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Okay, so Hi, everyone. Good afternoon. My name is Elizabeth Dick and I am a radiologist based at ST Mary's Hospital, which is part of Imperial College in London. And although I'm a radiologist, that talk that I'm going to give you now, first of all, it's going to be interactive. And second of all, uh, I'm actually going to be getting you to think as if you're working in the emergency department. So basically, this session is going to be a quiz, and I'm going to get you to answer, and you can send some messages through the chat. But I'd also love you to answer via this polling up. This address is going to keep coming up in subsequent slides. So what we're going to do is we are going to basically help you build up your own list of causes of acute chest pain. And I also hope that I'll help you to recognize what is the typical history in certain causes of chest pain. And what are the typical examination findings. And then finally, um, I hope that you'll be able to understand how the radiologists can help you, um, to make decisions about what's going to happen with your patient. Okay, so we're in the emergency department. It's Friday night. The patient's are coming in, and you and I and everyone else on this call is all in the emergency team. And we're all trying to sort out these patient's who've got chest pain. So we're going to see a series of patient's each in a different cubicle, and each of these patient's has got chest pain. And so what we'll do is we'll see the patient, get their history. Uh, look at the tests and the imaging, and then we're going to make a diagnosis. Okay, so here's our first patient. This is a 40 year old female, and she's previously completely well, and she's coming. She's got a very high fever, and she's got chest pain. So when we do the examination and we put the stethoscope on her chest, we kind of can hear a funny rubbing sound. Centrally, we did some bloods, and the blood showed that she's got high inflammatory markers. So her c reactive protein is high. Her e s R is high, Uh, and white cell count is high as well. So that's what we know so far. about her, and I'm going to take you now straight to the CT scan of her chest. That happened. Um, and this is with the patient in the corona position, so as if they're facing you and as you'll see will come in through the chest from anterior to posterior, and I want you to focus on the heart and pericardium. So as we come through this, you can see, uh, the heart in the midline. Obviously, you can see the pericardium around it, so I want you to think about that that you can see the Hemi diaphragm and the liver below it. Don't worry about the lungs. Take it from me that the lungs are normal, but really focus in on the heart and the pericardium, and let's zoom in here. Now I realize that you may not have seen many cts of heart and pericardium, so I put a normal in for you to compare. So if we look in the top left hand corner, you can see the normal pericardium. It's it's very, very, very thin line, literally as if someone has got a pencil and drawn a line. And, um, it has fat outside of it and a little bit of fat inside of it, which is why you can see this kind of very thin line right here. So that's the normal pericardium. It's so thin that sometimes it's very hard to see, and the only place you actually see it is over the right ventricle. And it's normal to have a tiny bit of pericardial fluid, but you certainly don't expect to have a large amount. And sometimes I think a good way to, um, think about the pericardium is it's almost like So we call it in the UK cling wrap, Um, in. Certainly in Australia, they call it sarin. Um, sarin wrap. Um, I think there are different names across the world, but basically that kind of plastic stuff you wrap your food up in it's that thin. Okay, so let's keep coming through. Our patient's now and we're comparing the pericardium of our patient with the normal pericardium, and I hope that you can all appreciate that. Actually, here, this pericardium is very thick, so we've got one layer of pericardium here. We've got another layer of pericardium here, and then in between it, we've got all of this stuff which is fluid, very inflamed fluid. So normally the two layers of the pericardium are so thin that they're like two layers of cling film on top of each other, and you can't see them, Uh, tell them apart. But here they're both thickened, and there's fluid in between. And then I'm hoping that you can also see this, um, stranding, which is in the fat deep to the pericardial layers. So, uh, there's definitely something going on with the pericardium in this patient and let's go back and let's look at the rest of the images just to confirm is it on every image that the pericardium looks thickened and we're gonna come all the way posteriorly and then come to post your part of the chest Post report chat here just for anatomy. Here's the descending aorta that we can see. So I'm going to ask you to vote now and tell me what you think is the diagnosis in this patient. Do you think the diagnosis is aortic dissection? Is it pulmonary embolus? Is it pericarditis, or do they have a gleaner humeral joint dislocation? So the way to vote is to enter this address. Um, on your, um, phone browser or there was that QR code earlier. Now I'm just going to have a look and see. I can see someone to raise their hand. Um, would you like to just put whatever question you had in the chat? Whoever raised their hand? Hang on. Let me Let's put the chat here. No, it wasn't a question. I was like, I know the, uh Oh, I see. Ok, great. Well, that's fine. You can, um uh did you manage to answer through the poll everywhere? Chat? Yes. Yes, ma'am. Perfect. Okay, good. Great. Um, now it's looking like 100% of the people are saying pericarditis, and that is the correct answer. So that's great. Did you have something to add? Um, person just was speaking. Uh, no, ma'am, no. Okay, great. Okay, good. So the diagnosis is pericarditis? Absolutely right. Everybody's right. So, with pericarditis, instead of seeing that very thin layer of pericardium, you see a much, much thicker layer. The two layers are distinct as opposed to close together, and there's fluid in between. So the kind of history that you would get from this patient is chest pain. Um, a pericardial rubs. So when you listen over the heart, you might hear that kind of rubbing sounds a bit like hair rubbing together. If you do an e t g, you'll see ST Elevation. Now, in terms of imaging, what we can see here is that each layer of the pericardium was second. They are enhancing. We've given contrast there, enhancing. So they're brighter. They're taking up the contrast there. Is this a fusion and there's also stranding around. And if we were to do histology, we would see that there's a lot of fiber in and adhesions and