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Whilst I say hi to everyone. Thank you. Ok, guys. Um Please let me know if you can hear me in the chat. Hello? Can you guys hear me? Sa can you hear me? Uh Yeah, I can hear you. I think um some people are put in the chart, they can hear you as well. So, oh, I can't see the chat. Yeah, a few people have said, I think, I think we're ok. Oh, I can't see any messages on the chart. Sorry guys. All right. Fine. Um I'm Anisa, I'm sure you've been to the session before. You already know that I'm one of the speakers. I'm one of the people that put together the teaching program. Hamza is one of the f ones on the team and he's doing his um clinical scenario on chest pain. Uh Now chest pain is probably one of the most common things you will get bleed for when you're on call and it can be when you're clocking a patient down in A&E or it can be someone who's been admitted into the hospital and has been there for a while. So essentially everything that Hansa talks to you about in today's session. It's how to manage when you're on the wards and you're briefed for someone that has chest pain or if you're clocking someone in A&E that needs to be seen by the cardiology team. Um And the focus is on mis and just any of the differentials on what you should be thinking about and how to use your resources in the NHS. So I hope you guys learn from this session and you feel confident with your plans when it comes to anyone that's coming in with chest pain, I'm gonna let Hans speak now and I'll just switch my mic off. If you have any questions, please feel free to type in the chart. I'm not sure if you guys can use your microphones but just type it in the chat and we'll be happy to answer. I'm gonna stop talking now. Ok. Hi. Uh, can uh everyone hear me if someone just pops a message in the chart? Just so we know that everyone can hear me. Yeah, perfect. So, uh, like I said today, we're gonna talk about uh cardiac chest pain, uh just how to manage it in, in, in acute setting. Maybe when you're on your call, on calls and er, get bleeded about some chest pain just going through what, what, what we would do, how to manage it, what investigations we'd like to do. So we'll kind of start off by kind of going to a bit of a a case based discussion. Um So let's say we get a patient that comes in a 65 year old male has presented with chest pain. So if you want to just start typing in the chart, what questions you'd like to ask this patient? My what you'd what you'd start with? Yeah, you guys can just type some, just some questions in the chart. Perfect. Thank you. OK, so you got a few coming through. You got sight when it began. So can you think of any others? So usually what I tend to start with is I tend to start with my Socrates. So perfect. Thank you, Lennon. That's all. Yeah, intensity. Sight of pain when it started. Ok. So essentially, yeah. So what's important is, is the site. So where, where the pain is, where, where's it started? Uh, the onset, is it sudden, has it been gradual? Er, the character is important? Er, you wanna know the nature of the pain? Is it sharp pain? Is it stabbing pain? Is it crushing pain? Is it, is it like a tearing pain? These are the sort of questions that you want to look out for? Uh, again? Yeah, like you said that radiation, where is it spreading? Uh I guess important with chest pain. We wanna look for any radiation to the arm, to the jaw, to the back. These are important signs that we should look out for. Uh, again, yet associated symptoms. Someone has mentioned uh, sweating, shortness of breath, uh, some nausea and vomiting we can get sometimes, uh, the exacerbating factors are important as well. And, uh, er, severity again, er, what's important for Ard has pain is the character. One important thing to look at is a character. So the way they describe the pain, uh, what's very, what's quite, er, common in mis is we get this kind of crushing pain that's quite common. Um, again, family history, but we can, uh we can pick that up depending on. So if it's quite acute presentation patients in a lot of pain, you might not bother with a family history, but it is still important to try and pick, pick it up if we can. And uh past medical history is also we, we should probably ask about past medical history. Any risk factors that could have led to this, er, Mr or, or Mr or this c that might have led to this chest pain. So, m moving on. So some main important symptoms, as I mentioned. So quite important symptoms for an MRI would be like a central chest pain right into the back. So let's say our patient had these symptoms that we found so a sudden onset crushing that's radiating to his back and left arm and he's feeling a bit sweaty and clammy. So, er, next we'll move on to some of the differentials if you mind guys mind typing up some of the differentials that you'd you'd think if you, you met a patient with some chest pain. W what would get your alarm bells ringing? What would you be thinking about again? If you just write them out in the chart, we can just go through them. So you've got some, uh, the main ones. A CSM. I, uh, can we just think of any other differentials? Er, let's God's a good one and p perfect these ones that we should be looking out for these big main aortic dissection as well. So it is important that we look at the differentials, um, for some of the, for chest pain cos if it's not an M I course there, there are still some quite critical conditions that we ca we can have that can cause, uh, can be quite fatal if we don't treat them. Er, and someone mentioned pe, which is one that I wanted to start on by saying, uh, I'll just go through the ones that are, I've listed. So we've got M I angina P. So pulmonary edema can sometimes cause, uh, chest pain as well. So we've got reflux pericarditis and aortic dissection as well. So I think we got all of them, which is quite good. Ok. So in terms of investigations, so we wanna rule out some of these differentials and, er, again, we wanna rule in the ones that we, I think are most likely. So what investigations would we like to do for, for chest pain a game, we just type them in on the chart and we go go through them one by one. So if you're thinking, yeah, E CG. Perfect. Yeah. So Troponin is very important for mis it's good. Yeah. A CG. So can we think of any investigations that we do to maybe rule out some of the differentials we talked about also chest x-ray? Good. So we can check for uh pulmonary edema with the chest X ray and the D dimer. So this is D dimer is an important one. So, thank you, Lenny for mentioning that one. So why do we want to look at a uh ad dimer? Does anyone know what we're looking for with a, with a raised D dimer essentially? Yeah, the pulmonary embolism. Good. So I'll, I'll talk about er, er D dimer quickly. Just cos it is important. So why would we be doing the D dimer again? Like we said, er, to rule out the D pe and if the