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Evening everybody welcome to our part two series of this up to cardiothoracic um teaching series um Today, we've got nile um He's a fantastic teacher today. He'll be going through a presentation with a focus on coronary artery disease. Uh feedback forms will be sent automatically after the end of the session, so we would be really grateful if you guys could take some time out to fill those in for us as a thank you for now being with us today um Ok over to you now okay, so yeah my name is nile um I'm just gonna be teaching about coronary artery disease today, so I think there's a function from your end where you can make it full screen, so if you can just do that because it will just make it easier for you to see everything so just looking at the path of physiology. Um I think on, I think the other one, the other teaching session was on wednesday where we covered the anatomy, so you know the coronary arteries are what supply the myocardium and if we're talking about coronary artery disease, so it's obviously disease of the coronary arteries is that these arteries they get narrowed or blocked, which will decrease the blood flow to the myocardial tissue now, the most common type uh is atherosclerosis which is just the plaques on the walls of the arteries now. If you have a plaque on a arterial lumen, then obviously it's going to narrow it, which means you're going to get less blood to your tissues, which means you're gonna get less oxygen to your tissues um So there's two different types of plaque which you can see here. You have your stable plaque here and you have your vulnerable plaque um that just means that it's more prone to uh erupting um So with your stable one, you can see like the lumen is mostly uh taken up and the lipid court is kind of centralized um but the other one the vulnerable one the looming is pretty much empty and the fibrous cap is very small, so the difference between the two is the size of the fibrous cap. Now, the size is important because if you have a larger fibrous cap, which is the stable one, so it's less likely to um rupture and so you're less likely to get at m. I. So with a stable park because it's obviously stable, but at the same time it's still atherosclerosis, you will get symptoms like angina, stable angina, whilst the other one that will uh that has more of a likelihood of actually causing a myocardial infarct um Then just briefly because we're gonna go over this in a little bit more detail later, it's just some risk factors so when you have high levels of cholesterol if you're overweight, these are things that can be changed so by lifestyle, which is why you tend to try and obviously when you're working and you're trying to treat you always go with the conservative management first before you actually go on two medications and surgeries, so this is what you'd go for first um targeting your cholesterol levels and your weight and then nonmodifiable is your family history and then uncertain risk factors are things like age, hypertension, sedentary lifestyle, lots of alcohol smoking being a male or diabetes. I feel like these are just the standard for any kind of disease, not just coronary artery disease um so the first um thing that we're gonna cover is stable angina, so stable angina, it's got three typical features um I'm not sure what stage everyone is at, but if you're in med school, then this is like the typical features you're going to be getting especially if you're giving your exams, so you've got constriction in your chest, neck, arm, and jaw and usually well, always it's caused by physical activity, so you will never get stable angina, just sat down. It has to be caused by some kind of physical activity and the third thing is that if you use a g. T. N. Spray, your symptoms will go if you get a patient that is using g t. N and it's not working anymore, then you have to investigate it. Further um investigations will just be an e. C. G. C. T. If your e. C. G. Isn't showing enough and a coronary and you if if your ct and your e. C. G. Don't work um and then you just need to know the differences between unstable and stable angina, so does anyone know the difference between unstable and stable angina like in terms of presentation okay, so it's literally what it says so obviously, it's the um when one stable angina does that happen when you're resting whilst unstable, does um also with unstable angina. Like if you have an unstable angina attack, you can still after resting you will still feel the symptoms symptoms, so it's not um alleviated by resting whilst unstable angina. You take a g. T. N. You rest your okay unstable angina, doesn't work like that. Um management is obviously the thing that we said conservative, You always go with conservative first, so if you're overweight, then try and work on that um stop smoking, Work on your hypertension um alcohol intake, and the main thing is for stable angina. You use g. T. N. With a beta blocker or a calcium channel blocker, so it's either or um and then you have two different procedures, which is your c. A. B. G. And your PCI which we're going to go over and these are not really what you'd use first like first line, of course because first line is you're conservative second line medication third line is actual procedures, So the times that you're actually gonna need a procedure is if it starts getting worse and it's your symptoms are not being held by the medication okay, so you have your Pci verse, CDBG, so you've got PCI which is percutaneously coronary intervention and c. B. G. Is your coronary artery bypass grafting, so PCI is more cost effective. Um however, your c. A. B. G, it's got it's just got better prognosis. In the sense you can use it for um patient's that are more critical, so if you're over 65 years old or you have three vessels that have been occluded. You would typically go for c. A. B. G. Simply because it's it's just think if it's a larger procedure. If you've got more vessels that are damaged, you need to get c. A. B. G. Um and pcis they do not