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about the structure of E C G. Interpretation. Gonna talk about stable angina? Um, just cause I think that links quite closely to acute coronary syndrome. Um, we'll talk to the components of acute coronary syndrome, and then at the end, we've kind of got a one case based just kind of, uh, discussion kind of thing. Um, I have the chat function open. So if anyone wants to ask questions, um, at any point, just pop them in the chat, and I'll try to answer them at the most appropriate time. Um, if you guys have issues hearing me or slides again, just put it in the chat and hopefully we can remedy that. Um, so let's get started. So the first thing we're going to look at is E c G. Interpretation. Um, I've put here the structure that I use. I think it's a fairly standard structure. Um, uh, and I think E C. G. S are very overwhelming. And I think the the key thing is actually having a system that you go through E c g sec gs are also something that you realize as you go through med school and you start working that It's a lot about the patterns. It's very easy to look on the C G and go, Oh, God, there's ST Elevation in one lead. But actually, if there's if you don't have ST Elevation within a territory on consecutively, it's And it's not to say that you can ignore it, but you're It's far less worrying than someone who's got ST Elevation within kind of territory or in consecutively. It's things like that. So the way I think is so, First, you need to make sure we've got the right is to do for the right patient. That's quite, um, important in terms of you have oscopies or paces or anything like that. They're really keen on. Make sure you identify the right patient. It's really useful to know if, at the time the CT was taken, the patient was symptomatic. When I say symptomatic, I mean, did they have chest pain? Did they have palpitations or were they kind of hemodynamically compromised at the time? Um, the first thing I start by doing is really simple as heart rate. There's quite a few ways that you can calculate it personally. The easiest way that I find is your E C G strip is 10 seconds. So count how many are waves and then times up by six, and that gives you a rough heart rate. Your rhythm is divided into two things. So one important question is, Is your rhythm regular or irregular? And again, the best way to look at that is looking at the gap between the are ways just because they're the tallest point, um, on your e c G. If you're really struggling, you can sometimes get a piece of paper. And if you put a line like a plain piece of paper over one E C G line and put a dot for every R, I usually use the rhythm strip at the bottom. Um, it becomes a lot more apparent or clear whether or not this is a regular irregular rhythm. Um, the other thing with in rhythm is whether they're in Sinus rhythm or not Sinus rhythm, meaning that every QRS complex is preceded by a P wave. So again, just go through the rhythm strip and see his epi way before every QRS cardiac access is, um, I think probably the most difficult bit or bit that people get very confused about your cardiac access is essentially telling you roughly in which direction is the main pathway of conduction through your heart. So it should kind of go from your right shoulder down to your left foot is kind of roughly the way that it's It should go, And we talked about kind of if it's normal, left axis deviation or right axis, deviation and access. Deviation by and large either means one or two things. Either you've had ischemic damage within the muscle or conductive tissue itself, which means that it can't go left or right or you've got 11. Part of the heart is larger than the other, so it dominates. Um, looking. You look at Leeds 12 and three or a B F. For that, your P waves pretty much just looking at the size of them. So you should have 2 to 3 up to 100 and 20 so up to three small squares is normal. You can look at the morphology. I think that's quite nuanced, so looking for, like, p mitral or people Manali. But I think at this point it's more about seeing Does your P wave look too big rather than anything else. PR interval is should be less than five small squares. If it's longer than that, you're you need to assess for heart block. Essentially QRS complex again. You want to essentially find out. Is it narrow or is it broad? Um, normally, it should be less than three small squares. If it's wider than that, we would class it abroad. QRS complex Your ST segment. You're kind of comparing it to your P R. So you you. If you say your PR is your isoelectric line, your ST segment in a normal E C G should be around the same level as your PR interval. So you're looking as it is it elevated, or is it depressed? Your T waves. You want to know if they're very tall, Um, or if you've got T wave inversion, so T wave inversion is normal in some leaves, and we'll talk a little bit more about that when we go through kind of esque emmick changes on the C G. But you want to always look for T wave inversion. Um, and then your Q t C is essentially will be polarization time and um Q t. C is the corrected version, which is done automatically for you by UM e c G machines. It should be, um, less than 1 54 50 in males and less than 4 17 females. Um, if it's longer than that, you're at risk of arrhythmias. Um, just note Q t See length. When an E. C G calculates this at the extremes of heart rate, either exceptional tachycardic or exceptional bradycardic, the machine's calculation is often not as accurate. So sometimes the cardiologist will will calculate that by hand. You can basically look it up online the formula and put in the variables it needs. But, um, usually that be something cardiology did if you were very concerned about someone, um, I'm gonna just talk to you about territories of the heart because I think especially around acute coronary syndrome, it matters quite a lot. So it's actually divides the leads into what portion of the heart they're representing, and the portion of the heart or the kind of side of the heart is representing also, then corresponds to the blood supply. Um, when I was talking earlier about kind of ST changes in a single lead or ischemic changes in a single lead. If I had ST Elevation in both lead one A V, L, V five and V six. That would really convince me that someone was having some kind of a scheming event affecting the circumflex artery. Meanwhile, if someone had a kind of a lead three and maybe a V one, uh, I'd be attempted. I would be less concerned about that because it's not consecutive. Um, and it suggests that that might be artifact or there might be some other reason why they have ST Elevation on the E C G as opposed to it being a blood supply issue. Um, I'm gonna talk. Move on to about 17 before I do any questions about kind of the e c g e c g interpretation. It was kind of just meant to be a quick recap, because there are a couple of BCGs to look out in this, um, teaching. Everyone's happy. We will just move on. All right. Um, so stable angina, ACS acute coronary acute coronary syndrome. Um, looks at unstable angina and stemi non stemi stable. Angina is almost you're precursor, um, to these conditions. So it's essentially where someone has reproducible chest pain, which is cardiac in nature but is relieved by rest or g t n. And when I say reproducible, it should never occur at rest. If someone is having chest pain at rest, that's automatically an unstable angina. So nice actually talks about some diagnostic criteria. So your diagnostic criterias and vaginal chest pain, Um, the reason they kind of labor, that is, I think if I have to ask any of you what, your differences for chest pain, you're you wouldn't