inflammation around. Okay, so this is what pericarditis looks like. And now what I'd like you to do, please, is to name some causes of pericarditis. Uh, I have a question. Uh, it was regarding this pericarditis is like while auscultate in the chest. Uh, we can say there would be cardiac tamponade. Good. Well, it depends, of course, how big the volume of fluid, Um, in the pericardial space is if you have a big enough volume in the pericardial space, it could cause tamponade. But the reality is, is that with most causes of pericarditis, it doesn't cause tamponade. Okay? That's a good question, though. Obviously. You've got to think about that, don't you? Um, so anyone like to name some causes of pericarditis? I'm hoping this is coming up on your screen, and I'm going to have a little look for anyone who hasn't managed to vote. Uh, sorry. Who hasn't managed to download the boating? The votings address is, um, paul f dot com forward slash e d I c k 900. And I might actually just, um should I post that in the chat? Let me do that while we're waiting. Yeah. If you post in the chat we posted, I don't have the link, but if you could Okay, hang on. Let me do that, then. That's fine. Where's check here? So I know of old that what we can't do is put the QR code in the chat. You know, they don't like that. For some reason, Zoom doesn't like that. Okay, Good. So people are coming up with some answers. Dressler syndrome? Um uh, which I think is the post myocardial infarction syndrome. If I'm right, you can correct me if I'm wrong. Lupus. Definitely. So. Lupus kind of falls into that category. doesn't it? Of inflammatory? Um, kind of generally seronegative inflammatory condition, which can affect any organ in the body. Viral infections. Definitely. Bacterial infections. Absolutely. So those two causes someone's mentioned trauma? That's really important. Um, my cardial insufficiency. Yes. So I suppose that's probably part of the dress list syndrome, isn't it? That after an infarct, you are more at risk of pericarditis? Okay, Very good. So let's move on and see. I think I've got a list here. Okay, So the causes as ever you kind of divide it into a surgical sip. So you would think about infectious causes, inflammatory causes, metabolic causes neoplasm so infectious causes. As you've all said, you kind of think about viral and bacterial infection. Inflammation. Um, so that definitely involves connective tissue diseases like Lupus or rheumatoid or any seronegative arthropathy post acute myocardial infarction. That's the dress list syndrome that you were talking about, then coming onto metabolic so high. Um uh, your A levels uremia. Uh, sorry. Urea levels, not your eight levels. Uremia can cause, um, pericarditis. And then, of course, if you have funny little tumor deposits, or if you've had a radiation, that would also cause pericarditis. So that's the kind of list that we're thinking about. Okay, Very well done, Everyone, Uh, just to finish off, what's the best way to image the pericardium? Well, echocardiogram is very good. CT we've seen is good. Uh, m r is fantastic, but let's be practical here. It's a Friday night. You're on your own. Uh, you may not be an expert in doing Echo, and it's probably pretty hard to get an MRI. And so I think the reality is is that when you're on call, CT is your best bet. Okay, we're going to move on to our next patient, and this is a 25 year old male, and they've got severe epigastric pain, meaning pain in their upper abdomen, and they've been vomiting a great deal. So we're going to take a look at the chest X ray, first of all, and I'm going to zoom in on the chest X ray just here, and I'm going to point out to you what we can see on the chest X ray. So here we can see that there's this very subtle air outlining the mediastinum, and what the air is doing is it's tracking along the, uh, along the mediastinum underneath the pericardium. So remember how in the first patient I showed you the normal pericardium and I showed you how it's like this very thin sarin rapport cling film. So in this patient, what's happening is air is tracking under the pericardium and within the mediastinal space. So this is pneumomediastinum. So this patient's been vomiting a lot. They've got pneumomediastinum. And I'd like you to help me with the diagnosis. So we're going to go back to Paul everywhere again. Um, so you can I'm just gonna actually type the thing. Um, here we go. Uh, the address onto the WhatsApp group as well. While you're while you're boating. So Paul F E dick 900. So, um, if you want to type in what you think the possible causes are, So this patient's been vomiting a lot, and now they've suddenly developed epigastric pain, and they've got free air in the mediastinum. So what do you think might have happened to them when they were vomiting a lot? Rupture of esophagus? Yeah. Bore have syndrome. Very good. Okay, let's see if anyone has anything else, um, to add there or if you all agree with that answer? Uh, I think this is certainly the top consideration, isn't it? To think about rupture of the esophagus. Overexertion? Yeah, that's not a bad possibility. Um, kind of in general, you know, kind of that is a cause of chest pain, isn't it? Let's see what else is coming through. Okay, good. So while we're kind of waiting for more votes, I'll just explain to you what, um, bore Half syndrome is so bore. Half syndrome is indeed rupture of the esophagus. And what happens is it was described by a physician from Leiden. No, no. Yes, Leiden in the, um, kind of 17 hundreds. And he basically had a patient who had an enormously rich meal, and at the end of the meal, he actually kind of made himself from it because he was so full. And he got exactly this. He suddenly had terrible epigastric pain. And then basically, the patient died three days later. And then ball half did a postmortem on the patient. And when he did it, he found that there was a hole in the esophagus and there was a rough in the mediastinum, and he even found the patient's last meal in that hole. And so that's why it's called Four halves after After Bore have. So this is indeed esophageal rupture. Very good for a person who identified that ball. Half syndrome is the other name for it, and the classic history is someone who's been vomiting just cannot stop vomiting. And then all of a sudden they get epigastric pain, and that means that they've ruptured the wall of the esophagus. And then you may see the pneumomediastinum as well, because there will come out of the esophagus into the mediastinum. Okay, so now we know what it's likely to be. We have to work out how to diagnose it, and you're going to help me decide how to diagnose it. So we've got two choices here. Radiologists like to give something called contrast and contrast essentially stands out as white against the black X ray background, either because it contains