pe is positive, I just thought I'd mention this cos it is, er, it's important differential. So if a pe is positive, essentially what it is is it's a clot of the lungs. Um What, what we tend to wanna do for a pe is break down that clot just to help with that blood flow back to the lungs and help with the shortness of breath and pain that they're having. So it's important to start them on an anticoagulant usually we go for enoxaparin at treatment dose just to break down that clot. And um any long term er, coag anticoagulation to prevent any reoccurrence. Um, some of the causes of raised D dimer can be M I actually. So even if, if it is raised, it doesn't necessarily mean it is ap but important thing to note that if it's negative, we can rule out the pe so it can be caused raised by an M I stroke, it can be raised post surgery, it can be raised due to trauma. Infection can also raise the D dimer sometimes as well. So it's important to note that and renal disease. So I'm moving on to our, our, our next investigation and we'll be talking about Chon. So what, why, why do we think troponin is important? So, I don't know what troponin measures. It's ok if you don't, if you do, it's just good to know. Ok. If er, no one knows, I'll, I'll explain it myself. So, er, essentially din, it's a protein complex that we find in muscle fibers and it's a very important er, marker in er, muscle contraction. When heart muscle is damaged, we get this release of troponin, uh that essentially it is released due to the death of the heart cells. And a significant rise or prolonged elevation of the troponin is usually indicative of an MRI or some heart damage. It is important to do an e reporting if we can as soon as we are suspecting any sort of m I, it, it's good to do that early, early as we can and we tend to wanna do a repeat. Usually they, we tend to say it about six hours later, but depending on the clinical picture, if we, if there's high clinical suspicions, we can do that a bit ear a bit earlier. Um, and if it is raised, er, it points more towards an M I er, if there's no, if there's no change in um it's a bit or if there's no change or very little change in the troponin between the two results, then it's less likely to be an M I but that's not to say it's, it can be ruled out completely unless it's very low. So the next important thing is E CG you guys mentioned. So why is an CE CG important? So it helps us essentially to establish the degree of ischemia. So when a patient is having an M I, uh an M I is essentially a clot of the coronary vessels of the heart. So the heart's the, the vessels that are supplying your blood and oxygen to the heart essentially become occluded. This can be to a clot, it could just be general ischemia and an ST elevation is an indicator that there is ischemia. There can also help us identify the area which the, the embolus will be where the ischemia is depending on which leads are affected. So these are some of the er E CG findings that we, we, we tend to get with, uh with, um with a CS so we can get ST elevation. I don't know how m, how many E CG, how much of EC GS you guys have read up on. But uh essentially the main important one that we do want to look out for is this ST elevation. So if s the elevation to measure it, we wanna, if you can follow, if you follow this line, this is what we call the baseline isoelectric line. And we wanna measure the uh the difference from the baseline and see how much elevation that we have. It tends to be more than t two small squares is a significant finding and that's what we uh tend to call ST evaluation. You can also get ST depression. Uh You can get this in the reciprocal leads of the s um of the ST the in, in the leads that show ST elevation. But you can also get just ST est depression on its own. And you can also get some T wave inversion. So that same ST segment that's been elevated or depressed can also be inverted as we can see here. It's flipped and it's pointing downwards. So these are some of the main ones to look out for it's moving on. Uh Here's some er like, like we mentioned, so we've got the ST elevation, um reciprocal s TT ST depression, we can also get some hyperacute T waves which are indicative of early ischemia, pathological Q waves which are er tend to be a later finding. I'm gonna get T wave mo which also is a later stage finding and new left branch bundle block. These are all very important findings that we can see on ecg that point towards an M I. If you don't know many of these, we'll just go through them really quickly if that makes things easier. So the first one to look at is AQ wave, so this is a negative deflection that precedes an R wave. So I know it sounds a bit complicated. But essentially this is your R wave here if you can see me pointing at it on the screen and if you get this slightly er this this down stroke first, so it tends, it needs to be a deep, a deep line. So it's more than two millimeters on the E CG. And this is an indication of irreversible damage to the heart tissue. So this is why it tends to be a later stage finding that we tend to get um but it is important to look out for that. And then on the flip side, we've got hyper acuity waves, which is a sign of like more acute ischemia. So it tends to be quite in the early stages of the M I. And as you can see here, it's, it's, it's shown by this er this kind of dip and this er this peak in the um ST section, another one so far is er left branch bundle block. So this one, we get these dominant S waves in V one which is this deflection after the R wave and these monophasic ars in the lateral leads. Um We also have a few that I mentioned earlier. They're not present in this. That's an important finding of er left Bron branch block and we get this prolonged R wave time. So R wave time tends to be greater than 60 milliseconds. That's mainly in lead V five and V six. I know this all sounds a bit complicated. So, II will mention some er, websites that we can look at that can help us break down EC GS for E CG basics. Er, there's a really good website, er GKI medics. If you guys have heard of it, how to read an E CG, er, we'll just go through how go through how talking it'll go through an E CG from start to finish, essentially, starting with the rate, rhythm axis deviation, this sort of thing. So if you do get time, it would be worth er having a look at those and uh refresh, refreshing essentially. And to get more familiar with EC GS is another good website, Life in the, er Fast Lane. That's uh it goes through EC GS in, in, in a lot of detail from, er, from start to finish, breaks it down for you, explains it all one by one. So if you do have any ST if you do have struggles with EC GS, there are two websites I would recommend looking at. Ok. So I'll put an E CG up on the screen. Uh I'd say if you guys got a minute, if you wanna just start working through it, uh the best you can, um you uh just look, look for these important