only tell me that you thought it was a heart attack. You'd probably say something like, Oh, it could be heart attack. They might have a pneumothorax. They might have pericarditis. They might have reflux. There's so many reasons why someone has chest pain that you need to differentiate it a little bit between any old chest pain and cardiac chest pain. So, for for angina, it needs to be pretty convincing that it's coming from the heart. Um, and then you can either demonstrate that they've got, um, some sort of reversible ischemia on functional testing. So that's kind of your exercise, um, e C g s or stress echos. Um, or you can do a CT coronary angio. This is becoming far more common, at least in the London hospitals. We tend to go for a CT coronary angio first because it's very sensitive and secondly, that if we do pick up vessel disease, it really helps with planning as to whether this is someone who might need a cabbage or whether this is someone who needs E. C I or anything like that. Um, and then Nice also describes clearly what they what their classes anginal chest pain. Um, if someone came to you a stable angina, the kind of investigations to think about. So I've always divide mine into bedside blood's imaging and specialists because I just think it's quite as a useful system, and actually, it's often the order in which you do things. Um, one thing to be conscious of is nice. Always recommends that anyone who presents with chest pain in primary care or any other service if they're stable and they don't need emergency review in A and E or admission, they should go for a two week wait Referral to cardiology for a rapid access chest pain clinic. The primary aim of rapid access chest pain clinic is Firstly, it's run by cardiology cardiology. So they'll investigate or do basic investigations and order more specialist investigations for someone to identify the cause of their trips. Pain, Um, and they'll also give you guidance as to what treatments might be appropriate or how to go forward. Having said that, just because you're in GP and you refer someone to rapid access chest pain clinic doesn't mean that you shouldn't start some of the management before they go to the clinic, which we'll talk about in a little bit. Um, so I'd start with kind of your examination, your vitals, your E C G. Um, it's really, really useful in every setting. If you can get hold of a previous C C G. Now, not everyone has a previous C C G, Um, but if they do, having a previous CC'd to compare with really helps you identify whether something is an old change and therefore less concerning versus a new change. Um, in terms of blood says there's no blood, no blood test is such to test for stable angina. In fact, if you've got a tropp rise or your cardiac enzymes are elevated, that it's no longer stable angina, unstable angina. You're you're looking at an acute event then, so there's no need to do cardiac enzymes. But you should look for things that would make make angina worse. So cardiac risk factors. So testing for diabetes, looking at their lipid levels and then things that things that make but a higher strain on the heart, which thereby would mean that the scheme is worse because you've got higher demand for oxygen by the myocardium things like looking for anemia. Thyroid function. Test hyperthyroidism tends to stress the heart more than hypothyroidism because of the tachycardia. Having said that, hypothyroidism is not something you can ignore if you're concerned in someone with a cardiac background and then use the knees is primarily for the electrolytes. So things like your potassium, one of them cause an arrhythmia. Um, LFTs is really only just because you you always need to do LFTs before we start people on statins. So that's quite useful to have, um, in terms of imaging. So echo ct angio exercise, E. C. G tests, um, and then more specialist things would be your invasive coronary and you angiography. So sending someone to actually have an angiogram Very rarely is this diagnostic. This is really only done if you think that you you're going to proceed and put a stent in at the same time. And the Q risk score is something I think most people will be familiar with. It's your 10 year mortality prediction for a heart attack and heart attack or stroke in the next 10 years. Um, we say that if you're less than 10% then you've got fairly low risk. Moderate is 10 to 20 and high risk is over 20. You're really thinking about starting things like statin at over 10. Um, there are a couple of other non invasive tests, which nice talk about which I think are quite specialist, but they're they're good to at least be aware of what the names are. So it's things like a myocardial perfusion pet or an MRI perfusion scan or MRI, specifically looking for stress induced wall motion abnormalities. Um, usually you because they're scans. You don't actually get a patient to exercise, and that's how you stress the heart. You use drugs such as adenosine or dobutamine to stress the heart and have a look and see what changes you see on the scans and and so thinking about management or moving on to think about management. Um, I always divide mine into conservative medical and surgical. On this slide, I'm going to talk to you more about conservative and surgical, and then we're gonna talk a little bit more about medical just because that's a little bit more nuanced or complicated. So in terms of the conservative things health, education, I mean, I think that that goes for pretty much every condition. But angina is seen as a chronic health condition, so you need to tell them what the condition is. You need to give them warning signs, and, most importantly, you need to safety net them for when they need to go to A and E. So for things like if you give them a g t n spray, the advice we normally give is please, you use the G t n spray when you get this chest pain. If in five minutes the chest pain has not gone away, take another dose of the G t n if after the second dose. So we're talking 10 minutes after 10 minutes of consistent chest pain despite G t n they need to go immediately to a and E, whether that's far ambulance or they can get themselves there. That's, you know, a little bit patient dependent. But that's the advice that we would give them, Um, and then your classic, you know, cardiac risk factor. So smoking cessation. Think about our diet, exercise and maintaining healthy weight. Um, and surgical is surgically you only really think about. Once you've done all your scans and tests and investigations, and it depends a little bit on the vessels that are affected so immediately, both PCI and cabbage will improve someone's symptoms. They'll improve cardiac blood flow. And to be fair, the impact on mortality morbidity are fairly similar. The big difference is is that cabbage is very, um, intense for a patient to go through. It's open heart surgery. Meanwhile, PCI is going through a radial artery to put stents into the coronary arteries, so a cabbage someone needs to be quite fit. PCI. Someone could be a little bit frailer, with more comorbidities with standard. Um, the other big difference is that cabbage has a lower reintervention rate. So for young fit patient's, the cabbage is actually preferred because the chances of them having to need another operational intervention with PCI is quite high. And then well, if you had, like a 75 year old who's got a couple of co morbidities PCI is perfect because their their life expectancy after intervention isn't that long that you're going to need to do any significant reintervention. Um, cabbage is also preferred for multiple vessel disease, so thinking about drug or medical management of angina. So I think about it in