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Brilliant hi, everyone welcome to the case to session. Um This will look at the basics of cardiology um. The session is sponsored by the n. D. You so don't forget to give them a quick follow um and just to mention some housekeeping rules, please keep your mice and cameras on mute. Unless you have a question, please do raise your hand or ask in the chat function. Um Please do respect for them to chat and yeah if you have any questions drop them in the chat and yeah the session will be recorded just to let you know and do you feel in the feedback form at the end, but we'll send out the slides and recordings at the end um So yeah without further a do, I'm gonna let don't start now so take it away okay, so yeah we'll get straight into it, so uh I'm basically covering the anatomy of case to a lot of salt PCS, revisions, so we'll just go straight in. There is some radiology in there as well, um but I include these more in the sba, so okay, so years ago okay okay so just start off with the surface anatomy, so uh there's several bony landmarks that we can use um. And then we've also got these imaginary lines at how close to sort of define anatomically where things are in the thorax, so we've got our key landmarks. We've got a juggler notch. If we look on the right here, uh we started juggling not at the top and we've got the clavicles that come around, This is at the top of the thorax. Uh We've got the sternum in the middle with the external angle between the manubrium and external body, and at the bottom, got the xiphoid process and then the cost of margins at the side as well uh The sternal angle is very useful because it also marks a second intercostal space, which is where we can auscultate um uh heart valves, which are discussed later on. So, in terms of these lines that we use as well, so we've got the midsternal line in the middle of the chest, um uh Then we've got our to midclavicular lines at the front as well, uh and then come around to the side. We've got our anterior axillary and then our middle auxiliary and posture axillary lines uh and then at the back are scapular line which go to the inferior um angle of the scapula uh and then we got our mid vertebral line as well, so there's a really usefulness to know so that we can describe where things are um on the surface, natural authorities, so then looking deeper into uh into the thorax itself, so the thorax is the space between the superior thoracic fracture and the diaphragm at the bottom obviously below the diaphragm is where the abdomen is uh and then within that we've got our uh our lungs and they're pleur, er and then in between got the mediastinum, so I'm not going to talk about the contents of the mediastinum in this session, but as you remember from your anatomy teaching here in mediastinum, we can remember the content using bats and tents, and in theory mediastinum is divided into three parts antara million posterior and contains uh the acronym dates, so I put this in the notes with this session, which you can review in your own time, but the mediastinum itself. It's the central department explains all the viscera between those plural cavities okay, so moving on, so just quickly talk about the sternum, ribs and cost cartilage is in more detail, so the sternum is the flat bone, it's the breast bone at the front of the chest. Um It's got the manubrium, which connects into the sternum, uh the sternal body and then the xiphoid process at the bottom um. And yes As we said, I got the drug, a notch on the manubrium and the sternal angle at t 45 which is really important landmark uh and then connecting onto the stern and we have the ribs, so we've got seven true ribs, so from 1 to 7 these are the true ribs because they connect directly onto the sternum with their cost of cardiges, and then we've got the false ribs which are 8 to 10 and these are false ribs because they don't connect directly onto the sternum, but they connect through the seventh cost cartage and then we have the floating ribs as well 11 and 12 at the bottom, which don't attach this turn at all okay, and then we've got the cardiac surface markings, so we can use the cost of cartage is that we just spoke about to mark out where the heart is anatomically using these. So the heart itself lies behind the sternum, which is interesting because we used to take uh bone marrow from the sternum. As you can imagine the stone is very thin bone, and there's obviously a big risk of punching the heart, so I don't do it anymore, and we'll take it from the posterior superior iliac spine, so um yes, so the heart itself lies between ribs 2 to 6 um and the, the vertebral level of the heart is between 25 and t eight um And really importantly, the apex of the heart um is in the fifth intercostal space midclavicular line that's a really important place to remember uh and then the position of the heart itself to be marked out using these cost of cartilages oh sorry just slide uh at the bottom of this diagram here, so we've got our right third costal cartilage to our right sixth cost of cartilage that are left second to the fifth intercostal space midclavicular line of the boston, so now on to the actual sort of viscera of the of the thorax, we've got the pericardium which is around the heart, which is the loose fitting sac that surrounds the heart and and the roots, the great vessels and we can divide the pericardium into our fibrous, which is our tough, non dispense non distensible layer and are sarah's pericardium uh and the fibrous pericardium really important because it fixes the heart in the, in the thoracic cavity and it prevents the heart from over filling. If you remember your frank frank starling mechanism from from uh pcs. Uh If we overfill the heart, we're going to have a strong enough muscle contraction to project that blood um so that's really important and then our sarah's pericardium um has two layers who got our parietal layer which uh lines the inner side of the fibers, pericardium as you can see on the diagram and then we've got our visceral layer, which is actually our epicardium um which the it's not the part of the heart and in between this, we have the sarah's fluid that helps to lubricate and reduce the friction as the heart beats um And the pericardium is really important. So we've already mentioned it fixes the heart in the in the thoracic cavity. It prevents over filling of the heart and it also is lubricating the heart, but it also protects the heart from infection uh and in terms of innovation, so the the parietal layer of the, of the sarah's pericardium is highly innovated um and this means it's really sensitive to pain, to temperature and so when we have pathologies where we've got see a pericarditis or cardiac tamponade, the pain and the irritation comes from that irritation of the uh the parietal uh layer of the sarah's pericardium uh and this is why when we lean forward in the patient's with pericarditis or cardiac have not lean forward, these relieves their symptoms, so the inner heart this is sort of a sort of going back to a level biology uh got four chambers, two h 02 ventricles, uh, and then these chambers are separated by valves, so you've got your trikus bid, so you got your h right atrium and your tricuspid valve going into your right ventricle, which comes out to your pulmonary valve, which is a semilunar valve and then we go out to the lungs come back. We got left atrium, mitral valve, uh left ventricle, and then aortic valve at the top, um and our mitral valve is the only valve that has two leaflets, all the others have free. Um I used to find this confusing cause. Semilunar guest sounds like to but they do have three leaflets and they form a crescent shape um So, yeah and I just put in here a image of a echocardiography uh the heart um And it's just important to remember that when you see these images, it is flipped upside down to the atria, sort of sit on the bottom, you got the ventricles at the top okay um and then yeah just a little bit more in detail with the contents of the right atrium in the ventricles, so uh the right atrium we've obviously got our uh you know kava attaching into it, bringing blood back from the bodies, we've got the superior vena inferior vena cava and then we got the coronary sinus, which brings back venous blood from the coronary circulation uh and this sort of sits between the atrioventricular node and the inferior vena cava, so it sits here and then we've got this really important embry a logical remnant, which is the faucet vallis, which used to be the frame noval, which used to be patent, and it's basically a hole between the right and left atrium that allowed fetal blood to bypass the the pulmonary circuit because it's already oxygenated from from month and then the ventricle is really important structures to know is the papillary muscles and these attach onto the cord, a tendon, a, and these are really important to make sure the valves stay, taught that they don't prolapse back through because of the high pressures that are generated when the ventricles contract all right, so auscultatory points, this is a really really high yield thing to know and just what you need to learn um so, depending on the flow of blood is where we can hear. Uh the valve sounds as they open and close on the on the chest, so uh for the aortic valve, we we place the stethoscope over the right second intercostal space, pulmonary of the left second intercostal space, tricuspid, in the left 4th 5th intercostal space, and the mitral valve with the apex beat uh and a really handy way to remember this the way I remember it is sort of using atm sort of cash point so uh atm running down there and then pulmonary just off the side okay big as I said that's just something you need to learn um it's really high yield and then coming onto the lungs, so the pulmonary pleurisy. This is very very is, is exactly the same as the pericardium, uh The visceral pleura lines the lung surface uh and then between the visceral pleura and the parietal pleura, we have the pleural space uh and this contains pleural fluid. Um The pleural fluid is really important. It reduces friction to the membranes when we breathe and also helps the lungs adhere to the to the surface of the thoracic wall when we're breathing I/O and this is really important as you can see in this x ray here. There is a pneumothorax, where it's sort of uh there's there's no definition here so you can see here you've got these sort of striations and stuff of the of the airways. Uh This here is just where air has got into the cavity uh and has caused the lung to collapse um uh and that's when air gets into this space into the pleural space um uh and that trapped air has caused a lung to, to, to collapse in that way uh and then we have the parietal pleura side, the parietal pleural lines of thoracic cavity, and again this is the part that's innovated and it's sensitively pain pressure and temperature. And then just talking about the lungs, so the lungs they got the right and the left lung, so the right lung has three lobes. We've got the superior, middle and inferior, and then to have that it's got to fish is we've got our oblique fissure and our horizontal fisher as you can see on the diagram, and the left lung has only got two lobes um uh partly because the heart comes in this side