findings that we have mentioned, er, for mis and if you just write out your answers in the chart and we can just go through it once you guys are all done. So I'll give you a few more minutes for that and, um, if you just type it out in the chart and we can go over it together once you guys are all done. Um, and if you don't wanna go through the whole E CG from start to finish, you could just look at the important findings and we can go through those, um, just look at any pathology that you do see on the E CG and we can talk about those if you're on, right, more on the chat. Ok, good. So we've uh people start noticing the ST elevations in, er, leads two and three. So how do we know it's, er, ST elevation again? So we're looking at this, er, isoelectric line and seeing it's er, greater than two small squares of increase So if you see here, that's the ST elevation in lead two, again in LE three and again, a VF all done, there is also some ST elevation in V four and V six. So this is a lot, a bit harder to see, but there is a little bit of ST elevation here also. So you also want to keep an eye out for this. And again, in V six, this one's a bit more clear. He said at Johnson, he said there's your isoelectric line and again, there's your ST elevation. And if we look at the ST depression, so we come up to, like we mentioned, uh I think someone mentioned, er, in V two and V three. So we'll look at V two, V two, V three first again. So there's your isoelectric line and you see there's a drop of more than two small squares. So we're happy to say that's some ST depression. Again, if you look at uh V uh V three, we have some here as well. And again, in V one. So, although I think, er, most people, er, a lot of people, yeah, everyone's got that. That's good. So, moving on to another one. So this one's a bit more complicated. So I'll give you a bit more time to l look through it and work through it. So again, if you just look up for any of the patho pathologies that you, you've noticed on there and you can point those out. So I'll give you a little clue for this one. So some of the findings that we did speak about in the e slides were present here, so you can keep an eye out for those and see if you mention, er, see if you can notice them. Ok. So, so someone's noticed the uh the elevations in V 234. So if you can see this here, start looking at V two, again, it follows that same pattern of the er ST elevation from the er isoelectric line. And that's the same V two A V three, V four five and six. And then we have in V two and V four. So this is one of the um point fives that we mentioned earlier. So it's a sign for early ischemia, we have the er our hyperacute T waves. So if you, if you look back to the picture from earlier, if you look at this pattern, we can match that in A V two, V three and V four, I think you can see it best in V two. So again, this is a sign of a, a early sign of ischemia. We may have some T wave inversion. I don't know if you noticed this in A VL again, these are all very important findings er in mis things you should look out for on EC GS very indicative towards ECG I think uh Ram was er kindly pointing out er that there's also bigger mini, right? Would you wanna explain, er, what, er, bigger money is if that's ok. I mean, to be honest, I'm not fully clear about myself if, er, you'll type out on the chart and let everyone know what that is, if that's ok from what I remember it's um, is it the extra heartbeats, you have extra heartbeats are followed by a normal heartbeat. Um, I think I can explain it. It might be a, might be a bit better. So I think she's trying to, she's er unable to connect to her microphone. So I think for now we'll just carry on and when she's able to connect, we'll, we'll come back to it. So, one important thing about CG is that we can, we, we can use is the lead placements. So the leaf placements will help us identify where the area of infarct is. So we could split the EC GS up into essentially quadrants. And if you look at this diagram here, so your 23 and your A VF tend to be your infer your inferior side and uh it tends to affect these vessels here again, you later. So you one in EV O and again, in your V five and V six. So using, using this diagram, we can essentially identify the area of the infarct will B. So V one, V two B seal uh A seal arteries again, anterior and your V four and your V three So I guess that that's one of the important things of the EC GS, it not only helps us identify that there is ischemia, it can help us also locate the area of ischemia. So this can really be really important for further management down the line. So if we know where the er infarct is, it be makes just things a little bit easier to treat, especially when they go to PCR centers, for example. So just talking about what act, what A CS actually is. So this was our main differential from earlier. So essentially what it is is a reduced blood flow to the heart that leads to ischemia. And the ischemia means that your heart, heart muscles aren't getting enough oxygenation, which can eventually lead them to die out. And that's why you get this uh cell damage and the increase in troponin. So, uh we can first start by talking about unstable slash stable angina. This is not you reduced blood flow, but yet you tend to get a lot less muscle damage. Er don't really have any E CG changes and your biomarkers can be normal. Uh We've got non ST elevation M I. So it's like some pa partial blockage causing some type of damage to the heart muscles, but it's not complete. Uh E CGE CG changes we tend to see can be ST depression, T wave inversion, which we saw a bit earlier or there could be no E CG changes at all. Then we have ST elevation mis. So you might have heard of the stemi. So that's when you tend to get the complete blockage of a coronary artery and that causes a lot more significant damage. So imagine that the arteries is completely occluded, no blood is passing through and we're not able to oxygenate the heart muscles so that eventually the heart muscles tend to start dying out. And we tend to note, note this by ST elevation on our EC GST wave inversion, new left branch on the block and again with our raised biomarkers such as aponin. So this is a, a really important uh classification that we essentially use to classify the um essentially the risk of an M I. So if you, if you guys ever heard of it, there's a really a really good app that we use called er MD Coc and it's just got a lot of the calculators that we have for calculating risk or like wells score, Glasgow Blackford score. So, calculating mortality and risks of different conditions. It is really good app to download. If you haven't got it, you can get it on your phone. If not, you can just type it in on, on the internet and you should be able to get that up. So essentially using the history, the ECG findings as well as like risk factors on our troponin. We can essentially