terms of your relief, your reliever. So that's your short term nitrate, which is G t N spray. Then you need to start them on an anti anginal. Um, the point of the anti anginal is to essentially increase blood flow on a more consistent long term basis. So you can either use a beta blocker bisoprolol or a calcium channel blocker, and we tend to prefer the adult size and the verapamil group. Um, you should warn Patient's about kind of the side effects that would be two blockers. It tends to be feeling faint or kind of loss of consciousness. Um, if one or the other doesn't really work, then you can try the other one. If they're still not responding. You try both together. Um, the third line would be a long acting night. One of these four. So a long acting nitrate. So, um, such a Such as, um isosorbide mononitrate. Um, if a bridion or nick a Randall or ran ran old Selene, Um, you can start with this if someone can't have a CCB or beta blocker. So your classic patient's that can't have beta blockers might be, um, an asthmatic. And then if if they had a bad reaction to a CCB, you might just move straight onto third line. And your last line is triple therapy, I would say I probably would only do beta blockers. CCB in primary care. I wouldn't really be starting any of these other drugs independently as a G p. So that would probably something that you need cardio input for, um, in terms of monitoring these drugs. So you should start them, and you should review them 2 to 4 weeks after they started the drug. If they're still having regular chest pain, you need to intensify the treatment. Um, secondary prevention is essentially things managing other cardiac risk factors, and this is fairly standard you'll see these same kind of drugs come up quite a lot as we go through this, um, or a C s kind of, um, tutorial. So aspirin a sin him bitters at all for statin and then treating any hypertension. So your aspirin is an anti platelet, so that's reducing the risk of you having, um, an arthroscopic plaque that then, um, has a thrombus and blocks your blood supply. Um, ace inhibitors, They act firstly, is an antihypertensive, but also have an effect on cardiac remodeling as well. And then atorvastatin is your lipids, which is one of the major contributor to atherosclerosis. So you want to get lipid levels to normal level if you can. Um, we're gonna talk about a C s itself now. But if anyone had any questions about, um, stable angina and just wanted to ask them now you can either run, meet yourself or write it in the chat. Um, very happy, Whichever you would prefer to. Um, if not, we will move on to talk about what a C s is, you know, happy to move on. Okay, um, so a C s is a syndrome or spectrum of cardiac disease. where your perfusion to your heart is compromised. Um, it ranges from a spectrum of having inconsistent but critical ischemia, which tends to be a more unstable angina to having full blown occlusion of vessels, which would be most of your stemi is so full thickness. My cardio infarctions, the most important underlying causes atherosclerosis. Having said that, you can have other causes, so things like very rarely you can have emboli within the coronary arteries. You might have the coronary artery dissection, which would still give you a kind of my picture. Um, and you can have vasospasm. I think the really classic exam question is someone who's, um, taken a lot of cocaine and comes in and they've got chest pain and they've got a scheme. It changes, and actually it's related to the drug rather than having atherosclerosis. Your major cardiac risk factors, which I divide into non modifiable modifiable because you can't really do it, do much about things like your sex or anything like that. So you're non modifiable be age, so your risk goes up as you get older, uh, being male, a family history. Although this is only really if they have cardiac or heart attack before the age of 65. After 65 you would say that's aged related cardiac disease and less likely to have a genetic or inheritable component and then ethnicity. So things like Southeast Asians, your modifiable risk factors, uh, smoking, hypertension, diabetes, having any dyslipidemia a high B m I or having a sedentary lifestyle, Um, and then thinking about how these patient's come in. So the reason we kind of group them into a C S is actually when they come into the hospital, when they present to healthcare, they all present fairly. Similarly, they will all complain of chest pain. And we'll talk a little about about what cardiac chest pain is in a minute. Um, they can have some sympathetic symptoms. So essentially your body goes into a bit of a fight and flight response, and you'll get things like people will be nauseous. They'll struggle to breathe. They'll be sweating. A lot of people will tell you that they feel really anxious, and they've got a sense of dread. So they get quite, um, they can get quite worked up about that as well. Um, the one thing to be really aware of Are you? What? No, no, you're silent and my patient's So these are patient's where they have a heart attack, but they don't present in the way that we expect, so they tend to be the two groups. I think that's most common is either women or diabetics. They tend, actually not to complain of chest pain. They come in with a slightly odd presentations of being a bit confused a little bit off feet. They might have palpitations. They might complain more of epigastric pain than chest pain on the left side. Um, they might come in with the features of heart failure. So Palmer edema or kind of a failure of their cardiac output. So syncope, um, I would generally say, have a low threshold to consider an M I if you're getting over 50 and anyone who in a woman or a diabetic, even if they aren't presenting with chest pain, the simplest way to X to exclude whether or not they're having a heart attack is just to do an e c G, which is, you know, a very non invasive test, very low cost, and no one's really, ever going to get mad at you just for doing an E C g. Um, so cardiac chest pain we talked about kind of. I've mentioned it a few times. Um, what I mean by that is a sudden onset central crushing. So people say it feels like an elephant sitting on my chest or a person sitting on my chest. It feels like a lot of pressure. Um, it can radiate either to the arms drawback. Um, usually on the left side, I think it's radiating to the right. That's quite a typical. Um, it will be constant. It won't change with your position. So good way to differentiate. Pericarditis is pericarditis gets worse with position. Similarly, it won't change with their breathing, so it's not pleuritic in nature. Um, it can have a trigger. Well, it usually won't have a trigger if it's, um an A C s. But for stable and I would have a trigger. I exercise. Usually it gets worse if they try and do things. Um, even in a see, even in a stemi, they might feel a little bit better if they don't do anything and they have g t n. That doesn't mean that the blood flows all returned, and it's all fine. Um, but you're just relieving the pressure on the heart a little bit and improving the blood supply in terms of working someone up. So if someone comes into my a any and they have cardiac sounding chest pain, these are the things I'm going to think about. So you're bedsides are fairly standard. I think they're fairly expected. I've added in a respiratory examination just because your differentials for chest pain often include the respiratory system, Um, in terms of blood test. So the big things that your cardiac enzymes so troponin is very sensitive, um, and creatine kinase MB, this one, the creatinine is a little bit better for delayed presentations. Troponin tends to