iodine or because it contains barium. Those are two main contrast. When we're doing CT now, the difference between them is that I ordinated contrast, so contrast that contains iodine can go in any body compartments, so we will use it frequently to give an intravenous injection, for example, And then it travels around the venous blood stream, and then it will pacify the arteries and the veins. Barium. On the other hand, you can only give it when you certain it's going to stay in the bowel. Lumen Um, it's very good at looking at the bowel, Lumen, But if there's any concern that it might not be in the bowel, Lumen. So, for example, if you had a patient who was aspirating and you were worried the barium was going to go into the lung, you must never give it because it's actually toxic to everything except for bowel. So knowing that you've got your choice between I ordinated, contrast and barium, I'm going to ask you to help me decide which one we should use if we suspect that the bowel Lumen is interrupted. Now imagine you're in the middle of the night in A and E. You're the most senior person in the emergency department, and someone is saying to you Well, what should we do? Should we give iodine? Or should we give barium contrast? And so you kind of need to make a rapid decision about which one to give bearing in mind that we were suspecting that there's an esophageal rupture. So we're suspecting that if we give contrast, it will go outside of the bowel. Lumen. And if it goes outside of the bowel, Lumen, then we know, um, that potentially barium is very, very toxic. So, for example, say, um, as I say, if it goes into the lung, if it goes into the peritoneum, if it goes into the mediastinum potentially, it's toxic. Whereas we know that iodine contrast is very, very safe. So it's interesting. I see that most people seem to have voted for barium. I know it's coming up. It's coming up. I think we've got small numbers here, haven't we? That's our problem. Uh, the correct answer is I ordinated contrast. So in this situation, you wouldn't want to give barium because there's a high chance the bare room will pass out of the bowel, Lumen and into the mediastinum. And if it goes into the mediastinum, it would be very toxic and cause a chemical media Stein itis okay, So what we do is we usually give the patient something called omnipaque, which basically contains iodine. We give them we dilute it down and we give them one cup just before they get onto the table, and we're looking for a leak. So I'm going to take you through this CT now, and we'll have a look at all the images and work out what's going on. So here we are, at the top of the chest. This is anterior. Here's the sternum. Here are the scapula. You can see those. This is the lungs, which we're not going to focus on right now. Here's the trachea, and then here's the esophagus. And because we've given contrast, the esophagus is white. Now, as we come down here, as I say, we've given contrast because we've got the patient to swallow. Everything else we don't have contrast in. But this is the arch of the aorta that we can see and we keep coming down. As I say, this is the esophagus. This is the trachea, which is dividing into left and right main bronchus. Here we are. We can see left and right main bronchus and keep following the esophagus, and you'll notice that there's this soft tissue here on the left. Um and we've also got some gas now outside of the esophagus. So we keep following it down, and it's now kind of disappearing The contrast in the esophagus, Um, and it's kind of becoming harder and harder to work out what's going on. We can see, um, that there's a pleural effusion on the left. All of this is air outside of the esophagus, and then there's also soft tissue around the esophagus. So we've got to be around the level of the hole in the esophagus at this point. But I'm struggling to see where the actual hole is, and then when we come down a bit further. So now we're coming in fear. Really. We're at the level of the heart, which is here. You can now see there's contrast. This is not the esophagus itself. It's outside of the, um, esophagus. So what's happened now is we've got contrast in the paraesophageal space, so we know that the contrast to spilled out into the paraesophageal space and this little thing here is the esophagus, just with a bit of contrast in it. And if we just zoom in here for a moment, I think you can appreciate. So here's the esophagus, which has still got some contrast in it. Here's the wall of the esophagus, which is thick. Here is the contrast in the paraesophageal space, and there's airway it as well. So at some point there has been a hole in the esophagus at some point between the mouth and the diaphragm, and contrast to spilled out of it. But I can't show you the exact level. Okay, So with this patient, let's just remind ourselves they first of all had the typical history of bore halves. Which is would anyone like to remind me the typical history of both halves? Just speak up vomiting, uh, pain after vomiting, pain after vomiting. Perfect. Exactly. Yeah. So lots of vomiting and then suddenly horrible pain. So that's the typical bore halves History. Exactly right. They've also got we saw that they've got wall thickening. We saw they have gas around the esophagus and that the contrast is outside of the esophagus. And this pleural effusion is probably because they've been pouring out fluid from the esophagus. And it's collecting in the pleural space because the pleural space and the mediastinal space joint, um, communicate, don't they? Okay, so do you think that this is something that we can just kind of, you know, to charge the patient home. Or do you think that this is an emergency? Anyone like to make a suggestion as to which one you think it is? Surgical. We have to do surgery. It's a surgical emergency. Yes, exactly. Right. This is a surgical emergency. You basically got to phone the surgeon straightaway, haven't you? And they need to repair the esophagus. And even with the esophagus repaired and with lots of antibiotics on board, this has actually got a relatively poor prognosis because the media asylum gets so inflamed. Very good, well done for answering. Okay, so we're still sticking with chest pain. But now we're thinking about other causes of chest pain, and the next thing I want to think about is when you have a patient who's got chest pain and you're kind of thinking, Oh, is it cardiac or not? So what happens now is that when a patient in the community has chest pain, the ambulance staff decide very quickly whether or not they think the patient is at high risk of a cardiac cause. And they'll do that based on the E. C. G based on the troponin levels and the history, or whether they think there's a low risk. And if they think there's a high risk, then they think there's an acute myocardial