classify our patients into different risks of having an M I, and we can use that to guide our management of it essentially. Er so moving on to like our immediate management um of, of if, if we suspect a CS uh our immediate management. So the important things that we need to look at is er getting that pain under control. Um also try and return up circulation back to the coronary vessels. So uh nitrates is a good. So we, I use this um acronym Moner. So mona am being morphine. So for the pain relief, all oxygen. So that's only if it's needed. So if, if the patient is saturating, well, we don't need to put the oxygen on, but it's if it starts, if it start to desaturate. So oxygen starts to start dropping by like 94%. Uh we wanna put a bit of oxygen on there just to make sure they are oxygenated. Uh nitrates are very important. So, nitrates what they do is um they help open, they cause vaso dilatation. So this is really important cos this can help with the blood flow back to the coronary vessels, which can reduce that ischemia and reduce that heart er that cell death. But you have to be careful with nitrous cos it can also drop BP. So be sure to keep an eye on that. And the main one, very important one is the aspirin. So the aspirin is essentially gonna be your blood thinner, which is gonna allow that better. Blood flow to the heart. So, the, um, what we tend to do we use here is Aspirin 300 mg. And we're gonna give that a stat. So that's essentially immediate management for any sort of a CS. These are things that you wanna be, uh, you wanna be aware of. So, if being bleached about these are the medications that you wanna be thinking about and the management. So, um, so we've talked about our sties and Nstemi, um does anyone know how to manage a sty or what we would do? Uh it just popped up on the slide there for a second, but I don't think you had time to read it. So if um if you guys want to start start talking, talking through what um what management, you know, for semi you right answers in the chart. OK. Someone's mentioned uh PCI. So if it's been less than 12 hours PCI, OK, perfect. So to move on to the management. So someone's mentioned the PC. So this is very important. This is uh essentially what PCI is, is if the PA so if the patient is presenting within 12 hours and the PCI can be delivered within two hours, then PCI tends to be our primary choice. So what PC is, is we'll use a contrast dye to assess the blood flow of the vessels in the heart, which is what we call angiography. So we'll just use essentially fluoroscopy er to look at how the vessels are perfusing and we can locate areas of infarcts using that. Once you've identified the area of the infarct, we can either widen the lumen or remove the, we can widen, widen the lumen essential. That's with a balloon, which is what we call angioplasty. And then what we tend to do is insert a stent which will help keep that vessel open and allow blood flow to return to the heart And we can start re re oxygen that area of um area of s of heart tissue death. Another alternative, if the PC is not available within uh two hours, uh that could be depending on a numer of factors. Uh patients, not, you're not able to transfer the patient, um patients too unstable, er then we may consider fibrinolysis. So essentially what fibrinolysis is, is injecting a fibrinolytic agent that will break down the fibrin and the blood clot, which will. So essentially we break down that blood clot, we can get that blood return back to the heart again. So it's, it's a similar concepts but just acting in different ways. So we can use our fibro agents. So you might have heard of alter players, streptokinase. We use these in strokes sometimes, but it's, it's kind of a similar concept where there's occlusion and we're getting uh reduced perfusion and we're not oxygenating those, those, those uh cell tissues which is what's ultimately causing the Mr. So, um we mentioned stemi and uh I think someone also talked about uh dual anti antiplatelet therapy, which is good. So with nstemi, uh which they're a bit, they're similar to, it's a similar, similar management, except what we wanna do first is we wanna use a grace score and if anyone's heard of a grace score before, but essentially what we do is use a grace score to assess a patient's six month mortality. Again, there's a calculator you can find on MD card, which will go through it quite e er quite easily for you and you can put along information and it can tell you the risk. So if the patient isn't on low, a low risk, low risk of having a having ami what we can do is we can um start them on our aspirin 300 mg, which we should have already started and then our d antiplatelet therapy. So that's uh tigre 100 and 80 mg. And if there's no bleeding risk or no immediate PCI plan, then we tend to add something called ferox. So that's essentially our conservative management of an end dey. Um However, if so that's, if the patient is low risk, if we have anyone who's high or moderate risk, then we want to do something similar to the stemi where we do an angiography within 72 hours. So the difference here is, is, is, is the time frame and we can follow on with PCI if it is indicated at that point. So it's again, assessing the, the um the perfusion from the blood vessels. Um And if it's poor, we can carry on with our, we can do our PCI, but it's less, it's less of an important. It's, the time frame is slightly less important. It's still important. Don't get me wrong, but it's less important than with the Demi I'm just gonna briefly touch on uh stable angina and unstable angina. Um So these tend to be less of an emergency but it just good and important to know of them. So again, it's similar to an Nstemi where we should start a CS treatment. If there is suspected a CS and er depending on like the certainty of the Angina and the clinical picture, we wanna patient will eventually need a chord to see the G degree of either narrowing of the vessel or blockage. And then if there is any need for PCR Thrombosis, it would decide on that. But it's a, it's a, it's a, it's a less, less of an emergency presentation. So some b some patients will just manage medic medically and with secretary prevention and we follow the fold of me clinic, er, others might need to undergo PCR with stenting, but it just depends on the patient and the clinical picture. Oh, sorry slide that moved on. Thank you. I can give you a second, just read, but uh essentially it's less of an emergency. It's more, it's less acute you can, um, it can be dealer dealt with in clinics just, but again, it depends on the clinical picture, it depends on how much the patient is in pain. Thank you. So, er, moving on to, we're going to talk about some risk factors quickly. Um, so we'll, what we, what, how we split risk factors is into modifiable and non modifiable risk factors. I think we'll just start by talking about modifiable modifiable risk factors. So you