have a very fast increase, but then also a very short half life. Um, troponin is one of the proteins within the car cardiac cells, which are used for contraction. And essentially, when you have ischemic damage, your cell membrane breaks and you get release of the troponin to the exercise space, which we can then detect on your blood tests. Um, if you you should do a troponin on presentation and if it's high, you're still going to do a repeat. But even if it's normal and it's it's very convincing cardiac chest pain or they've got some changes on the C G. Then doing a repeat proponent in 3 to 6 hours will also help you. So even if they had mildly elevated and then it stayed the same, I'm more reassured by that than someone who's got a normal troponin to start with. And then it could ripples a couple of hours later. Um, I say 3 to 6 hours. So I think my trust says six hours. Um, it really depends on the trust guidelines, the longest I've seen in hospitals up to 12 hours, so you can see it very little bit. So I definitely check your trust when you start working. Um, and then in terms of the other blood, so a full blood count and using these again these are looking for things that would make the chest pain worse, will make the pressure on your heart worse, and then your lactate. This is a really good mark of how sick someone is with their heart attack. So if the lactate as raised, it suggests that not only is there heart struggling their heart's not getting enough blood, but their heart has been so severely damaged that it's their cardiac output has been compromised, and they're getting a skeptic damage in peripheral organs. Um, if someone had to raise lactate that I'd probably be talking to, firstly, cardiology. But also I see you HD you because they're probably going to need a fairly intensive support and then risk factor. So your glucose and your lipids imaging is your chest X er an echocardiogram Nowadays, um, if you go to a heart attack center, they'll have point of care. Echocardiograms. Um, they're called. They're called V scans just because they don't have quite the same definition or breadth of detail as an echocardiogram. Um, and the scans are really useful to help you confirm the diagnosis. So, firstly, if someone has an E. C G, that isn't very convincing of a heart attack, and you're waiting for their blood's to come back, if you have someone who can do a CT scan, they can quickly have a look and see if there's any what we call regional wall abnormalities. So essentially, when you look at the heart, the heart should contract in a kind of consistent, coordinated movement that that shows us or demonstrates a healthy heart in a heart attack. The area that's had a skeptic damage will no longer contract as well, and you'll have an area that kind of lags. So it doesn't really contract with the rest of the heart, and that would suggest that they've had some kind of insult. Um, the VQ scan can also help you if you if on an e c g it looks like it's an anterior, am I? If you VI scan them and the anterior wall is the one with the regional wall abnormality, it makes it really easy when you go for PCI because he's saying, Okay, we're just heading straight for that vessel. That's, um, supplying the anterior the anterior wall because R, E. C G and R V scan are concordant, Um, and then your specialist would be angio, which is also your treatment and then a grace score. So Grace scores are a predictor of six month mortality after a cardiac event, and it looks at things like your clinical history, your examination, the E C G and also your blood tests. Um, the Grace score doesn't really impact what you do for someone who has a stemi. But for someone with an end stemi, it will really impact what you do. So if it's a if it's over 3% it changes how you manage them. Um, just to be aware, your troponin can be raised for the causes that don't have to do with a C s. So just be cautious when you run a troponin. If someone has, if you know they have acute heart failure. If you know they have an arrhythmia or pericarditis on wildcard itis that can actually give you a falsely elevated troponin. Usually it will be between 10 to 100. You're not really gonna get triple figures unless someone's really on well, with another cardiac disease. Um, I think most heart attacks you start seeing convincing proponents will be over in the triple triple figures or in the thousands. Um, any questions about kind of just investigating someone before I very briefly talk about unstable angina? No. Um, there's actually not that much to say about unstable angina because it used to be quite different in terms of how you manage it. But the recent guidelines now have moved to kind of treat unstable angina in the same way that you treat an n stemi when they present into a any, um, but unstable angina is differentiated from an n stemi and that they have a normal e c g for them. So if someone had had a heart attack in the past, they might have abnormal ECG findings. But you don't have a new change. Um, and the biochemistry i e the troponin cardiac enzymes aren't in keeping with having had an acute event. Um, if they have these, then you think it's more likely unstable angina. You're still gonna start managing them as an end stemi. And we'll talk through that management. But rather than, um, rather than rushing them to PCI or anything like that, you've got a little bit more time to manage them. Patient's who are very well with unstable angina. You could potentially discharge after a few hours of observation within A and E. Um, but if I'm honest with you, most people who've got first presentation with unstable angina will come in at least for one night just to see just to ensure that that doesn't progress into something or significant um So we're going to talk about myocardial infarction now. So this is where you have, um, complete loss of or a critical loss of blood supply to the heart. Um, the major differences is you'd expect your cardiac enzymes to be elevated in both of them, but in a stemi, as the name suggests, you get ST Elevation or a new onset left bundle branch block. The ST Elevation has to be over 22 small squares in the chest leads or one in the limb leads. Um, that's what we would say is convincing for a stemi. And N stemi is someone who's got cardiac chest pain raised cardiac enzymes and any other ischemic features on the E. C. G. And both of these will need acute management. So just in terms of the stemi, this is these are the SCG findings you would expect, and, uh, the next few sides are a couple of BCGs just to demonstrate to you what they look like because it's all very well reading hyperacute t waves. But, um, actually recognizing that is slightly different story. So you start with hyper cute T waves. To be honest, it's it's quite unusual that you see this as the only thing on an E c G that would suggest, um, an M I. They can also resolve quite quickly, actually, because they can quite quickly, then turn into your T wave inversion. You ST elevation is kind of your classic feature. Um, you can have a pathological Q waves. And then, as time progresses over the early days, you would accept. Expect things like your ST to go back to normal. But your long term things that stand are your T wave inversion or Q waves. Sometimes the T waves go back. Sometimes they don't. This is why it's really useful to have an old E c G for patient's when they come in with chest pain. So Hyperacute T waves. Um, Hyperacute T waves are essentially T waves that are. They're very symmetrical, so they look very even. They've got a very broad based, though, and they look really tall compared to what you'd normally expect for a T wave. That's what we That's what I would call a