uh and forms this cardiac uh impression and the lingula, which is the sort of tongue looking shape down here, uh and then we got the superior and inferior lobe separated by one uh oblique fissure, and then the highlight of the lungs. This is the highlight of any organ is where the lymphatics the vessels and everything runs into the lung uh into that organ, So the highlight of the lungs they also have the bronchus and a way that we can remember uh where the broncos is on each lung is using the handing monica royal bank of scotland uh Rbs, so the right broncos is superior, so the right lung, the bronchus is sits at the top as opposed to left wing, where it's it's further down below the artery okay and then the diaphragm so the diaphragm is the bottom. It marks the bottom of thorax and the top of the abdomen, um and yes it acts as the floor to the thoracic cavity, and we have left and right dome, so uh the right domes it's slightly higher because the liver is pushing up under it and then we can remember the uh there's three hiatuses that that passed through uh and allow things from the thorax to convey down into the abdomen uh and we can remember these by using um this sort of handy uh also save you money, but it's not it's um this handy way to remember it, so we've got the cable hiatus, uh which carries have been a caver, the vena cava has eight letters, so because we've got eight letters, the cable hiatus come through that t eight, uh The esophageal hiatus, esophagus has 10 letters, so this comes through t 10 and the aortic hiatus chaotic hiatus has 12 letters that comes through t 12. Um This is also quite high. You would frankly like to ask about this quite a lot too, uh and then see 345 keep the diaphragm alive, the phrenic nerve innovates and supplies the diaphragm um um and then obviously got left you got to front nerves, you got left and right uh and they supply the left and right hemidiaphragm accordingly and then the costophrenic angle, so this is where the ribs meet the diaphragm, so you have normally on a CXR as you can see here, you've got this sort of dark um uh sort of sharply pointed downward indentation where it's uh meeting the sort of white hemi diaphragm here and the white adjacent thoracic wall uh and that should normally be nice and sharp and pointy like this. However, when we have uh blunting of this, uh this can be caused by pleural effusion, any any liquid or anything that's in this causes this to blunt. It's quite an important thing to look out for on chest x rays um. So I showed you I've put on this side here some causes for blunting of the cost, a phrenic angle. Um There's a pleural effusion, lung hyper expansion. Uh If you think of people with COPD and they got really hyperinflated chests uh plural abscesses and then also hemothorax uh cause the same thing as well so onto some s. B. A. S. Uh It's the first one, so uh atrial septal defect often occurs the site of an m, biological interatrial shunt present in the fetal heart, which the following embry a logical structures or features is involved in this defect. Don't know if I can launch the pole you, then I think you might have to apologies, give me a sick. I will give me 30 seconds make a calm pathetic upset more uh I think you should be able to yeah, I got that been quite cheeky with this one. I caught you out early on a lot of you have put d, and although that is sort of the right line of thinking, the answer is going to be see because I've said in this embry logical, so the embryo logical into atrial shunt is the frame and oval and the remnant of that shunt is going to be the faucet of alice in life okay. So let's question, a 96 year old man presents with the two week history of left shoulder pain accompanied with hoarseness of voice. Having taken a full history examination of the patient, The registrar orders this chest x ray, which is shown below which of the following is indicated by this chest x ray. This is a tricky question. I just want to get some of the radiology in there, so um it's a poem okay. I think in the history that he has left shoulder pain and see if there's anything on the chest x right, there okay, okay, so uh the answer to this one is d so I don't know if you can see on this here. Uh It's a very common uh well it's a commonly examined question uh This is a pancoast tumor, so I don't know if you can see on the Diovan, is a it's a bit of white here. This is this is the tumor and it often compresses onto the recurrent laryngeal nerve, which supplies the voice box uh And this is why we've got hoarseness of voice is a tricky question, though so um I think the common uh huh slide, so a 30 year old man has presented to the emergency department after seeing his gp with an intermittent high grade fever of two weeks duration. Um On examination, the patient has poor or hygiene and an audible end-diastolic normal, ask, irritation. The trans esophageal echocardiograms performed and that shows the fall and what does this image show sorry uh oh so we got another tricky question just trying to get you used to seeing those radiology of the anatomy um looks good so far actually remember which uh these chambers um which, and the valves in between okay those advances already most of you've got it right, so this is uh going to be a some mitral valve, so we've got our uh left atrium down here, the mitral valve in between and the left ventricle. As you see also, this is the biggest chamber which makes sense um and this is infective endocarditis. Persons got poor oral hygiene, which is which allowed bacteria to get into the, into the bloodstream uh and um in fact endocarditis most commonly effects that the mitral valve as well. Uh next one so India is a known asthmatic who has presented a sudden deterioration in his asthma. He is struggling to verbalize. Do two acute onset shortness of breath and sharp pleuritic chest pain. On examination has unequal chest expansion, but the patient's trachea remains central. This patient's chest x ray shown below what is the diagnosis. This is something we did talk about in the yes pieds, give you back more time with this one okay 15 more seconds. Yeah good job with this one as well. So um yeah this is easy. This is the right side of simple pneumothorax, so as you can see you've got the sort of loss of definition here because this is aaron the pleural space um and it's not a tension pneumothorax which a couple of you did put because the trachea is remaining central attention. Methorexate can push to the other side. Oh yeah there you go, so you can see this tension pneumothorax, so you've got loads of air in this country, really push the lung down and the pressure that's built up has deviated the trachea to the other side as you can see whoever did this chest x ray is going to be in trouble because it's an acute is an emergency, so they would normally put a put something in to relieve that pressure straight away. And then a 32 year old man is brought to Emergency Department coughing and wheezing after an episode of alcohol intoxication. On examination is reduced, breast sounds on one side imaging shows it is aspirated a foreign body, which is including an airway structure, which is the most likely location for this foreign body to be stuck in um slips the toe, so thinking about our that way, um okay to the time 3 10 more seconds, it's pretty 50 50 okay yes you guys have gone exactly 50 50 on b and c. Um The answer to this one is going to be changed. It is see so the bronchitis, so on the right side, it is steeper and it is wider than the left side, Which is why when we put people in the recovery position, we put them on the left because they're less likely to have things go down and aspirate and get stuck um in the left bronchus than than the right bronchus um so yeah because it's steeper and it's it's larger than things tend to get stuck down there because of gravity. And then a 74 year old woman presents with intense fatigue, shortness of breath and ankle edema. The doctrine called Oscar takes the patient's heart valves and the detection, rejection, systolic murmur heard loudest over the aortic valve suggesting aortic stenosis, where did the doctor place the stethoscope to hear this murmur. So just remembering our auscultation points that we discussed yeah we're feeling very confident this one which is good, um So yeah this is a second, this is a this is your right second intercostal space. If you remember, we've got that atm pneumonic way of the memory, things, so it's it's starting with aortic and the right hungary on the left. Trikus for den, mitral at apex beat okay. So next, hello is to describe the arterial supply the heart's a bit more and asking for me, I'm very but we'll get through this bit quite quickly, so the great vessels, so the aorta we can divide into three parts, so we've got the ascending aorta coming up from the ventricle and the arch. They also with these vessel doses, which were quite in a second and the descending water, which comes down through the thorax and into the abdomen, um the ascending and also so this is where the coronary arteries come off and the blood seeps into the coronaries during diastole and then we've got the artery water, so we've got these different branches that come off the top, which supply their head, neck, and the arms, so the breaking catholic artery then divides into rights of clave, in the right common carotid, then we have the left common carotids and then the left subclavian um yeah. So then talking about the coronary arteries, so as I said the coronary arteries they filter in diastole and this is because as the heart relaxes the pressure and the ventricles uh comes lower than that. An aorta and the blood wants to push down into the, into the ventricles, but as it does so, it shuts the aortic mouth and then the blood seeps into the coronary circulation as you can you can see at the bottom there, um so the right coronary artery comes around the heart. If you look at the diagram here, right coronary artery comes around, gives off the marginal branch and then also the posterior interventricular branch in the majority of people uh The right coronary artery supplies sort of r. S. A. N. Node which is really really important it gives off on the s. A. N. Branch um and then the left coronary artery gives off a left anterior descending. We've got diagonal branches that come off of the left anterior descending and we also have this uh complex branch, which comes around the back um and then the company needs we have our coronary veins, so the marginal branch of the right coronary has are small cardiac vein, the posterior interventricular branch has the middle cardiac vein and the left coronary artery. Uh The sorry the left anterior descending artery uh is a company with the great cardiac pain, and then these veins all merged together and form the coronary sinus which drains back into the right atrium um through the uh coronary artery. The coronary signers orifice um that we saw earlier. Um So yeah, so talking about the, so I said that the posture interventricular branch comes off of the right corner and the majority of people. Um However, this is sort of an 80 to 85% of people that are right cardiac dominant. There is a proportion of people 15, 10 to 15% that are left cardiac dominant where the posterior interventricular branch comes off. The left. The circumflex