guys can list off any modified risk factors that you know of that can increase your risk of A CS or M I. So if, if you, if you don't know what we can, what we can do is we can break it down into. So the M I, we know it's caused by an occlusion or reduced blood flow to the heart. So if you can think of things that would reduce your blood flow and reduce your perfusion, that might help gonna you list a few in the chart. OK. OK. Good. So low cholesterol hyperlipidemia, atherosclerosis, diabetes. So these are all conditions. Can we think of anything that aren't? Um OK, perfect. So stop smoking, lose weight. So these sort of things can also um contribute to your risk of having an M I hypertension also. Well done. So now can we, so, so we talk about some of the mentioned, some of the modifiable risk factors. So anyone know any of the non modifiable risk factors that can increase your risk of having, uh, NM I or A CS. So we've got male gender. So exercise. So that's one of the, er, modifiable ones. But, yeah, go to bring. So these are the non modifiable ones now. So age, age is one. Can you think of any other ones? Family history, well done. Um, in terms of a race link, er, in my, I'm not too sure if there is a race link, but I guess in a way that kind of is. So, for example, South Asian families are high risk of diabetes. Um, that would inadvertently increase your risk of having an M II guess slightly. Yeah. Um, so just moving on to the risk factors. So, like we mentioned, so we got the modifier ones are hypertension, diabetes, hypercholesterolemia diet and exercise and excessive alcohol consumption. What's really important to know of is the hypercholesterolemia one. So what happens when you have too much, uh, LDL cholesterol in your blood, it increase your risk of developing atherosclerosis, which is essentially these plaques that build up in your blood vessels. And, uh, if you continue building up these plaques, what's gonna happen is your vessels are gonna get narrower and narrower. Um, so the, this narrowing of the arteries will reduce your blood flow. So you, if you imagine you've got a tube and it's just been filled in on the inside, less of the blood is gonna be able to pass through that, which as a result is gonna increase your risk of having this ischemia and increase your risk of having an M I. This can also break off as well. So it's important to mention. Um So that's this part of the plaque can break off and that itself can actually lodge in the vessel. And that again will reduce that blood flow and CRE er and cause an M I and some of the non modified ones. So we mentioned age uh sorry we mentioned um yeah, so age is one to be, be aware of. So as you get older, your risks are gonna increase um your risks increase a lot more after 45 in men and 55 in women. So mo moving on from that men are a lot are a lot of a higher risk of developing an mi than women. Um and another one, someone also mentioned family history, which is really good. So being aware of any any early cardiac death in the heart in the in the family is good to be aware of, especially uh with the younger patients, especially below 40 cos there could be an other underlying cause for that. And uh so we'll talk about risk factors, we talk about management. Um So finally, we just talk about uh secondary prevention, how we can we stop this from happening again. So what's really important is we do send the patient home on aspirin to 75 mg and this will be lifelong. And why we do this is this will keep the blood, uh it's essentially a blood thinner. So this will help reduce the rec clotting if uh blood has been thinned and it stops, helps reduce the occurrence of developing clots and embolism, uh secondary angio platelet that will also help with that. So that'll be er like clopidogrel, for example, we can give that with it. Um We also have atorvastatin. So what atorvastatin does? So, no, we mentioned the um high cholesterol atorvastatin will lower your LDL cholesterol. So by lowering it, it reduces the risk of developing further atherosclerosis. So it's very important to make sure that patients are sent home with this because we don't want, we want to want, don't want to increase that risk of them developing any uh Mr S in the future ace inhibitors and beta blockers um help reduce heart rate and BP. So beta blockers, for example, help reduce the risk of arrhythmias. So if you keep your heart rate under control, uh you're less at risk of producing er clots and you reduce that strain on the heart as well. Allow for good blood flow around the heart. Ace inhibitors will help reduce your blood flow. But ace inhibitors also help with vaso dilatation of the blood vessels, which is really important, which will help with that blood flow that we need to the heart tissue muscles. Uh We can also provide aldosterone for those patients with heart failure. So, heart failure can uh increase that strain in the heart, which can also uh lead to uh Mr S. So, aldosterone is a, essentially acts as a, a diuretic which will help get some of that uh fluid off the lungs, which can make things will reduce that strain on the heart. Again, reducing your risk of having an M I. So I tend to go look at these as by as, as the six A essentially. So, er for secondary prevention. So, aspirin or antiplatelets or atorvastatin ace inhibitors like a Ramipril er Atenolol or other beta blockers. So you don't, we don't always use Atenolol, we can use bisoprolol for example, but I use Atenolol. Um I remember it as Atenolol. So we remember that as a beta blocker and aldosterone. So it might be a, so another important secondary prevention we should look at is the lifestyle changes cos these are tend to be the most important prevention. It's like smoking, diet and exercise. All like we mentioned are modify risk factors. These are these things we can get under control to prevent that risk of reoccurrence from happening. So it's really important to focus on these and make sure that our patients do understand that these are increasing your risks. And once we get, once they're able to understand that we can prevent them, we can try and prevent that this happening again in the future. So I think that's um everything on secretary prevention. Has anyone got any questions? Anything that they're unsure about? I want me to go back to and we can look at again. Ok, looks like everyone's everyone happy. So essentially, uh, what we're gonna do is, er, that's the end of the powerpoint. Er, so what we're gonna do is we're just gonna go back and, uh, kind of go through the case and, um, just see kind of test yourselves on, on what we would do. So if we, um, come up to the start. So as you come back to our patient, so we'll call him Bill. So Bill has come in with his chest pain. Um, should we go through some of the questions that we'd like to ask again if that's ok? And what they, what are they really important questions that we should be looking out for? Good