prolong, prolong your life. They just help your symptoms for a certain time but to actually prolong the years you've got left you would use a connery artery bypass craft. Um So if you go into acute coronary symptoms, you've got three types, first of all, um you've got your unstable angina, your n stemi, which is non st elevation eh my and my car, deal, infarct, or your st elevation m. I. And the clinical presentation is the really typical one where it's uh central or left sided, and it it radiates to your jaw and left arm. Patient will say it feels heavier constructing and then just the typical ones like your breath, sweating, nausea, vomiting um and you can appear pill or clammy, but the main thing is that sometimes it radiates to your jaw and left arm, or it's central and left sided okay, so the pathophysiology, so you'll have endothelial dysfunction, which can be caused by different things, of course like for example smoking um and this causes inflammatory cells to enter the endothelium essentially when you've got inflammatory cells entering the endothelium, you get fat deposits um so you're gonna get LDL low density lipids which are bad for you. Um They're going to, they're going to start depositing in the subendothelial space and then you get your monocytes differentiating into your macrophages and these are going to phagocytose the LDL which is a really important step because this is what forms foam cells so form cells are characteristic of a c. S. Um and then the macrophages are just going to die, which causes more uh inflammatory cells to come, and then eventually you get your um smooth muscle proliferates so it's just getting bigger and bigger and migrates from the tunica media into the tunica intima, so you're just going more deep into the layers, and then you get a fibrous capsule which covers a flat, a fatty plaque, so essentially what I've just described is this here how we make the plaque right, so it's just how you get your lipid court and then your favorite cup okay moving on, so a. C. S. Um Sometimes it'll develop in patient's who've got coronary artery disease and like we said it's because of the build up of fatty plaques and this obviously causes the main problems which you can guess are now narrowing and narrowing is bad, of course because if you get narrowed, then you get less blood flow, which means less oxygen, which means enjoying a like symptoms, so angina is chest pain due to insufficient oxygen reaching the myocardium during exertion um So that's number one you get narrowing and then the next one is you can get plaque rupture and this can include an artery and if you're fully complete occluding an artery, then you're gonna get absolutely no oxygen reaching the myocardium, which means you'll get my cardial. In fact, the difference between the two is that with the narrowing, you still get some oxygen but with a plaque rupture, you only get well, you get no oxygen, so you would end up with my um um modifiable risk factors are just a gender, family history, so these are things that you can't change. Obviously, you don't have any choice in these, then you're modifiable risk factors are smoking, diabetes, hypertension, hypercholesterolemia, and obesity. Again for um investigations, you'd use e. C. G. Or cardiac markers like troponin, which you've used in an m. I. And the management for this is mona, so morphine oxygen nitrates, aspirin, it's the easiest way to learn it, just then mona, for a. C. S. Okay, so In terms of this, e. C g, can you tell me whether it's an n stemi or a stemi in the chat, please does anyone knows if it's an n stemi or stem, so n stemi is non st elevation, so it's kind of in the name and then s stemi is st elevation stemi, yeah, so it's a study because if you look at leads to three and Avf, so to hear three, I'm not sure if you can see that mouse so 23 Avf you can see the st segment so stemi um It's alleviated, so you can see that it's a stemi literally because the st elevation st segment is elevated right um what about this one does anyone know what this one is so a stem mural and steady. If I say to you look at leeds 123, avf, v 3456, what can you see yep exactly, so it's an end stemi cause If you look at it, so leads to three um a v f v 345, and six. You can see that there's deep st depression which you can see here yeah, so it's a end stemi, okay, so this comes up quite a lot and not just in exams um It just comes up a lot especially when you're on cardiology placement and they expect you to know this, so I'd say really do learn this, so you're circumflex is one v five, v six. You have to know your right coronary coronary artery which is 23 and AVF and then your left anterior descending v 124. These are really important to learn and I guess this has been recorded, so you can look back at it, this, which I got from past med, so can have a look at that um okay. So then you have different types of heart failure, which is low output or high output heart failure, so first we're gonna do low output heart failure um This is also known as congestive heart failure, so in, in this sense, the heart is not able to prompt pump properly and so you can't meet the bodies demands. This is important to know because in low output well, actually I can ask you this so what's the difference between low output and high output heart failure does anyone know yeah so essentially good, so in low output heart failure, it's either a systolic or diastolic problem, so it's literally to do with the pumping in high output heart failure. There's nothing wrong with the heart like the heart is pumping fine. It's just that you've got more mess metabolic demands in your body, so we'll go into this in more detail but essentially low output heart failure has got a pumping problem. Your heart is not pumping properly. High output high output heart failure. Your heart is pumping fine. Your body is the one that's got increased demands, so I know um output heart failure. Again, it's the same thing so it's caused by pump failure, which we said arrhythmias um excess afterload and excess preload. So