infarction, and they send the patient straight to the primary coronary center, where they will do primary intervention. So, for example, they'll do an angiogram, and then they may stent the coronary artery that has spasmed. But if they think that the patient is at low risk of a cardiac cause, they then bring the patient to us, and then we have to decide what to do with this patient. So this is what we're going to do next. We're going to talk about something called a triple rule out CT. So what a triple rule out CT does is it looks at three common causes of chest pain, and it demonstrates all three things on one C. T. So the common causes are coronary artery stenosis, acute aortic syndrome, same thing as dissection of the aorta and pulmonary embolism. And we're going to look at all three of those things. So before we get any further, I'd like you to help me, Um, revise. We're going to revise a little bit of coronary artery anatomy now. So could you name any important coronary artery, please? You don't have to name all three. Just one is fine. Because between us Well, name or three, won't we? And if you're not sure, just take a guess as to what you think they're called. Very good. Okay, so I like the way that this person has. Um um said right. Circumplex So you're right. So left and right is very important, isn't it? Yes. So And l a D stands for left. Anterior descending. So very good. See if anyone's got any more answers left Circumflex. Okay, very good. So between us, we've actually got the correct answers here. So thank you for answering that. Um, Now let's move on to next side. So cardio coronary arteries. You basically have coming off the arch of the aorta. A left coronary artery and a right coronary artery. And the left coronary artery divides into two. So it divides into the circumflex. So well, remember the person who said circumflex and it divides into left anterior descending. And if you have trouble remembering, uh, which one has the bigger branches? If you think about it. The left side of the heart has to do the most work because the left ventricle is under higher pressure, isn't it? So that's why it needs two big branches. Okay, very good. And if we do an angiogram, you can see the same thing on angiogram. You can see the right coronary artery coming off on the right side. You can see the left main coronary artery coming off on the left side and then dividing into left circumflex and left anterior descending. So let's think a little bit more about those now. What I'm gonna do is I'm going to show you side by side. We've got the kind of three D picture, and then we've got an actual picture, and this actual picture is at the level of the pulmonary artery. So it's around about kind of up here. So what we can see here is we can see the the aortic root. So where the aorta comes out of the left ventricle just here. And if we focus in a little bit more on the aortic root, do you remember from anatomy days that the aortic root has three cusps? Basically, it has a right anterior, uh, left anterior and a posterior cusps. And they're, like, kind of leaflets, aren't they? And as the blood passes through, they flap against the wall or they flat back again. So the right anterior gives right to gives rise to the right coronary artery. The left anterior gives rise to the left main coronary artery, and the posterior cusps does nothing. It just kind of sits there. It doesn't have any any arteries coming off it. So this is the aortic valve. Remember, In most people, it's got three, uh, cusps. Um, that's the best thing to be. Three cusps tricusp it and the right anterior and the left anterior give rise to coronary arteries. The posterior cusps does not. So let's go back to our CT and remember that on on CT, the heart is always a bit twisted around. And so here we can see. I'm hoping that you can appreciate the three cups, but they're kind of slightly twisted. So although posterior is back here, the posterior cusp is slightly rotated, and it's it's here and here. We've got the right and the left, um, cusp. And you can see that the left side is giving rise to the left main coronary artery here. And then if we come down a bit more, you can see the right coronary artery coming off the right cusp. And then, actually, you can start to as we go up and down, you can start tracing this left coronary artery, see how it starts to come out. It divides into two branches. Um, and these two branches run all the way down to These are the branches corresponding to here and here, and they're running all the way down so that you can, um, kind of supply the left ventricle and enable it to pump, pump, pump. And finally, if we just look at the level of the ventricles, here's the right ventricle. Here's the left ventricle. Remember learning, uh, earlier on how the right ventricle is anterior. Uh, and the left ventricle is more posterior. That's exactly what you see here. And you can see that the left ventricle has got this very thick wall around it, because the left ventricle is having to pump all that blood under much higher pressure. It's under arterial pressure, isn't it out? Whereas on the right side, the whole system is lower pressure. Okay, so let's come back to the triple rollout CT and let me just have a quick look. I just want to check. There's no people. Yeah, Okay, fine. Um, so triple rollout CT. We're looking at the pulmonary arteries, the aorta and the coronary arteries. Now, the problem we're looking at the coronary arteries, which is basically doing cardiac CT, is it's really difficult. There's lots of things you need to do. You need to have a very good quality CT. You need to give a contra an injection of contrast in two phases. So you give one injection and then about 20 seconds later, a second one, you need to have e c g gating on the patient so you only acquire your images at certain points. You need to make sure that the patient is, um has a relatively low heart rate, and the way to do that is to give them beta blockers. Um, you then need to make sure that they're not that the coronary arteries are completely dilated. And so for that you give them nitrates, and so actually you're doing a lot of things. You're giving them a lot of drugs. And for that reason you need to actually have a doctor present who actually knows about cardiac imaging. And that's actually not very easy. So quite often what happens is we don't actually do the cardiac part. So if someone is present in the daytime and we do a cardiac CT and we see that there's a very significant stenosis, so the artery is narrowed by more than 75% that's fantastic, because that is significant. We can send them to the cardiology sweet, and then they can treat that significant narrowing. The problem comes though, um, when we don't have a very significant narrowing on what happens next. So, having told you all of that, let's go back to our