hyperacute. It's slightly different from your tented T waves. Your tented T waves and potassium abnormalities are narrow based, so the big difference there is whether it's broad or narrow based. Um, they're quite classical of, uh, ischemia. If you see them, it very rarely means anything else. Your inverted T waves, they are a little bit more difficult. So and it should t wave inversion is totally normal and not concerning in a v. R um, in 23, aVL, aVF and V one and V two, depending on the patient and also the ethnic background, the T wave inversion may or may not be normal, and that's what I mean again when it comes back to previous CCGs. But, um, I would I would take any new T wave inversion that wasn't an avr fairly seriously. Um, and I'd probably get that checked just by a senior colleague Or have a look and see if you could find an R c c G rather than saying, Oh, it might just be a normal variant. Um, you definitely should not see t wave inversion and lead tooth two and V 32 v six. Um, other causes of T wave inversion just to be aware of is, um, in Children. Actually normal finding so pediatric e. C. G s are slightly different. I'm not really going to go into it just because they tend not to have stemi Zoran stem ease or ACS. But just to be aware, if you are ever given a pediatric E c g um, you can see t wave inversion, and that's totally normal. Um, other other causes of T wave inversion that are cardiac related to be things like a bundle branch block can sometimes give you t wave inversion because the repolarization is quite significant infected a PE hokum and also interestingly raised. Intracranial pressure can give you, um, inverted T waves. The next bit that we'll look at is ST Segment changes, so ischemia can either present as elevation or depression. If you have ST Elevation, you should have ST Depression in the reciprocal leads. And when I say reciprocal leads, I mean on the opposite side of the heart. So if you had an an anterior, am I you'd expect Leeds reflecting the posterior aspect of your heart to have ST Depression ST Elevation. Um, you can see that quite well. Here in um, the one and V two and V three, you've got that really high ST segment is almost a whole big square above your PR interval. Um, and then your ST Depression on this side, I think the best one to appreciate it in this aVL. And again, if you just compare it to where the PR interval is before the key RS, you can see that it's quite a few small squares below, um, again ST Elevation ST Depression on only because of because of ischemia. Um, ST Elevation in particular. So things like pericarditis but pericarditis. You get that saddle shaped morphology, um, other things that can cause it again. Left under branch left ventricular hypertrophy. Um, if you have a ventricular aneurysm as well, one really important thing to know which I think often gets missed when we talk about STDs and we talked about heart attacks, if we think back to the territory's, um, we talked about kind of anterior inferior lateral. We don't really recognize posterior as well. Um, the best way to I don't know if you guys have heard of kind of 15 Leedy CGs. So 15 lead E. C G is essentially where you add extra chest leads around going around the posterior of the rib cage. Um, we don't routinely do them, but we do them in patient's where we suspect a posterior m I. And the best way to determine whether you think someone has that on a 12 lead is if you look at probably the 12 V three. If someone had ST Depression in V one to V three, I'd be really suspicious of a posterior, am I? And I then want that 15 lady C G. And what you would expect to see is that the extra leads that you do then so kind of your your V 70 your V eight. They should have an ST elevation that you then see, um, our theological Q waves. So Q waves are a normal part of your QRS complex. Um, and they should be fairly small now. Pathological key waves are when they're over one millimeter, one small square wide when they're over two small squares deep, or if there, if the depth of the Q wave is more than 25% of the height of the overall QRS complex, so that it can be a little bit tricky to text. The ucg here that I've put is a really obvious, clear example. In real life. It can be a lot more subtle. You wouldn't really be expected to pick pick up really subtle, pathological key ways. But I think here I hope everyone can appreciate here. Then if if you follow along, you've got your P. And then as you can come into your PR, you see that it really dips down quite significantly before it goes up to your R wave. That really significant dip is a pathological key wave. These are late findings of ischemia, and they tend to persist for quite a while. So that's a good sign that someone's had a previous heart attack. Um, and then the last thing So left bundle branch block a new left bundle branch block. The rule of thumb is if someone has a new left bundle branch block with chest pain. You treat it as an acute ACS event until proven otherwise, um, left bundle branch block. So but every bundle branch block essentially will give you a broad QRS because your conduction pathway down into the ventricles is affected. And so you get that widening of the Q r s instead of these nice, narrow ones. So the first feature is abroad QRS. You'll then have. Um I don't know if you're familiar, but we isolate as William and Marrow. So a w kind of in your V one V two versus, um an M shape in your V five and V six would be a left bundle branch and then marrow. So the opposite and m kind of shape versus a W would be your right bundle branch block. To be honest, it's quite difficult to appreciate that I think here is actually quite a typically CG in terms of If you look at V six, I think you can all appreciate you've kind of got a double notch on your QRS complex, and I can kind of convince myself that that's an M. Um, and that's kind of the main sign that this would be a left bundle branch block again. Your your B one V two. You can't really see the w that well and actually in in in most patient's, you won't get a beautiful textbook w and M. But if you see one and you've got QRS abroad QRS, I'd say that's probably good to be enough to say. That's left bundle branch block. Um, I have a couple of E C G s now which either, like someone to shout out if they can see the abnormality, or you can put it in the chat. Um, I'll give you guys a couple of seconds just to look through the c d. Um and then just walk you through that, um, once you've or talk you through the main findings. So if anyone can see and fancy starting out or putting in the chart what the main findings are for this first E c g. Yeah. Great. So someone's mentioned an inferior stemi. Um, so and someone else has talked about right Bundle branch. So we've got ST Elevation quite convincingly and lead to to and lead three. And I'd argue that you can see it in aVF as well. Um, and that is all three of the inferior territories, and that would be supplied by your usually by your right coronary artery in most people. Um, so I would say that's quite a convincing, um, inferior. My you can also see in aVL, which would be your reciprocal lead for an inferior stemi. You can see a bit of ST Depression, which helps me decide that this is This is definitely an ischemic event of some form. Um, someone mentioned right bundle, bundle, branch block. So I can kind of see why, in terms of that, the QRS complex is at least in the early chest. Leads look a little bit broad, but there are actually, I think, just on the borderline of three or just above three. Um, and actually, as you go through two v six, they're not consistently broad across the across the whole, um the whole e c g strip. Um, what I