or Socrates? Ok. So let's say our patient has told you that he's got some central crushing chest pain that's ready into his back and he's feeling sweaty and clammy. So, what's our first investigations that we wanna do? Where do we wanna start with? So I tend to use, I tend to use this, er, acronym Bliss. So, what we start with our bedside? So what bedside investigations would we wanna do for investigations? Ok. Brim. We'll come back to secondary, er, prevention at the end. We'll just, er, we'll talk through the case a little bit again and then we'll come, we'll er, we'll mention that again. Ok, good. So our E CG. Yeah, that's our main one at the bedside. So then, so next we're looking at our, our labs, our laboratory results. So what kind of blood results are we gonna be wanting to do? Let's say Bill's a bit short of breath as well. So he's not got, got the chest pain, he's got a bit of shortness of breath as well. Good. So Paul's also mentioning the er ABG here, which is a good point. So if we, if we got any patients with shortness of breath, um we're unsure what the cause is and ABG is always important to do and the troponin, of course, so our markers for cell damage but our patients short short of breath. What's the um what's some of the results that we want to look out for shortness of breath, chest pain? Ddimer? Perfect. And uh again, we do nd IMA to art which is P D down, we mentioned troponin. So E CG. So I don't know if you guys remember, but so let's say this is Bill's E CG. So again, one of the important findings that we should notice on on this E CG, just the main ones point pointing towards a differential. Yes. So Iman, so yeah, so um for Macron was place so all I tend to use is is I'm sorry, I didn't finish that off earlier. I should talk about it. A little bit. So I tend to start with my bedside investigations. So your observations, any, anything that you notice clinically, anything from your examination, um, you might listen to the heart, find some heart sounds. So you mostly, mostly your bedside, tons of l that's your laboratory investigations. So any important bloods that you wanna look at, uh, for eye, um, that's your, your imaging. So whether you need an ultrasound X ray echo, these sort of things that you wanna look out for er S is your special test. So any specific s er special test that you wanna look at? Um you wanna notice how you cause more breathing your Murphy sign, these sort of things that comes in new special test. So I II tend to use that, that helps me out er good. So, um so man mentioned here so that the er inferior leads have ST elevation. So we just took that step foot further um and er tried to locate the area of the infarct, which is really good. So again, like I mentioned earlier, these EC GS we can use, we can use the area of the infarct, er sorry, the area of E CG change, we can match that up to where the area of the infarct would be. And it's a really good diagram to have a look here. So you can just follow the artery down and you'll, you'll know more or less where the occlusion will be or which area it will be in, it's well on them on. So, so what would the uh immediate management be for this patient? That's what we would do initially. So he's in a lot of pain. His, his, his chest really hurting. He's desaturating his uh oxygen sats to about 92%. What we wanna do. Shouting out in pain. Nothing seems to be helping. He's got some power seats small and needy. OK, I just run right, right in the chart. What our immediate management would be. Yeah, good. So I wanna get that pain under control. So we'll go for the morphine first. IV. Yep. Again, if it's desaturating, we'll uh give her some oxygen. So, but that, that, that's only if the patient's desaturating, if they're not desaturating, we don't need to give any oxygen. Um, so round about 9490 anything less than 94 we'd put him on some oxygen. So what's another important medication that we should give for uh the pain relief? And uh also mention it was for vasodil dilation earlier. It's really important in A CS. So uh so 300 mg, aspirin. That's good. That's for the uh the, the blood thinning aspect. I know. Two. Yeah, perfect. Just one more medication. That's uh that we missed out so far. That's really helped, can really help get the pain under control. Sometimes you're in emergency situations. Er, you can give this medication very quickly and uh it can cause it can, it can tend to get the pain under control almost immediately. Sometimes it's important to be aware of it. Perfect in the Keto and nitrates sublingual. So we tend to just give her one or two sprays under the tongue and a lot of times it come, it acts really quickly. So if you're ever worried and you haven't given it yet, it's, it's, it's a really important one to give, it can calm the patient down as well. It's uh it's really useful nitroglycerin. Perfect. OK. So moving on. So then we've got our, so let's say so we noticed that our patient has some ST elevation in the inferior leads. So we say so we think he's having a, he's having a infarcts of his right coronary artery, for example. So what would your immediate management be sorry, not your immediate management? So your man, so you've given the immediate management, what would you do now? What's the next steps mentioned earlier? So it's actually we've con confirmed our occlusion of uh being in the right coronary artery. And patients been presenting for this pain started six hours ago and the closest PC center is half an hour away. So PC, so he needs angiography. Perfect. And if it wasn't suitable for PCI, let's say it's, it's been 12 hours since the presentation, but the PCI center's three hours a day, what will we do instead? Perfect fibrinolysis. And um so let's say a patient was having an N Dey. Um but they, we did a grade score and the score was low risk. How can we manage this patient? Yeah, so we can just do a, a lot of times we can just get away with doing dual, dual antiplatelet therapy. So, aspirin tag and if there's, there's no bleeding risk or no PCR, we can just add some kind of paranox, but we do want to monitor them and uh they may need to repeat, uh may need angio to er make sure that the occlusions fully gone. OK. And then uh just finally moving on to, so we aware of the risk factors. So just secondary French anybody wanted me to just uh talk about it again quickly. So what's important here? So actually, we'll ask, I'll ask you guys actually, what the um so what, what would the second prevention be for a patient who has had an MRI has been treated for it? What medications we wanna give and what lifestyle changes would we recommend? So you might have noticed I do like my acronyms. So uh there's an acronym I mentioned for this one that might help you guys and if you can't remember all of them, you can just off a few of them and we can go over it again. OK. So Nikita's mentioned some of them here in the chart. So Aspirin Ace inhibitors