patient, this middle aged man, he's got atypical chest pain. That's what the ambulance crew have decided. And so they think he's at low risk of a cardiac cause. But he came in in the daytime, and because my cardiac colleague was around, we actually were able to do the triple rule out, and I'm going to show you the coronary arteries here. So here we can see is the right main coronary artery, and then as we keep coming. So this is the aortic root. Yeah. And as we keep coming down now, you can see the left main coronary artery coming off. And that left main coronary artery then divides into the left anterior descending, which is this artery here. And then lower down. We'll see. Um, the left circumflex. So I would like you to tell me where the problem with the left anterior descending artery is. I can tell you now. There is a stenosis in it. It's narrow. But where do you think that is? So I'm going to get you on the image to vote on where you think that, um, narrowing is so All you have to do is just touch it. This is very good. Well done, everyone. Keep boating if you want to. I know there's I know we're a small and select group today, but that's okay. Okay. Very good indeed. Now every one of you is right. Actually, So there is certainly a narrowing here because the contrast, which is outlining the Lumen of the coronary artery, just disappears at this point, doesn't it? But some of you put a point here, and some people put a point here, and those are also narrowings. So this person has got very significant stenosis of the left anterior descending artery. Definitely more than 75%. So they would be a good candidate to have a stent put in so they go straight to the coronary department. Well done, everybody. And just to kind of complete it as we come down here, this is the left circumflex, and you can see that's nice and wide, isn't it? It's not narrowed at all. Okay, very good. Okay, so we've seen one coronary artery study, and now your experts on the coronary arteries, I'm going to ask you to look at one more. So this patient is in his thirties. He's super fit. He loves going to the gym. And while he was at the gym this time he got chest pain. Now the chest pain is completely settled down, but, uh, he came in and we decided to do a cardiac CT, and you are going to help me work out what's going on. So you're very good now at all of the anatomy. Here's the aortic root in front of it is the pulmonary artery, and we're going to start searching for the coronary arteries. So there's an artery here. I'm not quite sure which coronary artery it is, but let's follow it. Radiology is all about following things, so we're going to follow it and you keep following it. And it's definitely giving off the left anterior descending artery. You can see that here and then. It also has a kind of branch here, so let's keep following it. What is going on with this artery? Oh, and here's the right coronary artery, which seems to connect up. Uh, so it's actually quite hard to work that all out, isn't it? So let's go through it again. So here we've got the right coronary artery coming off. And actually, what's happened is all three coronary arteries are coming off the right anterior cusp. So they come off the right anterior cusp where the yellow arrow is give rise to the right coronary, and then the left dives off that single origin. It goes between the pulmonary artery and the aorta, and then it kind of comes forward here to the left, anterior descending and left circumflex. So there's a single origin of that of all three coronary arteries and the main left main stem, which we all know is important. Um is running between the pulmonary artery and the aorta. So I now want you to think about why do you think the patient got pain when they were exercising? They've got that coronary artery between the pulmonary artery and the aorta. Why was exercise making it worse? And you got to think a little bit laterally. Think about what happens to the aorta and the pulmonary artery when you're exercising or when you're increasing your cardiac output. Very good compression. Exactly. Keep going. Keep going. Very good. Okay, good. And just see, there's a little bit in the chat. I just wanna see anyone said anything else. Oh, look, someone's written an essay. Thank you for that pulmonary artery and a. Or to squeeze the origin of coronary branch with this individual anatomical anomaly. Fantastic. And someone here has said ischemia. And that's exactly right. The ischemia is due to what you've just described, which is the coronary artery is, um, squeezed by that pulmonary artery and aorta. Fantastic. Well done, all of you. So, um, basically, this is actually called a malignant course and It's a malignant course because you could imagine that unless the person stops exercising, they could actually just drop down dead because that left main coronary artery if it gets completely squashed, there is nothing going to the left ventricle. And without a left ventricle working, you are not going to kind of keep um, pumping blood out. And so then all of a sudden, you could literally drop down dead. So well done, everyone for that. That's good, right? OK, so, um, we've talked a little bit about cardiac CT. I think I've explained to you that it's useful if you can do it. If you can see a stenosis, it's very useful if it's normal. But the reality is, is that an awful lot of patient's, who we do even managed to do cardiac CT on. They have a bit of stenosis. It's somewhere in the middle and not enough to justify putting a coronary artery stent in. And the reality is, is that in the middle of the night, we certainly don't have time to be doing all expertise to do coronary um, imaging. So usually what happens is the triple rule out CT becomes a double rule out CT, and that's what we're gonna talk about the rest of the session. So, um, double rule out CT. Basically, we're looking at the pulmonary arteries, and we're looking at the aorta. Okay, So the next patient, um, is, um, a patient who's very elderly and frail, and he's come in and he's got into scapula chest pain. So at the back, and it feels like it's tearing him apart. And I'd like you to tell me what you think that history makes you think of. Is it an aortic dissection? Is it pneumonia? Is it a pulmonary embolus? Is it too much gardening? So have a think about that. What do you think? That history. So it's tearing, and it's inter scapula. Good. I can see Taiwo has, um, said be, uh, Taiwo. Are you a twin? Yeah. Lovely. Um, very good. Anyone else we want to answer here? I think most people are answering aortic dissection, aren't they? Okay, so aortic dissection is the correct answer. So, um, Taiwo, as you, um as you answered me just now, would you mind describing to me with aortic dissection? What are the what are the things just remind us all. What are the things that the patient might complain