think can sometimes look like a right bundle. Branch block is actually here in 23, where your ST segment is so high, it looks like it's creating that m shape. And it looks like a continuation of the key RS. Um, but it's actually just it's just the ST Elevation there. Um, so I'll move on to E C G two and again if you want to shout out or put in the chat where you think the abnormality is. Okay, so we've got a couple here, so I'll talk through the answer. The main things here is I have a look at this E, c, g, and I'd probably say V two V three. Um, the 506 definitely have ST elevation and lead one. So I probably say that this is a little bit of an Antara lateral m I, um if you have a look, you can see ST Depression in three and aVF and that would suggest because that's inferior. So that would be in keeping with kind of an anterior lateral. Um, and it would be the circumplex artery that's affected. Yeah, um, in terms of the someone's mentioned left hyper tree. So yeah, you're you're quite right. Actually, the QRS here are really deep now in someone who's having acute chest pain. I would if if this was someone who was previously well and fine. I you know, that's I think it's quite reasonable to query left hyper tree in someone who's having an acute event. I e. They're saying I have chest pain at the time of E. C. G. The first thing that you need to be concerned about is actually more left heart strain. So it suggests that something is putting the left side under a lot of a lot of strain, and that would be in keeping with having an m. I obviously, if you treated there are my and this persisted. Um, I would be more concerned about hypertrophy, and then an echo would be really useful to evaluate kind of the thickness of the cardiac wars. Um, I think people talked a little bit again about bundle branch block. It's bundle branch block is really difficult. Um, again here. Actually, I find bundle branch block the easiest. If you look at the rhythm, strip along the bottom, which is usually your lead to. And if you look at the QRS complex is here, they're actually still pretty narrow. If you're looking from the first point the bottom point. So I'd still say that's actually that's still acceptable. I wouldn't necessarily be concerned about bundle branch block, but it does. I do appreciate it because it comes quite difficult when you start getting a lot of ST segment changes to differentiate where your QRS complex ends and your ST begins. Um, again, unfortunately, one of these to come with a little bit of practice, but keeping your structure really helps. So this is your last one? Um, this one's a little bit trickier. Um, but again, if you just want to take a little bit of time and have a look and see what you think might be going on for this patient with the C c. G. So if anyone can spot any abnormality, um, just pop it in the chat. If not, I'll walk you through what I think I can see on the C C G. Yeah, So the really big things are your ST depressions in V one v two V three and you do have a little bit of elevation in your lead to so that lead to I would worry a little bit less about your two and you're six. Um, just because they're not they're not consecutive with anything as such. Um and they're not. They don't belong to the same territory. But the big big thing is V one to V three, your ST Depression. And so this would be an E c G where I'd be really worried about a posterior, um, m I. And that's where I'd want to get 15 d d. C g um, and the thing about posterior am I so they can be a little bit difficult when it comes to treatment. because 70% of people are known as um, right right dominant in terms of their coronary artery circulation, which means that the right coronary artery will give most of the posterior supply in a couple. It will be supplied by both the right circumflex and the left circumflex, in which case you can get a little bit more of a complicated picture. Um, firstly, heart block. I think it's just on the border, so I'd probably say, Probably say that's on the border of what's acceptable. I might repeat that, but I think it just comes to five small squares from the beginning of the end. Um, but it's a little bit difficult to see on this, but yeah, it is. It's very close to being prolonged. Um, and then so thinking about management so acute management we talk about them is an unstable angina, So I've kind of written it out. It's kind of a list or step wise, because I think that's quite useful to think about, um, your standards. I suspect most people know of the the pneumonic Mona bash, so your morphine, oxygen, nitrates, aspirin and then bash for your long term. So beta blocker ace inhibitors that statin, um, and so forth. But I think it's quite useful. We're slowly moving away from it. It's really useful just to keep those. Those are the basic principles. But just to be a little bit aware of some of the other kind of things that we think about so oxygen we no longer give to everyone. Um, we're becoming more and more aware of things of the damage of, um, over oxygenating someone. So if you over oxen, it someone, you increase the oxygen free radicals and that can be just as harmful as having low oxygen levels. So we actually only give people oxygen. If they're saturations, require it. Everyone gets loaded with 300 mg aspirin. Um, I think this is one of the doses that you should just memorize off by heart. It's the standard for N stem ease and first Emmys, and it is barely. It's one of the critical medications I think that you'll ever have to give in your career. Um, then g t n spray be careful with G T n spray. So, um, it's an excellent, excellent drug. It can really help someone. It can really settle someone that can improve their saturations the people to be careful about g t n with are people who are hypertensive. So if someone has had such a big heart attack that they're they can't keep maintain their BP, giving them g t n, which forces vasodilate Asian, I can put them in an arrest or put put them in quite a dangerous situation. So just if if they've got a really look, if they're hypertensive already, I would just hold off the g t n and either get senior advice before giving it or just say, Actually, let's let's try the morphine and the anti emetics first, um so, uh, cardiologists really love either morphine or die morphine and the anti emetic of preference for cardiologist is either metoclopramide or ondansetron one or the other. Um, uh, the reason why metoclopramide is probably I'd say, first line on a national second line. Metoclopramide won't cause attack a Codec tachycardia. Some of the other anti antiemetics um do so you want to avoid those, um, and then your antithrombin treatment. So that's your funder paradox or low molecular weight heparin? Um, we tend to go for funding Paradox. Um, this is only if they're not for immediate PCIO if they're not very high risk of bleeding. Um, sometimes if your hospital has capacity, which, to be honest, is very, very rare nowadays, um, and stemi patients will still go for an immediate PCI. Which case? I wouldn't load them with a blood thinner. Um, and then at this point, kind of Step five is when you do your grace score ing, I still do Step six in regard. Step six is not dependent on the Grace School, but it does depend. Step seven and eight do so. Step seven. Essentially, if they've got, um, if they've got over, I think it's 1% on their grade score. You'll give them the second anti platelet. So either prasugrel ticagrelor all is the one that nice recommends. We're all very familiar with clopidogrel. Um, we It's now advised that you really only use clopidogrel people who are at high risk of bleeding or already on some kind of blood thinner. The reality of clinical