statin beta blocker. OK. So I'll put it up on your screen. Uh again. So what I tend to use is, is the six days you might, you guys might want to use something different, but this is how I remember it. So the very important one is the aspirin 75 mg. That's gonna be lifelong. That's the most important one to remember. Er, and sometimes a second gender platelet, it's not always the case but can tend to give her a secondary platelet as well. Er, atorvastatin is important. Uh Does anyone, does anyone remember why the is important? Ok. So essentially the atorvastatin is gonna reduce our, our LDH cholesterol build up. And what's why, why that's important is when we get too much build up of LDL cholesterol, we can get this atherosclerosis that can build up in the vessels. So it's essentially this plaque that will um fill up the vessels, reducing the blood flow, cos it causes narrowing and this narrowing cos le less blood flow is passing through this narrow passage. We're gonna get less blood flow return on the opposite, on the opposite side, on the opposite side would be the heart muscles, the heart muscles. So if your coronary arteries get narrowed, you're gonna have less perfusion to your heart muscles, cos they're not getting oxygenated, they will eventually die off. And this death of the heart muscles is what causes the pain is essentially what your M I is. And then our beta blocker uh and our ace inhibitors, they're really important. So, uh firstly, the ace inhibitor will reduce your BP, but it also allows for vaso dilatation. So opens up your blood vessels to allow more blood flow to pass through them. And your, your beta blockers will reduce your heart rate, red, reducing the strain that you have on your heart allowing for proper perfusion. So it's to do with your preload and your afterload. Um and we also, yes. So it reduces the strain and it decreases the risk of any arrhythmias. So, for example, where atrial fibrillation is one risk factor. I forgot to mention er for developing uh a heart attack. So in atrial fibrillation, uh your heart's, your heart's not contracting properly at the same time. So what happens is you get stagnant blood and that blood will allow for clots to form. So that's why a beta blocker is important. It gets to prevent your risk of developing arrhythmias as well. And the lifestyle changes are what are the most important, one of the most important preventions the way I see it. Um because you smoking, diet and exercise are all things that you can change almost immediately and can start reducing that risk of developing reoccurrence. Ok. I think that brings us to the end. Has anyone got any questions or anything that they, they weren't too sure about? They want me to go over again. Sorry, I know that took a while. I appreciate your patience guys. Thank you very much. If no one's got any questions. Er, I'll hand it back over to Anisa if she's still here. Hi, thank you, Hamza. You did really? Well, um, I have a few things to add. Actually, the first question I want to ask is if in this case we had, let's say a 90 year old, male or female doesn't matter, but a 90 year old with multiple comorbidities, er, with a clinical frailty score of about six or seven. How would your management change for this patient that I've mentioned? How would your management change? Just type your answers in the chat. So, do you think a 90 year old that severely frail would be fit for PCI? Is my question? Yeah. So it depends on the patient. So if you have 50 60 70 it doesn't really matter how old they are, I guess as an sho or an F one, you are clocking someone with chest pain that probably has an end to me. Um, you start them on medical management and if you think it's someone that's frail and probably wouldn't have PCI, think the smart thing to do, would it would be to start them on medical management and write in the plan that you want to optimize medical management for this patient and you don't think this, this patient's fit for PCI, but you're going to admit them anyway, you'll always let the consultant sort of either the AM U consultant with uh would like sort of decide whether this patient should be referred to cardiology. But ultimately, I think what we all tend to do is refer to cardiology anyway. And let cardiologists decide whether or not they're going to do a PC. And I say that because I have seen a 90 year old in very good health who had a valve replacement surgery. So I guess cardiology is really unpredictable. Sometimes they do take elderly frail patients and do some sort of invasive er procedures. So clock the patient start them on medical management. Remember the, the plan is to optimize medical management and refer to cardiology, but you think that they might not be fit for any invasive procedures. In which case, the consultant who then post takes the patient might put a DNA R on the patient and optimize medical management and send them home. Or if they think actually this is a, a fit and well 90 year old that might cardiology might take this patient. Um They'll refer to cardiology but if you're not sure, I guess, speak to your seniors and if they say actually like it's just gonna be medical management at home, you can always put that in your plan and not refer, don't put the referral into cardiology because cardiology will see all the referrals and it's slightly inconvenient if you've referred someone that doesn't need seeing. Um but just discuss it with the senior if you're unsure and remember about the DNA R. So if it's again, a 90 year old very frail patient who's coming in with an N time, he has multiple comorbidities. You need to put a DNA R on that patient. Um I think I had one more thing to ask as well. Yeah, sorry. There's just one more thing I wanted to explain. So some of you will be working in A&E some of you will be working on the medical team. And I guess the difference between the two when you see someone with chest pain is if you're in A&E you're expected, you will see semis and, and semi. So if you're seeing a semi, you're expected to understand that the whole sort of getting a PC done within the time frame um and medical management aspect of things. And if it's an NSTEMI, if it's an N Sey and you're working in A&E your job is to give the patient, their loading doses of aspirin and ticagrelor and refer them to medics. The medics would then start the patient on the medical treatment, which is everything you can see on the screen. So the secondary prevention, this is everything you start the patient on. So when you start your patient on Aspirin ticagrelor, uh the daily dose and atorvastatin ace inhibitors, Bisoprolol, um you need to check the patient's medications. A lot of the times you know, some patients have already had previous MRI S and they might already be on antihypertensives and statins. They might be on like a small dose of statins which you need to increase to 80. Um, they might already be on Ramipril or they might