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Hello everyone. Good evening. Hope you're all doing well. Um Could you just indicate in the chart whether you can hear me or not? And if you can see our screen or presentation, can you hear me guys? Can someone just type in the chat, please? Ok. That's fantastic. We'll just wait like a minute just to let some other people join and then we will go ahead and start. Ok. Do I think we're gonna just get ready and start? So welcome everyone to our final talk in the series on the Medical Cracking series. And thank you for joining us this evening. Um Just a quick intro about B SSN. So we're the Bulgarian Student Support Network. Um We assist and help students that are studying in Bulgaria especially. Um after you graduate, we are trying to facilitate the process of transferring back to the NHS and trying to make it more smooth. So if you do have any initiatives or any ideas that you think we can implement in your universities, please do let us know we can reach out, reach out on Instagram. Um Please do let us know and if you could also follow our page on medal. So you can be um updated about whenever we do have talks and webinars. I'm gonna be sending a feedback form after this talk so you can get your attendance certificate and we'll also have AQ and a session at the end as well. So I'm gonna hand over to doctor Dawson. Thank you so much. Thank you very much J and welcome everybody and good evening. Um Yeah, this is our, our cardiology talk, our last in the series of medical clerking. Um and if you wouldn't mind keeping any questions, burning questions to the end, and we will have a couple of polls uh along the way and just to outline what we're gonna talk about tonight. So firstly, what is a CS or acute Coronary syndrome? Uh discuss what a typical cardiac chest pain history is like and discuss maybe a more classical case. Then get into talking about troponin and there's something that's easily requested but sometimes difficult to interpret. Um And then we're gonna maybe mention a case that simply not all raised troponin and chest pain is always myocardial infarction. And we'll talk about some differentials that you can have. And then we'll summarize things with uh a second case as we go. So the aim of this talk is to give you a flavor of what cardiology knowledge you need to understand, to be able to clar patients who come from A&E and admitted into the hospital and the medicine um And it's very much a practical understanding rather than the in depth discussion. Um And this will keep you really safe and really um knowledgeable when you're working on the wards, which hopefully will be quite soon. So if we get into the first section, which will be uh our cardiac history. So the top tier, this infographic is from the European Society of Cardiology Guidelines, the E SE guidelines. They've updated them in, in 2023 this year. And what they said is the clinical presentation of what was chest pain. But I want you to use the word chest discomfort can be anything from oligosymptomatic or completely asymptomatic and then progressing up. So it can be increase in chest pain, it can be persistent symptoms and then on the more severe side cardiogenic shock. So if you've had a big M I that's then had an infarct of the myocardial wall, that part of the wall isn't pumping, you're gonna have a pump failure, the blood's going back up into the lungs, you're gonna feel breathless, you'll probably be on oxygen. Um The presenting symptom may be breathlessness, but it's not a lot to do with the lungs. It's gonna be about the heart and then of course, cardiac arrest, which is a very much a separate talk. So in the new guidelines, they changed the word chest pain to chest discomfort. And patients may describe anything really but pain, pressure, tightness, heaviness, or sometimes a burning sensation in the chest and that can be the leading symptom. And then there's three separate categories for they, they like to use. So historically, it was anginal, chest pain, it was atypical anginal and then non anginal and those terms have been removed. Now, what we're talking about is cardiac, chest pain, or possibly cardiac, chest discomfort or likely non cardiac. And I want you when you're clerking patients or you're seeing patients in the future, what I want you to do is get in the habit of talking in, in these three categories. When it comes to the patient who's presented with um chest pain or possibly a CS or query M I or anything like this, you wanna be categorizing in their history into three categories and hopefully a pneumonic that you've all used before. Um But it's incredibly useful even as you get more senior and as you go through foundation medicine, so the sighs typically central, the onset almost always sudden, the character, the discomfort can be a bit of anything but crushing and heavy is, is absolutely, you know, typical what you'll be hearing and the radiation of the pain to the left arm, the left neck, the jaw, uh in the