artery, or even the left anterior descending actually comes all the way around the bottom of the heart and comes up and supplies the back, so majority of right dominant. Then a few are left um and then talking about e. C. G. Territory. So this is also a really high yield thing to know is some of the you cover again in year two. In your case 12 So the e. C. G. Um leads represent basically different terraces myocardium depending on the place with the electrodes uh and since the anatomy of the coronary vessels is relatively predictable, um we're able to predict with relative accuracy the pathological vessels causing em eyes. So, if you look at the trace at the bottom, I'm sure you've heard um In your teaching that the inferior leads a sort of the boot of the e. C. G. So you got 23 in a. B. F. Here, um but I learned a really funky where you could remember it on placement uh recently which is using the pneumonic sally, so if we start from v one to v six, we've got s the two s per ceptcell uh and then we got our anterior and d three, and before then we have the five and b six being lateral, and then if we sort of go back and draw backwards, sort of l, I guess up to a. B. L. And lead one uh This is the l. And then we've got the inferior leads 2 to 3, and AVF, so I hope that makes sense it sort of, makes sense in my head that you've got uh sally there uh and then each of these corresponds to an artery as I said, so uh aricept also uh do you want to be four, are left anterior descending uh lateral leads represent the left circumflex artery and then as I mentioned because of the difference in cardiac dominant, the inferior leads, which are the posterior interventricular branch either represent pathology in the right coronary or the left circumflex, depending on where the pasta interventricular branch comes off okay and then the last slide before the s. P. A. S. We can go back to the great vessels of the thorax, which is the uh looking at the veins so we've got the superior vena cava coming here and this is formed by the merging of these break a catholics uh and these break a catholic uh the right and left breaking phallic are formed by the right and left subclavian vein coming in from the arms and then the internal jugular veins coming down from the, from the head and neck um and importantly, we use the right internal drug in a vein when we examine uh people for jvp, because this gives us a representation of uh the atrial, the right atrial pressure because it's like a column straight above above it, which is why we use this one um and then the inferior being cave that comes up from the bottom is formed in the pelvis by the common iliac veins um and it can collect all the blood from the abdomen uh parks upwards uh and it drains into the inferior right atrium as we saw earlier, Okay, so now on to the s. P. A. S, so a patient is presented to the Emergency Department of new onset chest pain and shortness of breath and the cds performed, which shows st elevation in the anteroseptal leads angiography shows the occlusion of the coronary vessel in which artery is the inclusion found. It's a little bit on those e. C. G. Territories spoke about which I hope I spent okay, don't think confuse you too much for that um it looks good so far yeah get a few more seconds, yeah all of you got it right so that's good to see uh This is the left anterior descending okay, so just put it on, so max is playing an intense game of rugby and his heart rate has increased to meet the oxygen support, oxygen demand of his muscles. The heart received its own option to pump at this increased rate through its coronary circulation. When is left coronary artery, blood flow highest, uh moving more support, yeah uh huh yeah that's really good, okay and the pole there, so all of you have put in diastole, which is really good. A few of you put late diastole. The correct answer is early just because when in early diastole, blood flow is going to flow into corners quicker because the pressure and the pressure difference between the ventricles and the water is going to be higher, so it's going to come down with more force, shut the valve and seep into into the coronaries. Okay. Next question, emily is revising the anatomy of the aorta and she remembers that the aorta can be divided into three parts and that each part has different vessels branching from it. What is the third branch of the arched aorta. Yeah you you got it right again which is really good um So yes gonna be d left subclavian okay julia is an f one working on the cardiac wards. One of the patient's in the world has recently experienced an m. I. Which resulted in a third degree heart block. This was because the BP, h. A, ventricular know was compromised, which coronary vessels is responsible for supplying the avian with blood. I, I don't think I mentioned this actually, I did say about the s. A. N. It is the same artery that surprised both of those, so who knows the pole nice, yeah really fast on that, that's really really good yeah, so this is the right coronary artery, so and the pole there um yeah very good to the right coronary. It supplies the the sinoatrial node and also the atrioventricular node, so it's really important so when people have um pathologies, know you can get heart blocks because the the blood supply to the atrioventricular node was compromised, but that's something to uh forward on inter, second year, uh but it's good that you know the anatomy there and what it supplies. Naomi a sec, is a second a 63 year old female who has had a son AM I and is now representing the symptoms of heart failure. Her heart is not pumping sufficiently and so as a bachelor blood from the heart. This can be assessed on clinical examination of the cardiovascular system by visualizing the pressure in one of the great veins in the neck, which the following veins do you. Use. Thank you. That's so cold, it's been very quick on this. You're doing really well okay a little bit more mixed now okay. I might have gone over this a little bit too quickly. The diagram um yeah okay. I'll end the poll there, so the majority you have actually put a which is the right external jugular vein which isn't correct um It is it is see it's the internal jugular vein um So yeah because this vein sits directly above the right atrium as you say, we can use it as sort of a accurate sort of measure of the pressure in, in that um in that circuit because the backflow will come straight up into that vein, so when that's raised that sort of showing that the pulmonary circulation is um it's sort of blocks okay uh and then I think this might be the last question. Uh The posture interventricular artery supplies the posterior third of the interventricular septum uh interior aspect of the my card in which cardiac pain runs alongside the posterior interventricular artery, so okay, yeah that's good yeah, the majority you got that right again, so uh this one is these it's the middle cardiac veins. A small cardiac vein uh drains the right marginal artery, middle cardiac vein is the posterior interventricular artery, great cardiac vein is your left anterior descending. The coronary sinuses what these three uh come together to form which drains into the right atrium and the esophagus vein comes up from the, from the abdomen. It drains into the inferior vena cave. Okay. Let's be done um Great yeah mm I think owen is next, so he will talk you through um lipid metabolism and transportation. I think the first ones endothelial function uh 31 2nd okay here is a mood, so yeah the first of all I have is the endothelial cell function and so I can let me get the pulls out of the way um interfered function and how it's associated with aging. So first question uh I'll start of the questions. Um patient presents at the g. P. Uh during wintertime uh complaining of pain and swelling in the fingers both hands. Uh All the thing is this happens after running apart. On the examination, you found poor nail growth and palate in the fingers, palette means paleness, toes, and air lobes. There are no signs of systemic inflammation and patient has no other medical history, which of the following diagnosis is the most likely can we start full. Please I'll start it uh and the pall then yeah, so the majority of you answered it right um and very good uh The correct answers. Um option A that's Raynaud syndrome and I'll go on to explain what that is. So Raynaud syndrome is idiopathic vasospasm. Um It's a reversible constriction of the small vessels usually in hands, ear lobes, and the nose um and it spasms up and blood doesn't get they're mainly in the small arteries and the symptoms can be frogging pain, paleness, cyanosis, and definite treatment is nifedipine, which is a calcium channel blockers, which helps relax your blood vessels, so second question type two diabetic patient suffers from hypertension and is being treated with the following drugs ramipril, bruce, opera low value fall certain metformin deepa glyph lotion presents of signs of Raynaud syndrome, which of the following is the likely cause. Oh sorry I need to stop the fall again. Mm yeah we've got a just one more and then we're in the pool there yeah we've got nine, so we're mainly split between option A and B and the correct answer is option a principle oh so principle oh is um b two blocker and I'll go on to explain which so uh press opera low is a selective beta a receptor blocker, but it does bind to be to to address address allergic receptors, so it does affect to some extent um beta two receptors and these receptors you can find in bronchial smooth muscles and or thelial muscles and fat cells and the blockage of these receptors. Sometimes it causes an exacerbation of Asmus, copd, and in this case peripheral smooth muscle basal spasm and just want to bear that in mind, especially asthma. That comes up in questions quite a lot and yeah that's just a side effect of beta blockers. Okay Next question which of the following is basal constrictor is a vasoconstrictor released by the endothelial cells, Don't start the pool again, mhm, but I mean it's not just need to check the sides. Uh These questions correct right, so majority of years ended B and a feeling one and that's the correct answer and on the next slide uh just share the table, just I don't think there's a need to explain this mainly just memorization of what's released. What does what so the top table is what's released by the endothelial cells. The bottom table I've separated um is, are the, are the size kinds chemicals, hormones released from other compartments and the body, other tissues um yeah Just something to learn uh This will be sent to you in the answer in the sBA pack, so I won't bother going through this and then next question which of the following is not an effect of aging on endothelial cells, start with four, again sorry uh there was soon yeah underlined the not a bit all right, we've got six people answer. If breaking news get a couple more, This question is a little bit harder all right, I'll end the pool there um majority of the majority of you managed to get the question right. It is, option D the ab, abnormal folding of the federal in one protein. This is an effect of Marfan Marfan syndrome, which is a uh autosomal dominant uh autosomal dominant mutation, uh which goes for this protein and the ms folding of this course is um abnormal abnormities