have an intolerance to Ramipril. So you need to make sure you check the medications they're already on instead of just blindly smacking them on er, secondary drugs. But essentially if you're clerking the patient and you're on the medical team, so they've been referred by A&E just check and make sure that this patient has already had their loading doses for aspirin and ticagrelor. So if they have already had that, you need to prescribe the secondary prevention meds and you need to admit the patient and refer to cardiology. It's cardiology team's job to then decide whether this patient's having a PC or not, that's all going to be done on the cardiology ward. Um But as a medic, it's just putting the patient on secondary prevention and referring them to cardiology. But keep in mind things like age and clinical frailty score and comorbidities. Uh because there's no point referring someone to cardiology if they're really not going to take that patient and again, speak to a senior if you're confused. So yeah, as a medic, you probably won't see a semi because sties are handled by A&E team and they go directly for PC. Er, it's usually end semi. Can you get down to the difference? That's the difference between the two teams. Uh I think Rahma has something to say So if you guys have any questions, please ask and I think I'll let Rahma speak because she probably has something to say. Can you guys hear me? Yeah, I can hear you. OK. That's good. Uh I struggled a lot with that, Mike. Uh I agree with you, Anisa, everything you said. Uh Temi is a medical emergency if you see and it's the elevation and it's missed a lot by nurses or who, whoever is aging, the patient, we've seen stemi and even tic. So that's an emergency. We have a window for PC or uh fibrinolytic agents. So act immediately if you see uh an ST elevation uh and even non sties like even troponin aggravations, like always speak to a senior about it because a lot of them are a high risk. Uh Some of them will need telemetry uh or repeat troponin. See like if there's a troponin rise or if the chest pain is ongoing, just repeat the ECG if there is like a changes in the ECG that that might mean that the, the clot is still ongoing like there is still ongoing uh damage to the cardiac muscle, that's high risk. Uh So those patients like always be wary of them. Uh Do you guys have any, any questions? I think I want to add definitely. If you're unsure and you feel like the ECG is something you can't read, get a repeat. ECG please get a repeat. CG uh It doesn't matter how many times you do, it just ask for an E CG. Yeah. Yeah. If you guys have any questions, please feel free to ask. And also if you have any f one related questions definitely ask because s is here today. So now's your chance. I've also put the feedback form in the chat for you guys to definitely try and put in things that you've learned from the session that you didn't know about before. Oh, and one more thing with regards to um grandma, can I ask you to switch your mic off? Oh, sure. Thank you. Um With regards to um VT E profile axis. So this is something we spoke about in the previous session. And the one before that and Mi Rahma both mentioned that for every patient that you admit, you have to do a VT E form and you have to start them on enoxaparin and it's usually 40 mg or 20 if they have a lower EGFR or body weight. Uh Now, if someone's coming with chest pain and you're starting them on medical treatment for an nstemi, um and they need VT E profile access, I'm sure in the presentation Hams has mentioned Fonda Paradox. So in these patients, instead of giving them ox, we'd give them Fondaparinux instead. And then after seven days, it's changed to enoxaparin, but you probably won't even see that patient in seven days. It's just a general thing like if you're on ward sorry, I was going to say ward, er, if you're in cardiology, you'll notice that after a, a couple of days the Fond is switched back to Enoxaparin. But if you're clocking the patient, bear in mind you're starting the patient on Fondaparinux because this is the better, it's the better medication to use for patients with, um, Nstemi. Um, and you don't need to put them on ox cos, then you'd be giving them too much. Just keep that in mind. It's Fonda Paranox instead of enoxaparin. Um And later down the line, someone will change it. If anyone has questions. Now's your chance to ask and remember telemetry, I don't think that was mentioned, but a telemetry bed is just to make sure you're monitoring the patient. I think the 1st 24 hours is it or 48 hours is crucial for someone that's come in with an Nstemi, you just need to make sure they don't end up in cardiac arrest. Um So any patient that's got an Nstemi and you're admitting them, you need to sign a form, a request form for a telemetry bed. Um I I'm not sure how it would work in other hospitals, but it's usually a telemetry form that you have to sign off for an Nstemi. Um You can also use a telemetry bed for other other things as well. Like if someone has a new Af or they've come in with some sort of arrhythmia, there's like a whole list of indications for a telemetry bed. Definitely have a look at them. So you know who, which patients need a telemetry bed, but if someone's had an enemy, you need one, and the patient should ideally go to the AM U ward and then cardiology ward on a telemetry bed. Um just keep that in mind as well. Ok, I'll let you guys ask questions if you have any. Um I think the next session we have is on arrhythmias. So we'll be covering the presentation, loss of consciousness and collapse. And I think the main focus is on heart blocks. Uh That's a common one in A&E and for the medics as well. So try and attend, I think one of the I MT twos is presenting. So, yeah, so I added on that bit because I think there's a difference in how it's treated for any doctors that are working in A&E like me personally, I work on the medical team. So I've only really seen N se um and I know how to manage N Semis, but with semi, I've not really got much experience with them. Um It's usually the A&E team that are sorting it out. I think we've also mentioned doing an echo. So anyone that's admitted with an end, you need to get an echo, you need to order an echo for them. Um I mean, at least I do, I think most people, most doctors do. It's good to have an echo done if they're being admitted. So that the um the size of the infarct, infarct and any like hypokinesia, it, you can see it on, on the echo and it's already done before the patient reaches the cardiology department. And they would appreciate if it's already done as well. So if you're admitting someone that's possibly for PCI, get an echo. If you guys have questions, you can drop them in the box. Sorry, in the chat. Otherwise you can do the feedback form and remember to save your certificates in the same file, please use them for your appraisals and thank you for attending as well. Thank you.