throat. Sometimes people describe a symptom and then associated symptoms. So, diapsis or sweating, that's because of a sympathetic activation response and that's why you get any excess sweatiness time course. So typically longer than 20 minutes and again, with your patients, what I want you to get a flavor of is, is asking, did it last seconds, minutes, hours, if they say minutes, then delve into that, try to find uh being, being as accurate as you can exacerbating features. So, is it exacerbated with movement or relieving features so eased with rest or GTN spray under the tongue that patients may already have prescribed and then severity is typically on the more severe end of things. However, um patients can even have big stemmy infarcts and actually even not come to the hospital or have no pain at all. So, um it's a combination of all these features is how you're gonna um is how you're gonna classify things. So again, using the A CS spectrum, so you've got the clinical presentation, which is on a spectrum. The very next thing the patient has when they come into hospital, they see the triage nurse and they see a pa a patient with a report of chest pain. The next thing they get and the recommended guidelines say to have an E CG within 15 minutes of presentation and they're not gonna have a malignant arrhythmia. These pe people who have walked into hospitals because they would be on the ambulance or, or in cardic arrest. The one patients who have the ST elevation, they'll be flagged and A&E will deal with their patients and they will send them to the nearest big hospital that deals with um PCI. So primary cutaneous intervention or percutaneous intervention. And that's gonna be stenting essentially. Um where medical larking comes in is where you see patients who have normal or abnormal E CG which has like ST segment, depression or T wave inversions or hyperacute T waves or something of this nature. Your task then is to say that do they have a non ST elevation? A CS event? The next step will be talking about the troponin And the words I want you to use is even non elevated or elevated or abnormal. Um high, low is a bit vague, say elevated or non elevated and then we'll come to our final diagnosis. So the stemi patients have already been taken away, hopefully. So is it a is this patient gonna have a non tey unstable angina, unstable part being that the symptoms have come on at rest and then on the less severe side also and, and not seen here in this infographic would be angina symptoms or angina. You have to have symptoms on exertion. They relieve with rest. They last typically less than 20 minutes and they can be relieved with GTN uh Glycerol trinitrate spray. And that's all your criteria for stable angina. So we're gonna talk about a case and our first case is a, a 68 year old male who attends A&E after 30 minutes of really severe. A nine out of 10 central crushing chest pain that developed suddenly whilst watching TV. Last night at that time, he felt short of breath s ob and nauseous, but the pain went away. So he didn't come in during the night. He attributed the pain to indigestion. Has he not long ate a meal? He attended hospital the next morning as the pain woke him up from sleep early at 6 a.m. So that's his history, his past medical history. So he has hypertension, high BP. He's on Ramipril. Um He's a retired lorry driver, no significant family history. His initial observations of BP, respiratory rate and heart rate were all normal. He has his blood test taken and he's awaiting the result and his CG NSR so normal sinus rhythm. So there's nothing to tell us no bloods yet. E CG is normal. We've just got a history alone at this point in time. So I want you to try and classify it as chest pain as to which um which category you wanna put it in and if we're able to start our pole. So, is this a likely noncardiac chest pain, possibly cardiac or you're happy that this is cardiac? Truly cardiac chest pain? Where would, where would people like to classify um this patient's symptoms and I'll just give you a few moments for the poll. Ok, great. So we've got eight responses and people are torn really between possibly cardiac and there's some who are brave and, and said, treated as cardiac chest pain. So you, you're all thinking almost all of you are thinking along the right lines. And so with this history, personally, I would think this is cardiac, chest pain. I would be happy to go that far. Um, possibly cardiac. Yeah. Um, you, you're definitely thinking along the right lines but the severity, the 30 minute history, um, he has a risk factor for a CS and that'll be the high BP. Although he doesn't have a lot of past medical history, he doesn't have a family history. Um and his E CG is normal, but other history alone, I want you to be able to classify things. Um Although the patient attribute it to eating a meal. Um The fact that it then woke him up at sleep at 6 a.m. is probably inconsistent with any gastro related causes or indigestion of anything of that