in type one collagen and this can cause major complications such as scoliosis and this caving in and caving out of the of the sternum. You can have a increased risk for aortic aneurysm and dissection. You also have an increased risk to myopia, cataracts, and glaucoma. Um Your skin will be thin, translucent, and will bruise easily. Um you're likely to have pulmonary fibrosis yeah and also in terms of management, you wanna watch out for aneurysm and dissect, dissections. Because that's the most severe and management for the muscular skeletal um complications would be surgical and also they would need to be prescribe pain management because a lot of these complications can be quite painful and people with Marfan syndrome are likely to develop it. Eventually, so, next question which of the following anti clotting agent is produced by anti clotting agents is produced by endothelial cells uh. It was autumn yes, I have uh huh and the pool there we've almost got even split between option d. N. A. And the correct answer is um is um tissue factor pathway inhibitor and Eathorne been three, I believe is released in the liver yes, um so yeah, um anti crossing function of the nefarious houses listed here. The things they release is tissue factor pathway inhibitor that prevents factor 10 A binding prostate gland side um process cycling and nitric oxide. I don't directly have anti clotting effect, but they help with blood clots, so prostacyclin has anti inflammatory, so they so it acts against cytokines that promotes clotting and then nitric oxide helps relax the blood vessel and increase blood flow. Help you flush small blood clots away if if possible and antithrombin three is produced in the liver and the mass cells produce heparin and yep. The motive axion is um of heparin is accelerate the action of an teeth from been three. Therefore, it is dependent on this protein and we change the order of how we present, the all those bits a bit, so we'll do l 06, 1st so lipid transportation of metabolism in relation to cardiovascular health and disease which of the hormones below stimulate like pollicis, It's a simple one, we'll start with and work for a few more answers, okay, we're gonna pull their yep. This is some of those annoying pcs, questions, so yeah the correct answer is glued to con luca, gone Glucagon, yeah not much of that is just happening to memorize and then next question which of the following protein is affected in familial hypercholesterolemia, affects, comes up a lot in um s one, s two, and so I think I I think I remember it coming up once or twice in pt, So good thing to know about yeah and the pool there. Um It's split between B and A and the correct answer is a is the low density lipoprotein receptor which is used to um absorb low density lipoprotein, so these lab of proteins that contain some fatty acids, some try try astragalus rights, and some cholesterol into the liver and when you don't have that receptor, you have a lot of fat floating around in your um in your bloodstream and that can cause complications like after, after road sclerosis and causing mild cardio infarction and etcetera. So in terms of inheritance, it's autism is dominant and you have two copies of this gene, when two of them are damaged, you have extremely high levels of LDL and you are extremely high risk of complications, mainly myocardial infarctions. In terms of management, you can have um lifestyle changes, try to avoid fat um and then high intensity statin this prescription and then is that in nz tim mono therapy, um also referral for endocrinology, endocrine specialist for homozygous, which is the more severe form of ethics. Okay Next question question which of the following is is responsible for bringing excess cholesterol back to the liver from extra hepatic tissue er one pull there. Most of you answered e and that's the correct answer that's high density lipoprotein which just contains mainly cholesterol and I've put in the table what each of these do t. A g style for try a star glycerol, but it's a ride or glycerol and yeah you can read through this later, I won't bother going through them one by one, but in terms of HDL that mainly just contains cholesterol esters and yeah this is what it does uh. Next s be a question, so we've got which of the following is the mode of axion of uh atorvastatin stop that starts the book, Yeah yeah statin is one of those. In other words, I tend to forget quite often when I was in Year one and two. Okay well in the pool. There we got a split between a. B. C. And the correct answer is option A, which is the Hmg, coa reductase and yeah and option b. Oh sorry, if we go back, option B option B would be about, asks the question psk nine is a protein that's responsible for absorption. Know inhibits psk nine is a protein on your liver cells, which down regulates l d, l, d, r, l, d, l r, and this psk nine is a new class of drug inhibits the down regulation of l d r, l, d, l r. So you have more of those receptors, and it help you absorb more fat into your liver, so that's not a sin I believe and then and then activate p a r for increased uptake and oxidation that is another drug you don't need to know vin you wanted to and to continue sBA SBA which of the following is a contra indication for uh all the statin okay well. Six people answered seven yeah wonderful there. Um The majority of you selected E, unfortunately not the correct answer. It's uh chronic kidney disease. If you're if you picked, e, you're thinking of aspirin. Yep sounds similar, but no uh so chronic disease. Chronic kidney disease. Why can you not prescribed a atorvastatin just to explain that is. Um If you have chronic kidney failure, you won't be able to filter out the drugs as part as well and you have the increased pharmacological effect of a trevor statin and you get side effects from that and option E, that's a contract indication for aspirin, you get red rainy syndrome. I believe that's how you pronounce it. If you give aspirin to younger children, but sometimes it's indicated okay can everyone see the screen alex, is it clear okay, nice, so yeah my elbows will be on L3 and five, so we'll start without further a do so for L3. Is gonna be explain the physiology of cardiovascular function including cardiac muscle, the cardiac cycle and cardiac output. So first start off with an s. B. A. So you're a medical student and you are asked to analyze the histological sample, what is the sample showing I gave you guys 15 seconds and so this should be pretty straightforward. They should take you back to pcs I think they've changed the pCS three now, so this should uh be recent revision okay. We'll end it there, so we're getting a mix of answers here, so we've got some and even spread of answers. The answer is actually be so it's going to be cardiac my muscles now um cardiac muscles will have inter kelated discs um and they have less striations um and they have a bit of branching as well, so interc, elated discs are going to be the parts where they allow for cardiac myer sites to act as a sin city um and that's where they all work together. Um scalise and muscles are going to be quite uniform and quite straight um and they'll be on branched and very striated um smooth muscles will have no striations at all. Um Now dense irregular tissues will contain collagen and fiber blasts, which are embedded between them and dense regular are going to contain parallel collagen fibers and fiber glass will also be embedded within them. Okay next question and just to mention that his his histological sample was quite vague so bored in whoever got colleague Meyer sites sorry, um So you asked about the cardiac action potentials and you record that there are five phases to this process in which phases um sorry which phase do L type calcium channels open, so we'll be talking a bit about the electrical activity in the heart as well five more seconds okay. We'll end it there another even split, so most of you have gone for be, but unfortunately the answer is actually phase two, so phase zero is going to be considered the points of deep polarization and this will be the upward gradient on your graph. Phase one is going to be you're slightly polarization after phase zero um sorry re polarization and that's going to be caused by a transient outward potassium and chloride channels. Phase two will be the correct answer because that will consist of calcium channels, letting calcium into the cell, whilst those potassium channels to release potassium into the extracellular matrix and that causes that little plateau that you see in them that action potential graph of cardio, cardiac minor sites, phase three is to phase where the cells are being re polarized um and this will consist of slow delay um potassium channels, letting potassium out of the cell alongside the rapid delay potassium channels, and phase four is going to be the phase where potassium re enters the cell to recharge for the next action potential and this is gonna be facilitated by your inward rectifier condoms. Okay. Next question so you're a medical student on your emergency block and you were oscar tasting the patient's heart valves. Upon completion of the examination, the fy one asks you um what this sounds represents what is the lab sound indic, indicative of okay. Three Astra polls, all right, we'll give you guys five more seconds ok brilliant, so most people have actually gone for a and that is indeed the correct answer, So there's gonna be two physiological hot sounds in adults, so s one and s two s one is caused by the closure of your Avey valves during systole um whereas s two is caused by the closure of the, they will take compartment, revolves um and systemic pressure overcomes the pressure exerted from the heart. Um so a few extra heart sounds that you might want to know. Two s three is going to be known as atrial gallop. Now, this sound is caused by the rapid filling of the ventricles, which causes the cord, a tendonitis snap open and usually um the closure of the valves um causes a sound but because this rapid filling will elicit a sound, um which gives you that extra s three, this is normally um physiological in pediatric patient's s for, however, is not so physiological um so it's more pathological this is when blood is forced into a stiff and noncompliant ventricle um due to hypertrophy and thick thick wall so that's yeah ventricular gallop, so atrial gallop is called that because it's um s free uh free, so atrial gallop is called, so due to the s three and s one sounds being closer together and s three will happen before s one, whereas ventricular ventricular gallop is called that because as far an s t u r closer together and as for what happened before. S too. Next question, so you are revisiting the cardiac cycle and the pressure changes within each chamber. Uh ventricular systole cannot occur forever and you know that when the heart relaxes, there is an event where when the aortic and pulmonary valves were shut, what is this called okay. I'll give you guys 10 more seconds all right, we'll end it there brilliant, so, the majority of you have gone for e, and that is indeed correct answer, so that's going to be your dicrotic not for urine to zero, so a v. Valve closure will happen when the ventricular pressure is higher than the atrium, which push the blood against it and the valves were shut. Now, the