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Hi, everyone and welcome to our Queens Cardiology Society Teaching series. Um Thank you all so much for joining today. It's gonna be our fourth session. Um and the second half of our Cardiac Physiology series, um kindly presented by TTH. So I'm gonna give forward t and let him take it away. Thank you very much. All right, perfect. Um Am I audible and visible to everyone if you can just put up with thumbs up in the chat or anything? That'd be very beneficial? Perfect. Um OK, so for those of you who don't know me, I take the last I take the last lecture that was the cardiac physiology part one. I'm the, I'm a second year medical student at Queens. And today we're gonna be focusing a bit more on the cardiac physiology, uh specifically diving into systems such as the rash, the angiotensin, all the system. We're gonna be looking into a specialized circulation, which is known as the fetal circulation. And then finally, we're gonna do a few MC Qs on cardiac physiology. So the and angiotensin allis, your own system is a specialized system which is responsible for elevating BP in in times of need. Uh In order to understand the last system, we're gonna have to come back and look at the kidneys. So the kidneys are organs that are present. We've got 22 kidneys, um, one on the left, one on the right. And the basic uh the basic filtration unit of the kidney is known as a nephron. Uh What we have on the right here is, is what a nephron looks like. The crescent. The crescent shaped structure is known as the Bowman's capsule. Following that, we've got the PCT of the proximal coated tubule, we've got the loop of family and then we've got the D CT of the test correlated tubule. What I'd like you to pay attention here is the two blood vessels that go into the crescent shaped crescent shaped structure known as the Bowman's capsum. We've got the ether arterial, which is responsible for taking blood to the nephrons and the ether arterial, which is responsible for taking blood away from the Nephron. So whenever the blood travels in the afer arteriole and enters into that little uh junction there, known as the glomerulus, that's where it then enters into the bowman's capsule and then downstream into the nephron, the efferent arteriole has a wider lumen as compared to the eer arteriole and that helps maintaining pressure. So that's uh that's what you need to know about the nephron. So far, we're gonna look into some of the facts of the Nephron. So the Nephron, it filters around 100 and 20 ml of blood per minute. So that is referred to as the glomerular filtration rate. The kidneys, the main function of kidneys is to filter the blood. And nephrons are like I mentioned, the basic filtration units within kidneys in a day, there's about 100 and 80 L of filter that we produced. However, as we're all aware, we don't, we do not um space out all 180 L, there is only 1% of that filtrate that is removed from the body as urine um making that 1.8 L. And as a result or rather what that means is 99% of the filtrate is reabsorbed. So when the blood is passing through the a fat arteriole and then makes it way, makes its way into the Bowman's capsule. It is then known as af it's then known as the filtrate and not the blood anymore if that makes sense. So the regulation of BP is done via the ra system, as I mentioned earlier. And the R system needs to be activated. And in order for it to be activated, there is multiple different stimuli. Once it stimuli, what we're going to focus on in this particular slide. If you look at the afi arterial in the top right corner, there, there is a group of specialized cells, these cells are known as juxtaglomerular cells. And the reason why we call them specialized is because they've got two main functions. Number one is that they detect se they detect uh changes in pressure. So any any cells that are sensitive to pressure or other pressure sensitive are known as bio receptors. So this group of cells that so the, so this particular group of cells that we've caught in the afer arterial are Chmela cells and they are para receptors that is the detect change in pressure. Specifically in this case, a drop in BP. The second reason as to why they're specialized is because they've got the ability to release renin. Renin is the first component in the renin angiotensin system. And the downstream effects of rin is what we're gonna look on. We'll look into later on in the section. Um So the, the key takeaways from this particular slide is that we've called chto glomerular cells in the a arterial uh that are pressure, itive. So they are bors and whenever stimulated, they then tend to release renin, which then leads to the activation of the renin angiotensin system. So one stimulus is drop in BP which is sensed in the afer arteriole by the josta cells. The second stimulus here uh is then located in the DCD. Uh And I