nature. So if we look at the blood test, so the next thing we're looking at is so he's got a full blood count and F PCA 109 which is just under normal, his white cells are normal C RP 12, which is grumbling along. Um Importantly, here he's got troponin. So troponins back and the trop is 15. And in the hospital, I work out um very sensitive test. So anything less than 13 is completely normal and his drop is abnormal or elevated his renal function. So his eeg fr is OK. And so are his electrolytes. So then we need to start thinking about a final diagnosis. If we think his chest pain is possibly cardiac or I'd prefer cardiac chest pain. He's got a normal E CG. So that takes out the sting. He'd have, um, has he got an unstable angina or does he have a non stemi? And does anyone wanna be brave and type something into the chat about what they think the diagnosis may be? I give us a moment with the chat and if I talk through. So with ast elevation M I, you've seen it on the E CG that's definitive and on that there, we got a non a CS diagnosis but from the history, we think that this is possibly cardiac or cardiac chest pain. So I think that leaves us with two choices in the middle there. So is it a is it a non stemmy or is it unstable angina? So unstable angina shouldn't give you a trop rise, but we have a slightly elevated trop or non normal. So that then leads us to non non ST elevation, myocardial infarction. And that brings on to the the second sort of category of uh our talk tonight and and that's chopping into TRS cardiac drops. So some really brief and and short facts about troponin. So what is it? So we use it as a biomarker of myocyte injury. So it has to be ongoing injury. It can't be an MRI that happened years ago or months ago, but it says dead heart tissue. So, dead myocardium does not result in any chop change whatsoever. So, in the UK, they're all high sensitivity troponin T and drop tends to rise within an hour after symptom onset. So, if you have a patient who lives in, you know, just 10 minutes away from the hospital and they get there really quickly and they get seen quickly and have their blood tests taken, well, unless it's one hour, at least from the onset of the pain, it's almost never gonna be high. Um So it's all about timing with a tropin test and taking the first drop is fine, but it really serves as a baseline upon which you compare, then other results as the patient um has future tests and trop so it remains elevated for a variable period of time with, with different people. And it can be as long as several days. And importantly, in, I'll stress, this tropin can be elevated for many different reasons. A CS is simply one of them and what can be the causes of elevated troponin. So there's cardiac causes, there's lung causes, there's completely unrelated causes. And then there's so the generation of TRS of the leaking of troponin from the injured myocardiocyte into the blood and then that being detected on your test and there's the opposite. So the elimination of troponin from the body, uh which is done by the kidneys. So, if your kidneys are not functioning, you have a chronic kidney disease, AC KD. What you'll find is your trop is statically elevated and it doesn't really change much. And that can, that you have to decipher out with clinical history and, and repeat testing as the patient remains in the hospital. So up here with the, the cardiovascular causes, um C HS or congestive heart failure can again give you a elevated drop that's not really going up, it's not really going down and it maybe lies around 4050 it never really changes cos it keeps coming all the time because the heart is under stress, although it's not proper ischemia, myocarditis. So, inflammation of the the heart, typically, you see myocarditis in younger patients after having maybe a viral infection and it irritates the heart and you get a myocarditis, you get chest pain, you get fevers and usually have sky high troponins in people who you'd never think would have ami. So that's maybe young, as young as in their twenties or teens with chest pain and a high chop. You'd think myocarditis aortic dissection. So that's ascending aorta. So there are type a dissections. Um your truck can be normal, it can be elevated, it can be super high, it can be any, virtually anything. And then you got sustained arrhythmias. So if her heart's beating up, you know, or going at 100 and 50 beats a minute for a few hours, that may well cause a little bit of uh myocardial injury giving you a tro release. Um, but again, that should be listed in the history of your, if you know your pa patient is having a, a significant arrhythmia, then that can factor into your history and your thinking and then your pulmonary causes. So, if you had a big pee and your right heart is usually pumping the blood absolutely fine. But all of a sudden you've got a blockage in the lung somewhere, the right side of the heart, which is only thin and nowhere near as, um muscular as the left side, it'll start