valves only open when the ventricular pressure has dropped far enough for the valves to reopen. Um Now, aortic um the aortic valves were open when the ventricular pressure exceeds the aortic pressure unless the patient has a condition called aortic regurgitation, where the aorta cannot shut properly um for which you will hear a little murmur like a whooshing sound around s too as blood, sort of washes back into the ventricles. Now. Also pressure does not have a sudden drop unless the patient has the conditions in their hearts, Ailsa, or when the aorta ruptures um or The patient has an aortic dissection, which may cause a slight dip in that pressure and the dicrotic notch is caused by blood being pushed against the aortic valve and it bulges slapped, built, bulges into it slightly, which builds a momentary pressure in that area and this will help with the pushing of the blood out into the, into the body because of the elastic elasticity, the arterial elasticity. Sorry Right next question, this is more on cardiac output now, so a patient is having a review of their heart function and the doctor mentioned that the injection volume is around 50%. You decide to revise your knowledge on cardiac physiology. I remember that cardiac output is governed by various factors, what is the correct equation for cardiac output. Sorry, give me a second cool, we launched the polls now all right, we'll give you guys 10 more seconds okay, nice, we'll end it there, so um everyone's gone for c um and that is the correct answer, but I'd like to add that there is also another correct answer, which is answer d. Um so there are actually two equations for cardiac output, heart rates and stroke volume or determinants for cardiac output. Um There is another one, so mean arterial pressure is governed by cardiac output, multiplied by systemic vascular resistance and if you rearrange this equation, you can end up with cardiac output being mean arterial pressure over systemic vascular pressure oh right just a bit about the cardiac muscle histology. Um It's just a quick vision over this. Um You remember that cardiac muscles are almost middle ground between scalise and smooth muscle. There long slightly striated and branched. The key determinant between cardiac muscles and the rest of them is that inter kelated disc between your cardiac myer sites. Now these will allow for your my sats, acts as that since City, um which is basically a fancy term for the all actors. One um adherence junctions basically anchor these maya sites together and they transmit the forces from one minor side to the other, and asthma. Zooms will reinforce the adherence junctions and prevent the separation during a contraction and gap junctions allow for ions to pass in between yourselves and that propagates your action potential and just the interrelated discs. Um They are these little um bars along the cardiac myocyte cool, so in terms of excitation, contraction, coupling of the cardiac myer sites um what happens is in 0.1 your action potential will arrive and that will transduce down to with your t. T. Bills, So stimulation of the calcium, stimulation of calcium entry happens from the extracellular matrix and you're are Y are receptors um detectives arise in calcium and initiate your calcium induced calcium release and this releases a large amount of calcium into your psychopathic reticulum, so then calcium oh bind onto TN, see the t n, c, b, n, t, and calcium, and then this cascade um of changes with uh will cause your TN troponin I to move off the acting binding site, so troponin I is actually this inhibitory component of the troponin complex and that stopped the myosin from binding onto your ACT in TNT is just a positional troponin and that helps your myerson bind onto the accent and terminations, is when um there is re polarization and the calcium um ions will drop in the concentration and calcium is taken out, so calcium will be taken off your t. N. C from um enzyme catalyzed processes, and that is resolved into your psychopathic reticulum by circa circa is just as fancy pump which pumped back calcium into your psychopathic reticulum. Cool um Just a few things about the phases of cardiac mine sites, so phase four as I said is when the cell is at rest and it's ready to depolarize. Phase four is when your cell becomes D polarized and this is triggered by your rapid sodium channels and that lets sodium into your cells. Phase one is when it repola rises slightly and there's potassium and chloride movement out of the cell. Now in phase two, this plateau is gonna be achieved by your influx of calcium into the cell, whilst potassium oozes out of the cell and phase three Finally, is your deep polarization and this happens via your rapid, delayed potassium channels cool and just a bit about the actual potentials in sinoatrial night sights so it's slightly different compared to your normal cardiac minor sites, so in the sinoatrial node um the action potentials are slightly different and there are there are changes to the phases and the amounts of phases so in uh sinoatrial cells, there are only slow sodium channels in the sinoatrial node um and this allows for a funny currents basically um which has its own intrinsic rhythm and automaticity and this is known as phase four. So in phase zero is that the polarization phase with calcium being the primary iron um driving this electrochemical gradient, so it's no longer sodium is actually calcium that drives this gradient, and in phase three is going to be that re, polarization of your myocyte and this is with potassium's so you're rapid, slow delayed, um If your rapid's slow delay and your rectifier channels, and all of these will work together to move potassium out of the sole cool and just a bit about cardiac cycles, so initially they can be quite confusing, I'm going to try and break it down a bit by bit just to try and make it as simple as possible right, so we start off with the start of the cardiac cycle, so you've got you want to think of it with three events right you want to think of it with your atrial events, your ventricular events and your aortic events, so I've marked out the different lines and the colors and what they mean so we're going to start off with the atrial events, so the atrial begins to fill passively and some of the blood will move in from move into the ventricles and at this point, the heart is completely relaxed, so it's complete diastole and in terms of the ventricular events, blood is filling impassively, so your pressure technically increases because there's no to space changes. Just blood moving in the aortic event um basically aortic pressure will fall as the previous cycle has occurred and blood is currently moving through to the systemic vasculature. So next next point, um for your atrial event, asia contracts and this produces your a wave and this is where the pressure bumps up slightly and pressure returns. Um. When blood moves out in the ventricular events, blood moves from the atrium into the ventricles and that causes a rise in the pressure and the ventricles will accommodate for this with your elasticity, elasticity, so the pressure then returns back to normal so that causes another bump. Um In terms of the autumn is still falling, the pressure is still um not really going anywhere okay and this is where everything sort of kicks off really so in the atrium, blood will bulge against the atrioventricular valves and this will cause a slight rise in atrial pressure producing your see wave now. With the ventricles, the ventricles are contracting and they shut the a. V. Valves against this pressure. Now, aortic and pulmonary valves will not open yet because there's still a higher systemic pressure in the air water as denoted here and that causes a bit of an isotope ice a concentric it is an isotonic contraction, so the muscles aren't really moving, but it's contracting if that sort of makes sense, um and the aortic events. What happens is aortic pressure will push against that. Aortic apartment revolve and that which results in the ventricles having to equate or surpass this pressure. Now this causes that isotonic contraction of the ventricles when they're pushing against the force that is still higher, therefore there's no net movement now. Eventually this pressure will become. Um Eventually this pressure will be overcome and the blood will rush into the aorta where the it would take. Um pulmonary vials will finally open and the next phase is diastole so that's really well then occur, and when the venture when the ventricle pressure falls below your atrial pressure over here, the a. V. Valves will then open, causing the blood to rush into the ventricles and dropped the atrial pressure and that produces your little v wave here and um in the aorta, the aortic valve will close and blood will rush back against the valve that causes a phenomenon called the dicrotic notch or the zero now where the blood pulls by the aortic valves. Um This causes a temporary rise in the aortic pressure and this helps the body efficient efficiently pump blood out as the also is quite elastic and it records quite easily so when there's pressure, so when there is passive pressure exerted, the also can use this to record and push the blood further cool. Hopefully that was helpful um so I spoke a bit quickly they're just trying to get through this as quickly as possible right so cardiac output, this is just some of the this is the equation, and these are some of the determinants of cardiac output. I'll let you read this in your own time because this table is quite lengthy, cool Now, we move on to L5, which is applying the principles of cardiovascular physiology to the regulation of BP, and onto our first L0, which is as follows so short term BP is maintained by feedback control system, what other two receptors involved in the system and what did they detect okay. We'll end it there brilliant, so the answer is actually a so barrel receptors are located in your karate's and your aorta, and this detects the high pressure, which triggers the control centers to vasodilate and therefore it decreases the heart rate and contractivity. Body receptors detect a drop in this pressure in the atrium, ventricles, and this causes your vessel constriction and an increase in heart rates and contractivity to increase the BP. Again nociceptor, Czar actually um sort of pain receptors and they're not really involved in this process, whereas Mcconnell receptors um is correct, but it's not the single best answer as borrow receptors and volume receptors are subtypes of these mechanical receptors. A 19 year old medical student has suddenly collapsed on the wards, sudden after standing up. They regained consciousness almost immediately and recall seeing stars in darkness there previously fit and well with no significant past medical history. They recalled that the night before they had been drinking with friends for which they are moderately intoxicated, what is the most likely caused okay, I'll give you guys 15 more seconds okay. We'll end it then brilliant, so the answer is actually orthostatic hypertension, so with a there's going to be a history of trauma and blacking out, followed by a little lucid interval, a sudden deterioration, um and with be it's going to be that classic thunderclap headache. You learn more about this next year in case 13 C