of? Mm. Yeah, well, I used to take a section, um, like, as described the patient. We have a very trap chairing pain and as well, uh, question my house as well described. Maybe there's a There's like a butte. Oh, yeah, absolutely. Abdominal bruits. Yeah. So you might hyo to Yes. Yeah, patient might have. I could. Severe potential. No, no, it's when it's ruptured. That patient, we have hypertension, but it is dissected the patient. Yeah, it might have some kind of, um um, question. I have was I was called, uh, um non uniform bp of writing the left upper limb for Mr Yeah. Brilliant. Brilliant. So you're absolutely right because of the dissection. And we'll kind of look at this in a moment because of the dissection. It may be that you're getting more or less blood to say the left arm or the right arm, and so they may have a different BP in both arms. And the other thing you mentioned, um, is they may have a bruit or a brew. It, um which is basically if you listen to the heart um, instead of hearing the normal sounds you hear it sounds like a kind of train is making all this noise. It's a terrible sound. Very good. Thank you, Tyro. Okay, good. So let's just revise a little bit of the anatomy of the arch of the aorta. I strongly suspect that Doctor John Curtice has told you about this already. But let's revise it. So, um, remember, we've got the arch of the aorta, and we've already talked about the coronary arteries which come off the bottom now, coming off the arch. You have these three vessels, don't you? You have the break, Yoka phallic first of all, which then divides into the right common carotid and the right subclavian. Then you have the left common carotid, and then you have the left subclavian artery. And after you've passed the left subclavian artery, you then get into the descending aorta. So if we were to section the aorta, um, the first thing you've got is the Lumen and the innermost layer is the intima around. That is the media. And then around that is the adventitious. So every vessel has three layers, basically, doesn't it? And the aorta is no exception. Now what happens in the dissection is that the intima tears and then the blood that is in the Lumen can pass out of the intima. And it goes into the space between the media and the intima, and you then end up with a false Lumen and a true Lumen. Um, and I often think it looks a little bit like a tennis ball. I don't know if anyone likes playing tennis, but you know how you have that kind of funny, um, U shape on tennis ball. It looks a bit like that. So that's what happens now just to remind you about the classification of aortic dissection. So it's very easy to remember if you can remember the first two letters of the alphabet. So if the dissection arises below be for below the subclavian artery on the left, then it is a Standford be dissection, and it can be treated conservatively. But if the dissection arises above the subclavian artery, and it doesn't matter whether it's only above or whether it's above and below, but as long as it's got the above in it, then it's a sending aorta, and that needs an endovascular stent. So that's the way to remember it. A for above or a sending aorta be for below and conservative treatment. Okay, great. So let's go back to our patient. And here he is. Here is the arch of the aorta that we can see right here. And as we come down, you remember I said it was talking to you about the tennis ball sign? Not sure if any of you agree that this looks a bit like a tennis ball, and you can see this kind of line within the Lumen. And this is the intima that has lifted up. And so one of these, um, spaces is the true Lumen. And one is the false Lumen. And how do you tell the difference? Well, there are a number of ways. Often the false Lumen is bigger than the true Lumen. And you can also use the density to help you, because the true Lumen will be denser. So as we come down, let's zoom in here. Okay? So the true Lumen is smaller and it's more dense. In fact, you can see it best here. This is the true Lumen. And the false. Lumen is bigger because There's, um, kind of less pressure on it so it can expand more, and it's less dense. Okay, Very good. Um, so a revision which, um which Lumen is generally smaller. Is it the false or the true? And would someone like to write that in the chat for me, please? This chapel? Yeah. True is small. Forces big. Very good. Okay, very good. Thank you. Excellent. Well done, everybody. Good answers. So there's a whole thing in medical education, which I'm sure you're aware of whereby, um, if you do kind of spaced repetition, so, like, you learn a fact, and then you kind of go back to the fact, and then you go back to it again, it helps to cement your knowledge. That was the reason why I asked you that. Okay, so where are we? So at this point, if we're looking So this is the ascending aorta, and this is the descending aorta. And here you can see this is the true Lumen. And this kind of gray area is the force, Lumen, and it's almost completely obliterated. The true Lumen hasn't it? And now if we keep coming down, Uh, by the way, this is the pulmonary artery. We'll be thinking about that a lot in the moment. Um, in a different patient as we come down, we've got false looming at the back, which is the gray we've got true, Lumen at the front, which is whiter. And then as we come all the way down, this is the aortic root. Remember, this is where the, um, coronary arteries come off, Can you see that contrast is pouring out of the aortic root into the pericardial space. And so now we're almost a bit like going back to remember our first case where we saw that the pericardium was thickened and had fluid in it. This is a bit similar. There's blood within the pericardial sac here that has come out from the aorta. Now I can actually see the coronary arteries here. So here's the right coronary artery. It's actually coming off the true Lumen. And the left coronary artery is also coming off the true Lumen, That is good news for the patient. Although there isn't much other good news for this patient because, um, the fact, of course, that he has blood within the pericardial sac is not good news. And then if we come down, I'm just going to follow the descending aorta coming down. Keep coming. Keep coming. Keep coming. First of all, you can see someone was asking earlier on. Weren't they about cardiac tamponade? Do you think you can write in the chat here? Do you think this is a large or a small? Um, pericardial effusion. You can just write it in the chat. More answers keep coming. Everyone can answer. Was it a sad he was asking in the beginning about pericardial effusions? Yes, ma'am, I think it would be. I think it would be because a large amount of blood is pouring in the pericardial space. So I think the tamponade will be possible here. You're right. So here, what we can see in this