there's two different types of pump failure, so your systolic or your diastolic heart failure, so causes of your systolic heart failure can be ischemic heart disease, dilated cardiomyopathy or my card itis, your diastolic heart failure is your hypertrophic obstructive cardio myopathy, restrictive cardiomyopathy, cardiac tamponade, and constrictive pericarditis, so once with low how low output heart failure is with your pumping and then your high output one is about your body's demands, that's the main difference that you need to know. So in terms of high output, this is what we've just said, so you're you've got higher metabolic demands, so your cardiac output is normal unlike the low output, so um maybe you were right. Um It's just that the metabolic demands are increased now the reason why they're increased is you can get. Um I didn't put this down on the slide actually, but really common cause of high output heart failure is obesity, so obviously for that you're gonna need to be pumping more right so your body's got more metabolic demands and because of that your heart's pumping, but your body just needs more so that's basically what happens and it just gets worn out. Um So other causes of high output heart failure is anemia. Your hbo venous malformation, paget's disease, pregnancies, thigh, toxic osis, and finding deficiency and then we have different types of heart failure, so we have left and right sided left sided causes pulmonary pulmonary congestion um Simply because obviously the blood is coming from the lungs right, so the pressure is gonna build up in the left side of the heart and because it's not getting pumped out into the rest of the body like there's a backflow that means you're getting less of oxygen being uh sorry, delivered to your muscle and tissue um Simply just like the symptoms are just the standard. Once again, so you've just got mainly shortness of breath. Um The main thing with left sided heart failure is the pink frothy sputum um that's that's keep pink frothy sputum and you've if you um sorry, if you auscultate, then you will hear by base or fine crackles, then you have your right sided, so this causes venous congestion, so the pressure is going to be building up on the right side of the heart, so you're gonna get pulmonary hyper perfusion because obviously your right side goes to the lungs so if it's not going there, then hyperperfusion um symptoms caused now. This is important because if you look back, if you look at the symptoms, so left sided is more about your shortness of breath on exertion, orthopnea, paroxysmal nocturnal dyspnea. Essentially, you're just being out of breath right and your pink uh for the sputum. Your right sided is different because you've got ankle swelling so edema um you're going to get that in right sided heart failure. You've got weight gain um abdominal distension, anorexia, nausea and the signs are your raised Jvp pitting uncle, sacral edema, societies and your tender, smooth hepatomegaly investigations for heart failure. These are just you know your standard e. C. G. Um which will detect any abnormality so like a fibbed anything like that and then you do your blood test so you obviously will do your user knees um for renal function and hypernatremia. I left es for hepatic and Tfts for thyroid, uh glucose and lipid ones. You can also check for those, um but those are modifiable risks aren't they so you can control how much um so basically your diet control right, so you're just you're just going to be changing your lifestyle um So you can use your echocardiogram and you can be use your bnp, so your B type naturalistic peptide and if you have high BnP levels, you know that there's been some kind of my cardial damage um okay, So this is what I found quite important. I'm not sure how other people look at it, but for me this is quite important so what you find in your chest x ray scan, so it's just a. B. C. D. E. F. And I think I should have put pictures up and I don't know why I didn't so I'm just gonna go through these quickly, but I would say like um just take a picture of this because this is really important for your chest x ray findings, So a is your edema, alveola academia, be, is, curly be lines, which is also your edema, see cardiomegaly, d, upper lobe blood diversion, E is pleural effusion, and F is fluid in horizontal fisher. I think these are quite important because um on placement. They do ask you this um and then lifestyle modifications is just the standard self to stop smoking, stop drinking, eat less soul um and then rehab and then we will go on to management so management for this mostly um so we said before was like your g. T. N, beta blocker or calcium channel blocker um for her failure is your ACE inhibitor or your beta blocker and of course you know if you're intolerant to Ace, then you'd use an arb, by intolerant, um what do I mean by intolerance, so what typical symptom does a patient come in with when they use a sin hip bitters, and then you have to switch them to arbs, Does anyone know what is let me scroll down yep, so dry cough. If a patient comes in with dry cough because of a sin, him bitters, you will typically switch them to a arb, um you can use loop diuretics such as furosemide and these loop directors. They just help with the symptoms. They don't do anything else in terms of mortality um spironolactone. If you've got your symptoms persisting and digoxin, for those with AF surgical management is the ones that we went over, so you're c. A. B. G. Or your Pci, so like we said, Pci isn't really that good for mortality, just for symptoms um. And c a. B. G. Again is for major um blockages. So for more any, if you've got blood vessels more than three more than three blood vessels, you would use a c. B. G. Um So this is just going over how the procedure exactly works and so essentially what happens is you have your blood vessels taken from either your leg, chest or your arm. Um I guess it's just a graph like I'm not sure if everyone's seen a graft, but they just take a vessel from one place and transfer it to another, and