is also okay 13, so it's actually damage to the bridging veins caused from trauma, gradual with gradual onset of these neurological symptoms. With d um usually, a loss of consciousness is caused by a trigger for example blood and spiders um whereas for e um this is actually caused by that sudden drop in your BP to the brain um either from standing up or standing too long. Um This can be tested using the tilt test, um but if you're gonna do a bedside test you'd use um just a BP um monitor for this cool Next question, a 50 year old patient presents to the g. P. For a routine checkup. They've had their blood recorded for which shows 14 545 95 mg of mercury. They have a past medical history of hypertension for which they usually take a PSA inhibitors and amlodipine. The patient admits they've they've avoided the medication too personal belief what stage of hypertension are they in okay you guys can just give it a guess um This is quite niche, I would say but it's quite good to know it's a little table that I can share with you guys later on, let's just give it a try, if you make a mistake not to worry nice ok, so the majority have gone for stage one and that is actually the correct answer, So stage one involves um having 100 and 4200 and 59 mg of mercury for systolic and 9200 mg of mercury for diastolic. Stage two is actually 160 to 100 to 180 for systolic and 110 and 100 and 100 and one and 100 and 10 for diastolic and for severe, it'll be anything above 100 and 80 mg of mercury and anything above 100 and 10 mg of mercury for your diastolic, there's a little table that would be more helpful than me just talking through it. Sorry, So another question is what is the long term regulation of BP. This wasn't part of the ellos, but I think it's something very important to know especially as you get um further one in the different years because this is what is targeted actually during um like when you give drugs to patient's, I think I think alex might have um sorry hold him might have mentioned it earlier okay Five more seconds okay, we'll call it there, so everyone's gone well, the majority have gone for the russ and that is correct, so the reticular, the rent, an angiotensin aldosterone system, and we'll talk more about that in a second and for the final question. I think so you are studying the effect of the ross, and you want to record the synthesis of the effect of molecules what enzyme is responsible for converting angiotensin one to angiotensin two and where does this enzyme come from okay. We'll call it there, so the majority of you've gone to see and that was sort of designed to trick you out. Um The answer is actually a so now a lot of enzymes are actually synthesized in the liver, um but the Ace is actually converse um converted. The Ace is actually produced in the lungs and we'll talk more about that later on, so just a bit about BP fundamentals, um So these are actually the very fundamental, so systolic pressure is the pressure exerted by the heart or the ventricles in particular and diastolic pressure actually relates to the systemic pressure that acts against the aorta um and this is the pressure that the heart actually has to exert to bypass and open up your aortic valve, which I mentioned earlier in the cardiac cycle, so diastolic is that little point where um the venture color pressure just exceeds your aortic pressure um so what is a healthy or unhealthy BP and this table just sort of summarizes it, Really I've mentioned it earlier and I'll spare you guys the laborious talk, so I'll just move on from that cool and physiological regulators of this BP and this is just a summary of what governs that physiologically. Um Your short term tends to be more neurological control, whereas your long term control tends to be more endocrine in nature and we'll explore um we'll be exploring, but the bar, affect reflects and russ later on in this talk, so yeah we're almost there so just to talk about the barrel reflex. Um So the baroreceptor reflex is the main short term regulator of your BP, and it's actually a series of detectors with a central and with the central control and defectors, so you've got two sensors, so sorry the two centers are the barrel receptors and the volume receptors and the control centers are the hypothalamus and the medulla oblongata. Now both will regulate the autonomic nervous system towards the heart and the vessels, and the bio receptors monitored the pressure in the aorta and coratids, whereas the volume receptors detect the pressure in the atria and the ventricles right um and for the relationship between gravity and BP. So due to gravity, the pressure above the heart is usually lower than the pressure below and this can lead to venous venous blood pooling in people that don't move around very often, so the muscles of acts um to shift blood back towards the heart, which is why most of most of the veins were actually located in big muscle groups such as your your quadriceps um. The baroreceptor reflex should serve to increase sympathetic output so um to increase the pressure above the heart if it drops too low, but there can be a few seconds delay before this happens, which explains the lightheadedness when changing porsche's too quickly so if you ever noticed that you stand up suddenly and you start seeing stars. This is sort of why so to talk about orthostatic hypertension or known as postural hypertension um is caused by an excessive delay in your baroreceptor reflex and this often triggers this loss of consciousness due to inadequate profusion of the brain. Now patient's often regain consciences on the floor, or when the blood, so when the BP basically evens out and diagnosis is actually done with the tilt test, which involves your patient being put on this device and that pivots it 90 degrees from flat and just a bit about vasovagal syncope. It's a common cause of loss of consciousness in patient's and it's often known as the neuro, cardiogenic syncope due to its uh cause being primarily from the vagus nerve. Now, there is an initial trigger that um that of which is either environmental or emotional, so for environmental triggers. This can range from standing for too long or excessive heat. Um emotional triggers involves your phobias and your distress um such as arachnophobia that can trigger this. Um The result is this paradoxical paradoxical activation of the parasympathetic nervous system and therefore it sort of induces bradycardia and days of debilitation. So the consequence of this is reduced um cerebral profusion. So that key difference between vasovagal syncope and your orthostatic hypertension is that vasovagal is triggered by this vagus nerve activation cool. Next, it's like oh that is it not it from me hold on where is it sorry okay. This is the last slide sorry, so finally for under crime control, um so the renan angiotensin aldosterone system is going to be this primary mechanism for blood for the control of BP. It's a, it's sort of a multi organ system and our journey is going to start off in the liver, so this releases your precursor called angiotensinogen, so as you've all realized with most things in medicine, um anything, with energon tends to be this inactive form of a of a molecule, so renan um is released from the kidney and this acts as a catalyst um for the conversion of angiotensin angiotensinogen to angiotensin one, so andrew Tencent converting enzyme or is shortened to Ace, is derived from the lungs and some parts of the kidney endothelium um and this sort of catalyze is a conversion um into angiotensin two, so from here, angiotensin two is the main effect, a molecule that has a lot of cardiovascular um effects, so for example, it will increase your sympathetic activity, increases your secretion of aldosterone by the adrenal cortex, and this resorbs sodium and retain your water to increase your BP. You've also got direct arterial activation um direct arterial uh arterial vasoconstriction in and finally got a. D. H. Secretions, which causes the kidneys to retain water and this system is a target of many BP drugs, for example ramipril and you get angiotensin uh sorry other stone receptor blockers, no angiotensin receptor blockers uh such as losartan, but you learn that more in case 12 so that's it from me uh kind of to Sonya now who will take us through the final bits so yeah, take it away, sanya, thank you and good job guys for making it so far in the dark, so I'm doing the last part for today and that is basically a crash course on coronary heart disease, which is primarily what case do is all about besides the annoying physiology that I never liked, uh but yeah I'll try my best to cover it as sure like quickly as possible, but I'm sure you can understand that that that has like there is a lot in this to cover. So do you wake you guys up from the long doc. I will start off with an s. B. A. And I will relaunch the bowl okay. I think it's 30 almost 30 seconds in and most of you have answered, so I'll end it right now. I think most of you actually went with D, which is the correct answer, but a few of you did pick b. C. And e. And I can definitely understand why. But uh if it helps you just remember that the posterior interventricular septum is actually uh it's like that that part of the heart, which might actually depend on the dominance. So for those of you who are actually gone with the left arteries, you may not be wrong, but it's just that in the majority of the heart uh Majority of the humans, the right coronary artery is the dominant one, which is why and like the dominance is more on the right side, which is why this part of the heart. The posterior intraventricular septum is actually occluded. Like if something happens to it. It's occluded by the right coronary artery, uh but yeah so that was it. I think if there any confusion just let me know and I think dom actually covered it in the beginning. When he spoke about anatomy, this question like the cvss be, and even this part so I will not go into much detail with it, but I think when it comes to coronary heart disease is and s two like as you move forward. I think med School loves to ask questions about this uh this artery was supplying this part and now it's occluded what like you know which artery is this and something like that. I think most probably most of the answers are with the left anterior descending artery, which is why It's also called the video maker because this artery supplies the left ventricle and the left atrium and the septum mostly. And if it's occluded a lot of your part of the heart is not being supplied by the oxygen and blood and yeah, it can lead to a lot of difficulties and I think e. C. G again, I know dom kind of covered this. I'll just add one little part in it that even with the CGS probably, I don't know if you can see my course, but I hope you can see it if not just let me know in the chat, that you can't but uh for example if there might be an st elevation or st depression in any of these leads, they literally come and ask you which artery is occluded, and I think that becomes a quite hard to at least for like a first year to understand that you know which artery it might be so for the simple, like because I was a visual, I'm still a visual learner, something that I used to help me decide is that I just remembered lead to three and AVF all right coronary artery, so if anything