pericardial space is a lot, isn't it? This is not like, Oh, I'm not really sure where to draw the line. It's, like, full of blood, this pericardial sac. So yeah. So the risk of there's a high chance of tamponade here, isn't there? Okay, good. And now we're going to follow the descending aorta down. Follow it down here. Now. Let's have a look at the kidneys. So there's the right kidney here. The left kidney here. And neither of them are a pacifying. Very well. And that is because if you look at the false Lumen, which is the gray area, uh, that is giving rise to the, um, renal arteries. Let me see. Hang on a second. Uh, where did I show? I want to show it to you here. Uh, yes. Well, anyway, I don't think I've included this slide. Sorry. Anyway, bottom line is that the renal arteries are being supplied by the false bloom and not the true Lumen. And that's why the kidneys are not enhancing. Okay, Very good. So now just a little bit of revision. Do you remember that Stanford be arises below the left subclavian artery, and Stanford A involves the ascending aorta. So you're going to tell me with this patient? What type of dissection do you think it is? Do you think it's a B or a with hemopericardium? Good. Let's see. I think I can see if people are closing, can I? Maybe. Maybe Maybe I'm actually confused. I'm actually confused between b and C, because it is. This isn't like yes. Okay, let's go back through it. So the correct answer is it's a type A dissection with hemopericardium, and I'll show you why that is. Uh, hang on a second. So let's just go back through the imaging. So first of all, you remember we talked about whether or not the A sending aorta is involved. And if we go back to the very first set of images, I mean, there's no doubt that descending aorta is involved. But can you see that the A sending aorta, which is here, also has the intimal tear in it, um, at multiple levels here and you can see that that's involved as well. And you remember as well at that point where the tear is in the ascending aorta. This is where the blood is actually coming out into the hemopericardium. So the ascending aorta is definitely involved. Let me just take you to my picture again. Here we go. There's no doubt there's a hemopericardium, but in terms of is the ascending aorta involved? Definitely, because that was what we were looking at just here. This is the region where the blood was pouring out. So does that make sense to everyone? It was the A sending aorta and the descending aorta that was involved. So it was actually this kind of picture that we can see the entire aorta, all the way down to the aortic root is involved. And, um, that's why it's a Stanford A. And then we also know that there was hemopericardium. Someone just said something lovely. Okay. Thank you. Okay, cool. So, last patient now and then you can go home. You can rest because you've had a very busy day. So this patient is 55 years old. They've got chest pain. Uh, they're very breathless. They've just got off a long airplane ride, and, um, they we've checked their d dimer is, and they're high, so we're very worried about pulmonary embolus. So what we're going to do now is we're going to do a study to look at the pulmonary arteries, and instead of focusing on the arch of the aorta, we're focusing on this. This is the pulmonary trunk. And as you know, the pulmonary trunk gives off a left and a right. Hang on a second. Right. Pulmonary artery. Can everyone see that left pulmonary artery and right pulmonary artery. Okay, So what I would like you all to do now, please. On this picture is show me where you think the clots are in the pulmonary arteries because there are clots. You just have to show me where they are. It comes up quite small on your phone, doesn't it? Very small, actually. So remember that the pulmonary artery is here, and it branches, um, into the left and the right. Okay, Very good. All right. So what we can see here is this rounded thing here is clot in the left pulmonary artery. And as I keep coming further, you can appreciate more and more that there's clot here. And these are the pulmonary arteries on the other side. See how the artery comes out, and then it's just filled with clot. I hope everyone can see that now. The problem with this is that if you've got a lot of clot in the pulmonary artery, you've got all this blood coming into the right atrium and then into the right ventricle, and then it's trying to get through the pulmonary system. But there's all this clot in the pulmonary system. And so actually it's really having to work hard to get through the pulmonary artery. And so that right side of the heart is really working, working, working to push blood through the pulmonary artery despite the fact that there are all these clots and usually it manages okay for a while, and then it starts to get really tired. So can anyone remind me what is the law of cardiac muscle? There's this thing about cardiac muscle and efficiency hypertrophy. Well, certainly hypotrophy. You need to see you sometimes do hypertrophy. But in the short term, you can't really hypertrophy. What is it about? It's a law which starts with s. In fact, you might actually have to tell me what the exact nature of the law is because I'm desperately trying to remember it. Anyone want to put this in the chat? It's about basically how the heart works. Well, until a certain point. And then it stops working. Well, uh, it's to do with the stroke volume. Yeah, this ringing any bells for anyone? I don't think so. Yes, yes. What's the question, please? The question is, what is the law? It's a physiology law, and it's about the heart and about stroke volume. And basically, if you put more blood coming into the heart. The the heart keeps pumping out more blood, Right? To make sure that it keeps going around. Uh, someone's got it. There you are, Starling Law. Frank Starling. Yeah, Exactly. Brilliant. Everyone's got it right. Banshee, can you explain to our Starling law, please? I have it in front of me on Wikipedia if if you can't. But I'm sure you can explain it much better to me. Hello? Yeah, we can hear you. Um, yeah. So the it is Frank Starling law, which reminds the amount of witness blood that comes back to the heart directly. So that's right. So basically, what it says is that the stroke volume of heart increases when you have increased blood going into the ventricles. Yeah, but then what happens at the end? What if you kind of what? If you over push it? Is there a point at which the heart starts to fail? Well, it definitely will affect the pre Lord and the actor dot so yeah, exactly. So it all works very well up until a certain point. And then, actually, the whole thing starts to fall off, doesn't it? And that's What? Well done, everyone. So that's what happens. Basically, um, in this situation, the first few hours, the heart is okay. It just