practice those that actually clopidogrel is by and large still the most commonly used. And that's pretty much down to a cost reason rather than an evidence reason um, and then your PCI. So if they're grace score is over 3%. They should have their PCI within 72 hours, and they should not be discharged before PCI. So if your Grace score is over 3% it suggests you've got quite a high six month mortality. These people need to be admitted, and they need to have an urgent PC. I Now, if your Grace score is less than 3% there's a bit of wiggle room. You would always admit these patient's because that you know you're giving the blood thinners. You're starting the monetary treatment. You need to educate them about the condition, the fact that they've had a heart attack, if you can get them a PCI within 72 hours. Most people would like to do that rather than send them home. But the reality of waiting list is that that's ready the occasion. So if it's less than 3% the whole point of admission is to stabilize them, make sure that they're m I does not progress and then give them, um, start them on long term treatment and then you discharge them with a view for an urgent outpatient PCI at the next available point. Um, so that's kind of in stem. Ease and stem ease are fairly similar, except that you don't calculate any score ing you give. Everyone gets this full list. Um, the only discrepancy being in the last point. So you'd always admit them a give oxygen aspirin, you would load them with either too Cockerel, prasugrel or clopidogrel. Prasugrel is the preferred, um, if they're going for PCI, it is also the most expensive and therefore actually not that common yet in clinical practice. G t n again. But be careful. Their BP and morphine and antiemetic and then the definitive treatment. So you want PCI, so it's within 100 and 20 minutes of them turning up at the hospital. So you've got two hours from the moment someone walks through a and E with chest pain, Um, and you can do it within 12 hours of their chest pain. Having started, Um, there's a little bit of a kind of gray area, so patient's who come in and it's been more than 100 20 minutes, or the chest pain has been going on for more than 12 hours. But who have either Continuing dynamic changes on the e c G i e. C g is continuing to change, suggesting that the ischemic ischemic insult is ongoing. All patient's who become critically unwell. So someone who can't maintain their BP someone who become, you know, has a loss of consciousness because of the m I. Realistically, these people in a life threatening state, it doesn't really matter when that started. If you don't clear that blockage to their heart, you're not going to get a good outcome. This does obviously have to balance the risk of putting someone on an angiogram table. Um, so just it's a bit of a discussion, but there is that gray area. But for the exam purposes, I think most of your cases will fall within this, um, within this kind of 12 hours one So 100 20 minutes of presentation and then thrombolysis is now only a PCI isn't available. Uh, in London, that's very rare. Outside of London, a lot of units still do thrombolysis and the preferences streptokinase and then must be in ICU when they have this. Um, so think about long term management. Long term management. The same for everyone with a C A C s. So we divide into two cardiac rehabilitation, which should be they should be referred and assessed by a cardiac rehab team within 10 days of discharge. They look at things like physical activity, so getting, um, slowly building up exercise tolerance lifestyle advice would include things like driving so you can drive one week after you have an angiogram. Um, if you've not had an angiogram, you need to wait four weeks after a cardiac event. Um, if you have a further planned procedure, you cannot drive until you've had that procedure. And it's been four weeks after, um, you advise as well about sexual intercourse, which something that's missed out a lot. Um, they should abstain for four weeks, really? And then it's fine. They can go back to as they wish. Other lifestyle advice would be smoking cessation and then think about kind of diet and things like that. Your secondary prevention is all around about reducing the risk of a future event. So drool, anti platelet therapy, aspirin and clopidogrel or ticagrelor prasugrel. Whichever one was started in hospital, they have to take both for one year. If they had a stent. They need aspirin. Lifelong. Um, if they didn't have a stent put in I someone who had a n stemi and then didn't need a stent. Um, then it will stop. Then you can stop the second agent after a further year. So, um, either two years of treatment or lifelong. To be honest, most people will stay on it. Lifelong, um, a beta blocker, Um, an ace inhibitor, Um, and high dose statin. So you're 80 mg of atorvastatin and then spironolactone. This is really only used for people whose, um, ejection fraction are affected by the M I. Um, the reason for that is it's really good for cardiac remodeling. Um, it doesn't really change the heart attack risk. It changes their risk of developing heart failure. Um, and then the other thing that's up and coming is not yet in the nice guidelines. But I suspect it will be in the next few years. Is your SGLT two inhibitors. You may be familiar with them, so it's you're kind of empirical flows in or your drugs ending inflows. And that I use for type two diabetes is not quite yet understood how, but it's, um the SGLT two inhibitors. Also very good for cardiac remodeling. Um uh, and a lot of cardiac centers are starting that in patients who are diabetic who have an ACS event, Um, and then thinking about complications, I added this in many because I think it comes up as quite common exam question. Um, we have a pneumonic or I had a pneumonic, which is Darth Vader. It's really I think lots of people are aware of it, but it gives you a kind of a brief overview, so d being death. A arrhythmia are for rupture. So either a septal papyri muscle ventricular tea for tamponade h for heart failure, and then your Vader's valve, disease and aneurysm dress the syndrome E for thrombo bowl thromboembolism and are for recurrence on the side. I haven't put that on there yet because I think it is also helpful to categorize why they happen. So you're ischemic complications. Are your re infections or your in fact getting worse? Your mechanical is essentially everything that happens because some tissue has died. So some if a portion of the ventricles died, you're at risk of heart failure because your heart can't pump properly If you're papillary, muscle has died. You're at risk of mitral valve in particular mitral valve regurge, which then in turn, puts your risk of heart failure. If a portion of your ventricles died, you lose muscle, then it becomes quite thin, and it's scar tissue essentially under pressure of beating the heart. Over time, you're at risk of that dilating and becoming an aneurysm, which could then rupture. Um, similarly, if you have an infarct on the ventricle so the heart bit between the left and right, um that become can become weakened. And that can also rupture It with me is basically, if any part of the conduction pathway, um, dies as a part of ischemic insult. Um, then you're at risk of arrhythmias. Um, and then the last, the last one Inflammatory Dressler syndrome. Um, not very common, actually. Um, massively, um, features massively an exam Question's classic dresses syndrome is a man who's had a heart attacks about 6 to 8 weeks ago presents to a and E with chest pain again terrified of a heart attack. But actually the chest pains pleuritic it changed with positioning. Um, dresses syndrome