to struggle to push against that pe and what you find, you get a right heart failure or right heart strain, you'll get a small rise in tropin and that's attributable to the right heart rather than a left heart myocardial infarction. And it's a similar story in CO PD. So airways disease, you've got strain on the right heart again, but not nearly as severe as, as in a pe. And again, you can have a mildly elevated troponin that isn't really going up, it isn't really going down. But you can consider that could be related to AC O PD rather than um any heart disease. There's a whole host of other causes. Um, so even in stroke, you can have um sympathetic release and sort of stress on the body which then injures the heart and you get a tr rise. So even neurological impairment or acute neurological impairment come in the heart strain later on. So timing is absolutely everything with a troponin. So as we see if this patient came in within 30 minutes, their trot may not be elevated to what we really think. Importantly, if they came in too late, you know, 67 days down the line, we may be missing the early part of the truck rise and fall and what's important. So other markers have, have gone out of fashion, certainly in the UK. So using um creatinine kinase or CK as a marker of myocardial injury, um I've never seen it used in the UK, a broad and in the textbooks, it may well say that because you get a quicker rise and a fall, you can actually use CK for is a reinfarction. So if you had an M I and then four days later, you've had another M I, you would see two peaks in CK, but it's not really much available uh in UK hospitals. So trop is always one that's um readily available, let's say, be aware of the, the rise and fall and reflect that in the blood test that you see for any patient. So we're gonna talk our second case and I've, as the end of our larking series, I've literally made this one a bit more challenging. So we've got a 68 year old male patient who attends A&E with three days of shortness of breath feeling generally unwell. He admits having a productive cough. So a a sputum, he's got intermittent chest pains, most notably on the left hand side of the chest. And importantly, so he's dizzy when standing his wife then called the ambulance over concerns over the chest pain rather than the shortness of breath that he was happy enough to leave alone. So that's our case history, moving forward to past medical history. So again, he's got high BP. He's on the first line drug, which is Ramipril. He's got chronic kidney disease. His eeg fr is about half what it should be the normal being above 90. He's anemic and he's taking iron replacement. He's a diabetic and he's got a high um HBA1C and he's got a bit of CO PD just on standard inhalers is social history. So, as I've said in other talks, it's really important if you've got a smoker, always try and identify how many pack years they smoke. So a single pack year is equivalent to smoking 20 a day for a year. Uh He doesn't drink alcohol and he's got a really limited exercise tolerance. So this guy can only walk 250 m or so even at the best of times. So he's not generally a well man. Um before this, this attendance and then I want you to keep using your, your Socrates and your monitor to identify what type of chest pain you may have. So, in probing more, when you're taking the history you're saying it's a central chest pain, it's sudden and short lasting, but it happens, it has happened multiple times and the character of the pain was sharp. Um, it has actually spread mostly left but occasionally to the right side, you're certainly short of breath. The pains comes and goes and it, he scores it around an eight out of 10 in severity. So these are the, the case history and all that you've dug into and the social history. So I'm gonna give you some examination findings for this patient. So, on auscultation of his chest, you've heard that he's got left sided crackles and the right side of his chest is absolutely clear. He's not wheezy. So that means your co PD exacerbation would typically give you a wheeze. So he's importantly, not Wheezy. He's got no heart murmurs. His capillary refill time is three seconds. So you could argue a little bit dehydrated and you look at the mouth and the mucosa and it's certainly dry. So you think this chap is certainly a bit er on the dry side and a bit dehydrated observations, hypertensive tachycardic, albeit a little bit. Um, he's breathing at 22 beats a breath per minute and he's saturating just about ok at 94% on air and he's 37 degrees. So, as we said, very much for the first case, you've got your history, you've got your observations, you've got your E CG and with the pole So your, your E CG shows T wave inversion in the later leads. And it's exactly the same as it was for this patient who had an E CG two years ago and there's no change whatsoever. Then you've got a blood test. He's got raised inflammatory markers. Cr pa 105 is, he's a little bit anemic. Actually, 78 is quite anemic