starts to work harder according to Starling's law. And then it starts to get tired, and then the patient gets basically acute, right? Heart failure and the way that we know the patient is likely to have acute. Right heart failure is by looking at the ventricles. And we look at the right ventricle and the left ventricle so we can measure the right ventricle, and we can measure the left ventricle, the diameter. And if the right ventricle is more dilated than the left ventricle, it basically tells us that the right ventricle is strained because it's working so hard and that that patient is actually at risk of going into right sided heart failure. Does that make sense to everyone? So, in general, you want the left ventricle short diameter to be bigger than the right, because the left ventricle is the kind of the workhorse, isn't it? So in this patient, it's the opposite way round. We can see that the right ventricle is bigger than the left ventricle. So this patient has got right sided heart failure. So then what happens? And that's the reason why actually, people die quite quickly with pulmonary emboli. The mortality in the first few hours is really high. And certainly, um you know, when you're working on the wards and I vividly remember this when I was a junior doctor, you know, we would have, like, post operative patient's who seem to be doing okay. And then all of a sudden, they would just deteriorate within a matter of minutes, and then they would die. And then basically, what happened was they had a massive pulmonary embolus, and they're right. Heart just couldn't push against it. So the reason why I put this case in is is that the radiologist can make a difference. Because what my colleague was able to do is, um, to put a catheter up into the pulmonary artery, and then they put in some thrombolysis and they were able to dissolve the pulmonary artery clot. And this is a picture of the A heart before and after the thrombolysis. And can you see how the dimensions of the left ventricle have now kind of come much more back to normal? So the left ventricle is more dilated and the right ventricle is less dilated. So basically, I had to finish with an example where radiology can do something, right? That's it. We have made it through Friday night in the emergency department. Uh, I hope that you've kind of found that useful. The things to remember, really are the history of the patient is really important. And you're all really good at picking up on history. Second of all, um, you know, in reality, CT is a very good basic investigation, and that's probably what you're going to be asking for a lot in the middle of the night. Um, it's always worth knowing your anatomy because it will really help you. And I think we've illustrated this afternoon that actually working as a team is really good. So I know you're all good team players, but I would strongly advocate continuing to be like that. OK, final question. Can you please share something that you've learned today? Mhm. While you're sharing that, as that has said, Uh, yes, yes, I have, like, I've heard something from like from one of my one of my professors. And, uh, it's regarding the pulmonary embolism. It is said that in all the time. So when medicine was in sixties or fifties, uh, pulmonary embolism was given the name of, uh, ambassadors Disease. Which ambassadors? Disease. Like the ambassadors. Ambassadors? Yes. Because, uh, the thing is, uh, the pulmonary embolism happens when there is a deep point from buses, which which goes through the wane and then circulates through the heart and then clocks into the in one of the permanent, uh, pulmonary arteries. He said that, uh, this is due to the excess of sitting on the chair or in a sitting position. So he he said that if if so, what does? Why does it makes a difference, right? Why is it called the ambassadors? This is because, uh, if if a person is having a sedentary lifestyle in an office, why doesn't he get permanently amble? Is, um uh, compared to the person who has who is more like a flying who is flying about the ground or in a plane like people who are pilots and who are frequent flyers have, uh, more, uh, susceptibility to get the pulmonary embolism. So he said, there's something to do with gravity. Like how much you are about the about the land. And he said that the name ambassadors disease was given because many ambassadors fly off to different countries. And while many, many times itself happened to ambassadors, when they just leave the embassy, they have a certain, uh, just pain and they fall off and they die. So it was like a rumor that ambassadors, when they go or they frequently Friday, die after they leave the embassy. So that's what I heard. That's also called us the ambassadors disease. I see. OK, great. Thank you for that. That's a really interesting story. It's a bit like the boar have story. It kind of makes you think about the reason is it does anyone want to share anything that they've learned today? Any kind of tips and tricks? Um, yes, the, uh it's regarding the aortic dissection. As I think I wrote in the chat. Like truly small and fall suspect. It's regarding the aluminum point. Isn't it great? Ok, listen, everyone, you've had a long day. Oh, triple double rule out ct. Great. Keep going. You've had a long day. So, um, I'd like to thank you all for your attention. and I thank my colleagues as well Who helped me to prepare this? Um, I don't I'm not gonna do any more teaching today. I think you've had enough. Um, but just have a little think about all the things that we've learned today and have a good evening. All right. Thanks a lot, everybody. Thank you, ma'am. Thank you very much. Thank you, Doctor. Thank you so much. Nice to meet you all. Um, could everyone please take a few minutes to do the feedback form? Um, as always, is very important for us. And any additional feedback you have, you can write in the chat. Um, anything you'd like to share? Anything you'd like to see in future lectures? Um, I'll give everyone a few minutes to do that, and then I'll post the certificate for this lecture. Thank you. Can I just ask for everyone here to indicate if they were also on the last lecture with Doctor Young? Could you raise your hands if you are? What? Doctor Young? Yes. If you were here for the last lecture. Yes. Yes, I was right. Was everyone else who's who's currently on here on the last lecture. Also Yes, I was I was, uh I was okay, right? So I forgot Little bit certificate for the last lecture. Um, I'll post it here now, because, uh, I have most of the time the class regarding my university, so I couldn't attend some lectures. But when I start, I attend further and further. Okay. I've played the one for for Doctor Young in the chat. Now, you could all please feedback for this one, and then I'll put on the certificate for this one. Also recording whiskey your is