is a It's a non infective pericarditis, and you treat it with high dose aspirin. So you just increase that aspirin dose, monitor them and see how they go. Um, so I've just got a case to go through. It's only got a couple of questions, so it shouldn't take too long. So I'll read the case out, and then we'll go through the questions and again if you just start them out and put them in the chat. So you've got a 65 year old gentleman who comes to A and E with central chest pain, which he describes someone sitting on his chest and the pain started 30 minutes ago and is going up his left drawer. He's vomited twice in his feeling, quite sweaty. He's never had pain like this before. He's a current smoker with a 40 year pack history. He's a type two diabetic on diet control with a B M I of 32. He's not on any regular medication with no significant family history. He comes into your Ernie, and his heart rate is 100 and 20. His BP is 110 of 80. His saturations are 92%. His temperature is normal and his respiratory rate is 18. So this is the gentleman who's come in. What's the most appropriate next step for him? Um, so whoever just pop it in the chart of what you think is the most appropriate thing. Mhm. So which one of their 1 to 5 which you say would be your of the options on here. So 125, which if it was an SBA, which one would you pick? Because I agree. 80 assessment is what I would do. Yeah, so exactly. So you would start with an 80 assessment and the first problem you would hit would be in his breathing because his saturations are low. So you're gonna start oxygen. Um, I'm really glad everyone picked up on this because I've done this before and everyone rushes to kind of give aspirin or E C g. Your a t e is essential. It doesn't really matter what is going on with his heart. If his airway was breathing is compromised, those are more important. The reason we have 80 years, because that's the order in which, um, the order of importance. So you start be so you you put my oxygen. He seems kind of settled. He's all right. You can start your assessment. So you you've done your cardiac exam. Um, and you can't really, You know, heart sounds wanted to Nothing else. Really? That convincing. So you ask your lovely nurse, you an E c g, and this is what you get back again. If you just shout out or put pop in the trap. What you think is, um what e c g findings you can see and what you think the diagnosis is? Okay, so I'd go through C, c, g. And first of all, I'd have a look, So the rate looks okay. I don't think he's Braddock Article hyper tachycardic. I'm fairly convinced there's a P wave before every QRS, so I'm happy with that. His access is, I'd say, borderline normal, even though so one and three, even though they're leaving away from each other and then which could suggest the left axis deviation if you then look at lead to the positive and negative in flexion of fairly much equivocal. So I would suggest it's physiological. So I'm not too worried about that. It's QRS look narrow. So that's good. And then I start looking at ST segments, and I agree. The most obvious outstanding is V two V three V four V five. They have significant ST Elevation. You can see the ST segment. It's quite a few blocks above the PR interval before, um, I would say that I think I can probably see a bit of ST Depression in V three and particularly look at the last one just before ABF. There's a little bit of ST Depression here, so I'd say if they've got ST Elevation in four consecutive leads, Um and that's kind of anterolateral izing anterolateral stemi is exactly what I would probably diagnose this patient with. Um, I'd also say here, actually, the T waves do look fairly hyperacute. They're quite tall, they're broad, and they're very symmetrical. So, um, that would also be in keeping with a stemi. So we've diagnosed are lovely gentleman with a stemi. So what are you going to do next for him? Um and what are you gonna do next and thinking about the thing that would treat the underlying diagnosis? So either 1 to 5, whichever you think is most important, give you a few more seconds to have a look at that and decide what you think. Yeah, great. So I think the thing that's really going to change his outcome here is me giving him a dual anti platelet. So, um, for this gentleman, I've I've offered you to Calgary. Lol. Obviously you'd go with whatever. Um, whatever is available at your trust. Um, and then I would, Yeah, if he's a stemi, so he's gonna have to go for PCI. So I'd load. Um, in reality, what you do is you load them and you basically fast people get in contact with your cardiology department, and they often have urgent cath labs. Um, I don't know how many of you have access to or have abilities to go on placement. The heart attack centers at your med schools, but if you have, if you have the ability to go, I highly recommend going, um, it's actually really valuable experience. Um, so So this lovely gentleman was admitted to hospital? Um, he had his PCI. We actually managed to get him to the PCI lab within 60 minutes of his arrival. We put two stents in, um, and he's been fairly well after, um, he's now coming up two day three of his admission, and we're talking about discharging him. You're the F one on the ward, and you've been asked by a consultant to talk to this patient about his cardiac risk factors. Um, and specifically, the ones that we can do something about. And this is all about in view, trying to prevent him having another heart attack in the future. Out of the five options here, can you name all of the ones that would be relevant to this conversation you're going to have with this gentleman? Just put the numbers in the chart. Give me a couple more seconds. Okay. So yeah. So 24 and five. So you're smoking. You'll talk to him about smoking cessation. Something about nicotine replacement. You might need to give them a little book counseling around that, Um, if someone has a cardiac event and as a type two diabetic. So if we remember, he was on diet control, but his b m. I is about 32 so I'd really be having a conversation with him about, um, starting medication for his diabetes. Um, And for, um, talking about losing weight. You If you have a cardiac event. You really want to have really good control of your blood sugar. So you're really aiming for well controlled HBA one c um, and then obesity. So it's B m. I was 32. So really, um, thinking carefully about would it be useful to in to have a referral to dietetics? Does he need to think about kind of his exercise and increasing how much excite he does? Um, so moving on to the last question, Um, so after his PCI, the patient is asking how long he needs to take his blood thinners or anti platelets for, um, for this patient, which one would be the correct answer out of the five? What would you advise him? I'll give you a few more seconds to read that one. Yeah. Great. So he needs to continue both for a year and then take aspirin. Lifelong, because we put two stents in. Um um, that's the end. So I have the QR here for, um, the feedback. I'd be really grateful if you could fill it in. Um, I'll stay on for a little bit if you guys, um, have any questions, um, at all. Just put them in the chat. Or you can ask me directly. Um, I know previously and talk. Some people have wanted emails, which I'm more than happy to give out again. If anyone wants it to contact me. Um, just ask in the chat. Great. Well, if there are no questions, I will let you finish sitting in the feedback. And I'm sure the organizers we'll, uh, go from there. Thank you very much in a, uh, I will close the meeting soon. So if you haven't filled in the feed book from guys, please fill it in. Hi. Hi. Can you hear me? You left. Hey.