and his troponin now is much, much higher than the other patient. And that's at 42. So tr 42 inflammatory markers raised E CG which is normal for him. So thinking all that if you're on the medical take and it's morning or it's evening time, the question is, would you treat this man as having an A CS event until you next get a review that may be sort of 12 or 16 hours later and going forwards things I want you to consider. So what type of chest pain does he have? Is it noncardiac, possibly cardiac or cardiac? His E CG. So he said that was normal for him. His top 42 and you know, it's elevated. So have a think about why it might be elevated in this patient. And I'll let you guys answer the poll and, and see what you think. So as to reasons as why the truck may be elevated, he could have had a new M I it could be just because of his renal impairment or he can only walk 250 m. Has he got an undiagnosed sort of cardiac failure in the past that he hasn't seen medical attention for and that could give him a rather than a up and down drop that could be giving him a steady elevated drop of around that number or what we said here type two M I. So rather than having a, a pure blockage of a vessel, what it could be is that your heart's under strain because of the anemia because of the CO PD, because he's got an infection that's put an additional strain on the heart that's giving a bit of chest pain, that's given a shock rise. That's certainly possible. So there's various things that are happening and I want you guys to sort of try and guess as to what you think is the most likely outcome and as the poll reflects what would you wanna do with this patient? And I see a few of you have um hopefully Avis A has already and it looks like you're not really convinced for a type one M I at least, which is reassuring. I'll just give us a few moments here and you in the chat has said about CFL EC GS. Yeah, that's a really good point. Um So his EC GS were normal as they were two years ago or at least normal for him. But what would be the gold standard really is to get at least um two or three ideally three E CG. So one at time, 01 at 30 minutes and one at an hour for a patient who's stable like this. And if you're seeing any changes along the way, whether it gets more normal or whether it gets more abnormal, but then you've got evidence that there's a dynamic change. So that's suggesting that at some point, there has been some disruption of the cardiac conducting pathway and in this context of chest pain and being admitted to hospital, that would undoubtedly be um because of ischemia or an ischemic event. So looking at the poll answers, so good to see that not many people are convinced for a type one. Am I actually everyone's been a bit skeptical and, and maybe correctly. So um to treat his a type two M I, it's a transfusion, treat the infection, give him some fluid or look for other causes of chest pain. So we said that this was intermittent chest pain, which is less characteristic of, of cardiac. So with this patient who I saw over the summer, so let's have a look what what I did with things. So definitely there's clinical uncertainty here and there that's reflected in the answers that you guys are given. So there's a bit of a split between type two M I and looking for other causes and it's at this point, it's really impossible to be sure of the cause of the chest pain. So what my impression here was that this was a lower respiratory tract infection most likely or pneumonia. And we won't be able to tell between both until we get a chest X ray. But secondly, in the impression was to rule out a CS. So that leaves, you're not putting all your eggs in one basket you're thinking about. Well, my primary diagnosis is an infection. However, you can't rule out that this isn't, you can't be sure that this isn't an M I or an A CS of any type. So if you guys gave a plan like this as sort of early f one doctors or foundation doctors in the NHS, this would be absolutely great. So you've got IV antibiotic, you've got fluids, but both of which treat and help the infection and we know that he was a little bit dehydrated. You get your chest X ray, which can either prove or disprove a pneumonia. And importantly, we said he had unilateral crackles, he had crackles on the one side that could be evidence to say that this is more pneumonia or an infection. More than true. A CS definitely repeat the drop. Um drop up an hour or two hours later would give you that dynamic change. And if it goes sky high to the next drop is 200 it's a bit hard to explain that as an infection. So at that point, you'd have to treat fully with a, with your A CS treatment as your hospital advises and then adding on ABM P. So BNP is elevated with heart failure. If his B MP was in the thousands, that would lead you to be able to explain the troponin rise um with heart failure alone. And definitely this chap would, would certainly benefit from getting an echocardiogram done in hospital. Typically, you can get these