happens to these three uh it's right right coronary artery and the rest of them I used to understand uh pretty much visualizing this picture in my head and these are nothing but your chest leads, so you can like you can literally see the position of them and that's like the anterior part of the heart and the lateral part and that's mostly anterior is mostly your lady and the lateral would be your circumflex, but yeah it's most like most of it. I think we want to be four is pretty much your l. A. D. And c five c six is your circumflex, so that's how I used to really help with my answers. Okay. So now moving on to coronary heart disease is first and foremost uh coronary heart disease, coronary artery disease, and ischemic heart disease all mean the same thing I remember, I used to get confused with this and this is pretty much what like ischemia is pretty much when you need, like the oxygen supply, doesn't match the oxygen, oxygen demand, and it can happen literally anywhere, but when it happens in heart, it leads to these kind of clinical conditions, so the most common cause of uh ischemic heart disease is at Lowe's, atherosclerosis, sclerosis, which is pretty much a build up of fat fatty plaque in the artery, but there are other causes. I think one of them is called visa plastic uh coronary disease, which is pretty much where the vascular or like the art, lee is constricted because of some like neurons and like muscles, the the nerves and stuff. I don't know if you did that in first year, second year, but that's also one of the cause, but I think the most common one and the most thing that you're also going to see when you become a doctor is this one and these are the risk factors for it. These are obviously the nonmodifiable, which you cannot change, and these are the modifiable one diabetes is an important one, especially when you move forward in clinical years because uncontrolled diabetes is a huge risk factor for this and hypertension and I think uh coronary heart disease kind of go hand in hand. I think you rarely see a patient who has a heart disease and does not have hypertension, so and I think this picture is actually from a lecture in first year. I don't know if you guys still have it, but this is how it just shows the progression of atherosclerosis in the heart and over this part, like this part is where it becomes pathological, and I will discuss that more in detail when we move on to stable and a. C. S. Pretty much, but I will move on with the next question. This is pretty much just asking how does start in help reduce his risk okay. I think most of like most of you have answered. I would say half of you have answered and most of you actually went with see we have these and knees and to be honest, this was very cruel of me because I knew that if I put a simple option, this answer would be really easy and if I put the actual mechanism of action of statin, you guys would like literally guess it like this, which is why I kind of changed the words and did it and the correct answer is actually e, and why I put this actually was to explain what I'm going to explain it further. And when you have uh these kind of blacks fatty plaques, the highest risk about them is that they, they might rupture any day. You know because they are just fatty uh like blacks just building up and there's blood coming over here in high pressure. So at after some time, even the tick of like vibrant cover they have, might actually break and it might rupture and that's the threat that we have because that rupture might we do a trump ast formation and that trump's might actually fully occlude the artery, and that fully occlusion leads to a like heart attack basically and that's not good which is why even in this question. First and foremost, this patient is a South asian South asian ethnicity are at a high risk of uh CHD. Then this man is having a high b. M. I. So again a high risk factor and hypercholesterolemia, which is again a high risk factor, so now he doesn't have a heart condition, but statins are generally given prophylactic prophylactically, and I think that uh this is definitely not for first year but just to give you a proper explanation. I think you do you use a score called key risk and considering the guys risk factors, you will pretty much give him a statin just to reduce this and that's because the statin will actually make sure that the plaque doesn't rupture and then lead to a full vessel occlusion or basically a trump's formation, so statin also, firstly you know reduces the cholesterol level and will help with his hypercholesterolemia, but also helps in stabilization of the plaque, and I think this question, if I probably stay stated what the statin do specifically to the heart, probably that would have helped you get the answer correct. I hope that made sense, but I think what I've been really talking about is coronary artery disease and you can literally see it through over here and the thrombus formation that I was talking about or with this part, which is the second like thyroid box over here is mostly where you get stable angina and complete block, it would mostly be either like a proper m. I. Or if it's like 90% almost full would be a non stemi or unstable, but I think I'm a visual learner, so I really put a lot of pictures in all my slides and I hope that helps you guys do so uh another sba, I feel like I should read it out, so janice is a 72 year old female who presents the chest pain that started in the last three days today. However, she describes the pain to be getting worse despite taking her gT and spray. An e. C. G. Conducted shows uh conducted shows, t wave inversion and st depression, but her troponin level was normal what could be her diagnosis. Yeah I think most of you were pretty spot on with this and were quick to answer, so it is unstable angina and this is what coronary artery disease is. So. Obviously, if you have chest pain on exertion, So if uh if you are like doing any physical exercise, which by the way increases the oxygen demand, and because there's some like 70% of occlusion, uh the, when the oxygen demand increases, the oxygen supply is not able to match which leads to ischemia because the heart issues are not getting enough oxygen that leads to anaerobic respiration lacked it builds up and this lactate is actually what causes the chest pain and that's why this pain of angina is so different from other pains and that's why I think when you guys do your cardiac history, you actually ask or is it doesn't feel like a crushing pain that an elephant is sitting on your heart or something like that so that's pretty much the lactaid build up that's causing this and this only happens on exertion because addressed the oxygen supply is enough to like match the oxygen demand, but now when this doesn't happen and you have just been addressed you have these three, which is unstable, non stemi, and stemi. I think as a first year. Majority of your lectures spoke about the difference between stable and unstable angina, non stemi, and stemi, but no one really spoke much in detail about difference between unstable angina and non stemi and that really confused me, but I try to like explain it clearly, Hopefully, so, the major difference between them is that unstable angina, unstable angina is still a ski mia, so there's no like it's just that probably the artery is 90% blocked and that's why when you like are even addressed or I'm just sitting and talking to you. Uh The patient like might get heart pain, but this is not that long enough that it has lead to like necrosis of the cardiomyo sides and this necrosis of cardiomyocyte is nothing but infection, which is why myocardial infarction is the death of cardiomyo sites and that's pretty much the major difference between unstable angina and non stemi and that's why the troponin level will only be elevated in non stemi and stemi and not an unstable angina and stable because these are just ischemia and these two are infections so that I hope that makes sense and because um if you look at the blood flow and the levels of the vessels, the sub endothelium or the sub endo cardio like the layer is the furthest from the coronary uh blood because it's the most inner one. That's why and like non stemi is most likely to be a sub endo cardio or sub endothelium infection, whereas I think this is blocking, so I'll move this year. They're stemi, is more likely to be a transmural one because all of your things are kind of gone, They're all necrose, they're all dying because the artery is fully occluded, approximately 100% because of uh the trombone step. I hope that makes sense because this is a very important part of case to so whatever I try to explain is also like visually described over here and I think it's a good summary sheet also to understand the infections and ischemia and the e. C. G. N. Troponin, but yeah you guys can probably look through this later. So again stable angina, only on exertion, it will have symptoms like shortness of breath and sweating and uh the investigation for uh for stable angina would be a stress test e. C. G. And a coronary angiogram. A coronary angiogram will pretty much just show how much the artery is occluded and which arteries occluded really but the stress stress e. C. G. Why it is stress TCG because they're normally. Cg address would be fine would be absolutely normal and you will miss such an important diagnosis, but in stress, e. C. G, they are more likely to get st depressions and t wave inversions, which would tell you this and its management would be by nitrate because nitrate are vasodilators, so you dilate the coronary artery and more the more blood is able to pass through and the blood supply matches the demand, so yeah it helps beta blockers and calcium channel blockers are actually more to control the rate of the heart because the worst thing you want unstable in china. If I can get a picture of a heart, probably here, yeah actually it's fine. I'll just explain it through my hands If you can see it properly, but um yeah. The last thing you want in stable angina also is for the heart to pump like have tachycardia or like the heart rate to get faster because that basically means that the oxygen supply, oxygen demand is getting faster and the supply is not adequate because the heart is just pumping very fast and the ventricles are not able to contract properly. So that's why beta blockers and calcium channels are more to control that the uh the stable angina firstly, doesn't lead to a. C. S. And it's more for, like prophylaxis, but it's also very important uh for the prognosis basically of the patient and these are the 4th and 5th line, which is again a rate limit and basal dilator and that leads to our next sba, Again, I think I was a bit cruel with this, sorry, I mean I can't really see who's answering what and even if you're confused just pick an option. Generally okay. I think because we're kind of running out of time, I'll just stop there and I think five of you answered which is fine. It is a hard question and I was very cruel because if I just put you know vasodilator. With the correct explanation, it would have been such an easy thing and I just wanted to be mean really, but um I think what I also wanted to indicate is at times. Um Med school you know if you, if you for example know that g. T. N. Is a like by the way