they like using the internal mammary artery because it doesn't narrow over time like I've run on the slide. Um Blood vessels from your arm and leg. They will probably well. They will narrow over time, but internal mammary artery doesn't so they prefer using that so the vessels inside your chest. Um You remove the graft, you make a cut down the midline of your chest and what they do at this point is like. I said there you get your blood rerouted to a heart lung bypass machine because it's going to pump the oxygen for you because your heart is going to be stopped During this whilst the grass are being attached, so you're getting a vessel and then you're putting it in right, and then the heart is going to start again by using electrical shocks, so this is before and after a pci. Um well you can see here like there's narrowing, you can't really see much and then in the second one you can see this obviously being debilitation okay. So that was mostly the content I have a few questions here, I think I've got around five. If you would like to have a go, so a 60 year old male presents to the gp, complaining of chest pain that begins when he exerts himself. He is obese, but he has no other significant medical history. Recently has been diagnosed with c. A. D. Due to reversible ischemia shown on his myocardial profusion scan. The g. P. Advised on lifestyle lifestyle changes, um he could use as well as medication to prevent his risk of cardiovascular disease, so what other medicine medications that he was prescribed, So this goes back to what we said before what medications are you prescribing, does anyone know the answer for this, so what did we say was the medication uh regime for prevention of cVD. So you know definitely it's gonna be g. T. N. And what two other things did we say which is one or the other but one is first line yep, see so bisoprolol, you know is a beta blocker because they end with lull, so bisoprolol, propanolol, um so GTM spray, and bisoprolol first line, then obviously, if that's not working, you'd use a calcium channel blocker, which is amlodipine and the next one is a 70 year old female has called the ambulance complaining of sporadic central chest pain. She describes the pain to be constricting her neck. It was also aggravated when she was physically exerted when she physically exerted herself and stopped when she sat down. Her e. C. G. Was carried out and there was no changes and her troponin levels are also 14, so that below 20 was the first line diagnostic investigation, so you need to first work out what it is and then the key thing here is pain on exertion and it stopped when she sat down. Yep. It's angina, so the first line for angina. Good yes stable type because it stops when she exerts herself right, so the first line would be ct and you're so d ct, coronary angiogram. Next one is a 60 year old lady with hypertension and hypercholesterolemia, so high BP, high cholesterol. It's admit admitted into A and e after having a 40 minute episode of chest pain with nausea, uh sweating, shortness of breath. She has no risk factors for venous thromboembolism and e. C. D. Was requested and she's got st segment elevation in the inferior leads. A request for troponin levels was made, but it's not returned so what's the most likely diagnosis for this patient, so she has had 40 minutes of pain, yeah so good D, so it's a stun e, so this one was pretty simple because it says st elevation, so it's for her stunning um okay this one uh for this one okay, so, I'm gonna read the question and then I'm gonna go back actually no I'm not because then that gives the answer away, but this is about the e. C. G. That um I said so each part of the e. C. G. Which correlates to each artery. So a 68 year old South Asian man with a past medical history of obesity, diabetes, and hypertension was brought in by brought in by the ambulance presenting central crushing chest pain that radiated down his left arm. On examination, he was pale sweat. He has got 1 40 heart rate and his BP is 90/55. E. C. G. Was carried out and they're suspected that he had an MRI, with the occlusion of his left anterior descending artery so where would you see the changes on e. C. G. Lead for left anterior descending artery, yep d, so we're looking for left anterior descending artery and I'm going to go on to this slide again, so you can see here. V one to v four is left anterior descending okay, so these are really important and then this is the last question, so an 80 year old female um had fallen unconscious at home and she was brought to A and e by the ambulance um okay, it says by his wife, so I assume I was okay, so 80 year old female and then she was just called in by her partner um okay, no mail because I keep saying he okay, so he was pale and sweaty. Um He's got his respirator which is 30. His bp is 80/50 oxygen is 89 on air and heart rate is 80 so his e. C. G. Is what's shown below so what artery is most likely to be affected. Yeah D this is because of the st elevation in leeds, v two, v three, and then if you could see the rest would be before 56 yep okay, so I think that was the last question. Um Again, this is the e. C. G. That you need to learn just in terms of the vessels um. Um Otherwise, that's it um is there any questions anything like that. Thank you so much now. Also interesting um me and I will stay for a little bit if anybody has any questions and put them in the chat before you guys disappear. I'll send the feedback forms out now um. And if you guys feel that in you guys will get a certificate for attending. Um So thank you so much everyone for attending tonight and thank you so much again now for a great presentation. Thank you. Um This is recorded right, so will they be able to access this if and what they wanted yes, yes, so um I'll get that to them as soon as possible, it should be available tonight even um in a couple of hours um So if anybody needs any of the information on the slides um just pop back to the sub two page on medal and it should be right there for you, guys okay, that's for you okay. Thank you.