done within sort of 2024 48 hours and it'll be really helpful for a couple of reasons if you're getting um his ejection fraction. So how much blood is he pumping out on each beat? And another thing you see is regional wall motion abnormality. So, is there a bit of the heart myocardium that isn't beating? And the rest of it is, and that would be echo evidence that there's an ischemic part of the heart. And as we said before, including in your plan, although it's harder to get EC GS repeated somehow, um repeat Ec GS or serial Ec GS would be extremely helpful. So that's how I left his case. And later on actually is Trump ended up being static. His BNP was raised. His echo did show a little bit of heart failure and ejection fraction was about 30% and his chest X ray, although clear, he did respond well to antibiotics and, and this man eventually got discharged home after some IV antibiotics and um having a bit of a work up by the cardiologist. So I just wanna talk about um some resources that we've used. So the European Society of Cardiology guidelines. Although it's a massive booklet, there's some really helpful infographics and a small, a few small um really good explanations about how to interpret chest pain and troponins. For EC GS. My colleague, Doctor, Doctor Moore gave a great um talk on the E CG interpretation. And in addition to that, what confidence that is uh life In the Fast Lane website, which is really good useful tool for er reference work which I still use even now or even learning some, some EC GS. And I think that concludes our talk just here and I've got a couple of questions from, from Yusuf. Yeah. Um So he had asked before about um if we could go for a serial ECG, I think that was before with the first question about chest pain. Yeah. Yeah. OK. And then there's some further questions. Yeah. CKD leading to fluid overload. I think you just answer the questions and the basal crackles which just explain the HTN. OK. Does anyone sorry, does anyone have any questions about um any of the cases or just anything in cardiology just to type in the chat? And then we can um and to go back what, what Yustef Yussef has said. So um he had this chap in this case, had unilateral crackles rather than bi basal. So if you did have five basal crackles, that could be more consistent with fluid overload. Um However, they're unilateral with a raised inflammatory markers with a productive cough. You can more attribute this to infection rather than heart failure and he was indeed hypertensive. Um who knows what his baseline um BP really was. This chap in this case, had a BP of uh 100 and 80 something. Um We don't know his baseline, his baseline of whether he's been attending his GP regularly for his annual check ups. Um But he's certainly not septic. So septic, you typically have a hypotension, a low BP, um saying that this man is infected and it may be a stress response that then is, is driving his elevated um blood pressures on this. So, are you gonna treat this man as a CS? So we didn't immediately at least, but if his trot was further elevated in a dynamic fashion than we would have. So it's um this is a complicated case that I want you to sort of bring in a bit of discussion and a bit of reasoning as to why you may want to do things. And it's with your impression or your diagnosis, not to put all your eggs in one basket. Think about your primary diagnosis on the one hand, but always look to rule out really important or serious causes of pathology in this case. A CS. Um but it is a bit of an art and a bit of a skill and as you get more experienced, you'll get more comfortable in, in taking on a bit of uncertainty. I'll leave you with our resources. Um Yes, we are gonna get the recordings of the meeting. Um They're gonna be on our metal page. So if you just go on to metal type in the Bulgaria Student Support Network and yeah, you'll be able to just see the on demand recordings and yes, you should be able to see neurology and Renal as well. Um And does anyone have any other questions or any other remarks? Anything you want? But I'm gonna send the feedback form right now. So please do fill in the feedback form so you can get your um attendance certificate which is gonna be signed by our president doctor he and pop off. So yeah. Um ok. Does anyone have anything else before we wrap up? Can we have the doctors? I go through um so through the um Instagram page for the Bulgaria Student Sport Network, um we can all get a advice there and then if there's any specific questions, um myself or James or one of us doctors would be more than happy to pick it up from there. Um We all have access to that and that's the central point where you can get further information from. So I would um advise you to message over over Instagram and we can get back to any queries. Perfect. Ok, so thank you very much for your attention tonight. And, and best of luck with things going forward. Thank you very much, Doctor Dawson. Thank you everyone for joining us. Thank you. Bye bye bye bye.