B is the wrong answer, uh is the correct answer, and I just picked up a different part of the mechanism rather than the most obvious one and probably this kind of detail might not come If they decide to be nice, but at times like they do not like especially for like s one and s stools. They do not pick the most obvious mechanism of actions. They might pick like the lesser common one, for example, they might not even give vasoconstriction visa dilation, they might just talk about influx or like reduction of see calcium and that might be the options you have to choose from so just be a bit careful, but I think this one is a bit too for like um like to niche, but this is pretty much the mechanism of action, so your nitrate will bind over here, will lead to a cascade of reactions, eventually decreasing the calcium influx, so that's why uh increasing the influx of calcium was wrong over here, so it decreases the calcium influx in the cell that leads to a bit more build up of myosin and leads to basal constriction. No sorry, razor dilation because myerson phosphate would lead to more construction. I watched this video and I think it was literally one minute so uh it's a very good explanation in case anyone wants to see a need more details. This is another s. P. A. Oh uh after you've read the options, I'll just show you the e. C. G. That's okay, I think just to help you kind of look at this because it's a bit more obvious and I'll just go back yeah. I think yeah, I think majority of you answered and majority went with C and that is correct. Um I think the graphics I'm sorry I tried to get the best picture possible, but when you copy from google, you really don't get a good picture, but this kind of prominently showed st depression and if you kind of zoom in into the picture later on, that is st depression over here instead of elevation, and since this patient's more acute, it's more likely to be non stemi, rather than any of the other options. I hope that makes sense, so again focusing on um Acs, I'm not going to go to the clinical presentations again, but what you were, but what like something to help you again, with the differentiation between stable and unstable and stem, ease, in like uh my is basically would be mis, would be more acute as well and unstable and stable angina maybe a bit more chronic, but I think the more definite tive understanding of that would be an e. C. G. And troponin levels. To make sure you know them correctly, and when it comes to management of them, I'm I think it's it's good for you to know, I'm not sure how much of this actually comes in first year, but when you have a patient presenting with acute, like stemi or like heart attack, you're more likely to give them morphine oxygen nitrates to dilate an aspirin uh That's the first thing you give morphine to reduce the pain oxygen because the patient's obviously hypoxic, so you need that if it's a stemi and the patient has come within 1 20 minutes, you are going to perform the angioplasty or the primary coronary. I forgot die. I think something something like that and your plasty basically, and in 1 20 minutes, just because after 1 20 minutes, the necrosis of the infection of the cardiomyocyte has increased so much that even if you put a pc, I nothing's going to really help and it it might do do it might do more harm than good, which is why you are kind of you have a deadline of 1 20 minutes and non stemi and unstable, are more of it like medical management of drugs and like drugs that you know about, but with the non STEMI. If the occlusions quite bad and patient has a lot of risk factors, you might look at the risk and calculate the benefit like risk and benefits, and then probably might have an elective PCI surgery and secondary management is just to reduce the risk factors. To make sure that the patient doesn't get an mRI again or get any like get an MRI in future. If they're presenting with unstable and a c. Like under is inhibitors are obviously to reduce your BP uh do acts or like aspirin or platelet therapies, is more for like making sure that the platelets not formed again, beta blockers, calcium channels are more for rate controlling and statins obviously to make sure the plaques stable and hyperlipidemia is kind of in control. I think this should be last few sbs left, so mr, jones is a 42 year old man who has, who has a past medical history of rheumatic fever, asthma, and eczema. He has been diagnosed with increased heart rate and unstable angina which of the following medications can be given to him to help him manage both his symptoms, so rate and unstable in china basically okay. I think I landed here. I think you guys can see the results, but I think if you want a few of you went for a three of you went for C and I think majority went for e. The correct answer is actually a. D. And I'll explain it why, so what you want to do here is you want to reduce his heart rate and unstable angina, so heart trade. Uh I mean if it was just unstable angina, you would have probably been okay with the ways a dilator, but really gt and spray is mostly just for stable angina, unstable. You're probably going to give them more medications, which is why is not the correct answer. Losartan is actually a aldosterone receptor blocker and that's more again for BP because you want to control the BP, so probably doesn't exactly impact heart rate and unstable angina directly. Again, it's just more of reducing the risk factor. Ramipril Again is also a sign a better and s in a better if you remember the r. A. S. S, the one, the rennin angiotensin aldosterone system, or just in a nutshell, it works on the kidneys to ensure that the blood pressures are normal, so ramipril is again for more for BP rather than heartrate and unlike ischemic events and yeah hope that makes sense losartan and ramipril are both for BP. Mostly, now, you have your left with bisoprolol and the alprazolam, which is nothing but a calcium channel blocker and bisoprolol would have been correct unlike unless and until this patient didn't have asthma or copd, but because bisoprolol is actually contraindicated in as thematic and copd, patient's you're going to give him a calcium channel blocker does that make sense, So I think the most common thing is that. Uh genuinely they give you a patient with the contra indication, so and you are asked to like prescribe them a different drug, so read the question properly, know about the contra indication. Because that's a commonly tested thing. I think another sba, I think to be honest. This is also probably a bit of the harder one, so don't worry if you really don't know these answers. I think for you, if you have answered so just for the sake of tamils, stop, but I think majority of it actually went with D, which is quite impressive because I probably wouldn't have known this in first year, but the answer is d and I'll explain it properly now, so but actually just out of curiosity, but you know what see would be. If I asked you what see is if anyone's to put in the chat, uh If not see, actually would be aspirin, so kind of just remember, aspirin is irreversible in a bit of of this, and this actually these two diagrams really represent all of the anti platelets, so this is your arachnoid acid, which basically uh triggers this part, which leads to a cascade of reactions and an adp induce platelet activation. Yeah I hope that makes sense, I'm trying to simplify it, but your aspirin will pretty much bind over here, so you're a, a, will not be able to convert into this, so your platelets I like not going to exactly form thrombus is and lead to occlusion and your do Acts, which is your direct oral anticoagulants, which is nothing but your this one, this one, and Clopidro. All these all are quite famous, do X really so these all bind over here, which is the p two y 12 hour thing and that really stops the direct activation of the anti platelets because this is pretty much the activation like the direct activation, which is why the names also do act and these ones are your g. P. To be three A innovators which are these kind of names, but they are pretty much acting on the activations, which is how these drugs also like most of the drug's kind of work, but I think the most important ones aspirin really. And I think if they ask you, probably, this one and one more thing probably might be a high yield one, but if the patient has a high risk of bleeding, for example, they have been on, like anticoagulants for a while, you will give Kloppitt the role instead of this, but probably that's more high level not the s. B. Should pretty much be, I think the second last one really yeah. I think most of you have answered and most of you went with E, which is the correct answer, so all of them are a good cardiac markers of em eyes, but the first one that rises is myoglobin and I think this again this graph is again from a lecture in first year. I don't know if you guys still have the same lectures, but if not yeah, it's important and my globe is the first one. Your troponin actually comes after a few hours uh of m. I. Which also kind of shows if the patient has been having an m. I. For a while of it's just immediate and creatinine kindnesses, also kind of along the along lines, the same of troponin, but my globe is the first one and also the first one to be reduced the fastest and when it comes to uh CK, just remember, it's less cardio specific. So you do not exactly just look at c. K. You kind of more look at troponin and myoglobin and mostly troponin and I just put this picture of different types of troponin. Just in case it comes, so you kind of have an idea what see, I anti, kind of, does, so you can look at that in your own time, I can't move forward, so I okay, I think this is the last question and one of the harder ones again. Oh I think most of you have answers. I will stop uh the thing I think most of you did go with C, which to be honest is not bad. It's quite good, it would be it would be a good answer to give and to do in real life, but I think what I was trying to focus more on was how unspecific CK really is and which is why when it's elevated, you shouldn't really consider oh my god, something's wrong with the heart because CK rises when there's a breakdown of any muscle and it's most likely to be high in false trauma or in like athletes who have done very intense exercise and don't worry. I think I kind of wrote my notes, also in like the slide notes, part, so when you get the slides whatever things were extra from my lecture, actually out there, so you don't have to worry about taking notes, but yeah these kind of these three things actually also increase the creatinine kindness levels, which is why in this guy, he is 32 so a young age has fractured his leg and his e. C. G. Issuing tachycardia which just could be because he has fractured and there might be blood loss, which is why his heart has to pump faster or this guy just might be in shock and trauma, which is why his heart rate might also be faster, but the rhythm is okay and the bloods only show a high creatinine kind instruments fine, everything else is fine, so probably this guy is okay and we can just advise him but nothing has to be really done anything about it. Yeah. I hope all of that makes sense if you guys have any questions. Please let me know because I know I kind of went fast over a few things.