mentioned earlier on that we produce around 100 and 80 L of filtrate. However, we end up uh reabsorbing um 99% of it. So most of the reabsorption within the Nephron takes place in the PCT of the proximal tubule. And that's around 65%. Then within the l of family, there's 30% reabsorption that happens there. And then the final 5% is reabsorbed in the DCT. Now think of a scenario where a person, a, a person is hypovolemic or they're hypertensive. That means the blood, which is traveling in the afi arteriole is under very low pressure. If it then enters the Nephron via the Bowman's capsule, because it's under very low pressure, it's going to, it's going to move through the Nephron at a very slow pace, meaning it's going to spend more time in the PCT, the, the LR family and then finally the D CT and if it's going to spend more time there, that just allows for more reabsorption. So the second stimulus for release of renin is uh the specialized cells within the DCD known as macular tensor. When the BP is very low and sodium has been reabsorbed throughout the way. Uh And when it finally reaches the DCT, uh the drop in sodium concentration in that filter is sensed by macular denser cells. These macular denser cells are known as chemoreceptor cells. So they sense a decrease in the sodium concentration because the BP is low and it's been traveling through the Nephron at a very slow rate allowing for more absorption. So what the macular denser cells then do is they stimulate the juxtaglomerular cells which if you can look at the picture, they're very ne they're neighboring basically. So they then stimulate the juxtaglomerular cells to release. And that is the second stimulus that we have for activation of the ras third. Here, this is quite simple. It's just sympathetic activation. So, uh stimulation via adrenaline and no adrenaline uh on the beta one receptors of the juxtaglomerular cells then lead to production of venin. So just to sum up everything we've done. So far, the stimuli for activation of ras that is the release of renin is decrease in BP in the A and arterial sensed by juxtaglomerular cells. These are para receptor cells. Second is a decrease in the sodium concentration in the distal coated tubule which is sensed by chemoreceptor cells known as macular tensor cells. These macular denser cells then stimulate the juxtaglomerular cells. So then release renin and third. And finally, we've got the sympathetic stimulation of juxta glomerular cells. So this now we're gonna look into the Randin angiotensin and joint system. Uh The purpose behind the rin angiotensin joint system is to increase BP. So that's, that's basically the point that I'm echoing in this particular slide. The rash is activated whenever the BP falls and its main purpose is to increase BP. Ranin is the first enzyme to be released. Uh And the downstream actions of Ranin then lead to an increase in BP. So we've got the first question for today. Uh which of these does not cause release of renin. We've got five options and I think we may also have a pool here. So if you can just go ahead and release that pool, you know? Perfect. OK. Um I see the most low glomerular fil electrolyte levels. Uh We've also got a few people who have been low plasma electrolyte levels. Uh And uh well, my friend and I had a debate about this question because it does make sense that low plasma electrolyte levels would lead to low glomeru filtrate electrolyte levels. But I think we're talking about the direct stimulus for another the direct stimuli which lead to release of renin. And that most appropriately would be low glomerular filter electrolyte levels again, just to brush up on what that means is within the glomerular filtrate. That is low sodium. This is sense in the DCD by the macular cancer cells moving on now to the second component of which is the angiotensin. So if you see the number five there, we've got increased. So we've got renin secretion from the juxta glomerular cells. The sixth component there is angiotensin Ogen, which is produced by the liver. This is the precursor of angiotensin two but not directly. So what happens is angiotensin Ogen is converted to angiotensin one via renin or by the by the, by the use of renin. This angiotensin one is then converted to angiotensin two via ace, converting via ace or angiotensin converting enzyme which is produced in the lungs just to quickly brief this up or summarize this. We've got tannin which acts upon angiotensin. No, to convert it to angiotensin one. And then this angiotensin one is converted to angiotensin two via ace which is present in the lungs. So, angiotensin two stimulates aldosterone secretion from the adrenal cortex. That is the third component of the renin angiotensin aldosterone system. Um What that basically means is angiotensin two stimulates the adrenal gland, the adrenal gland uh al also known as suprarenal gland. Uh We've got two of them, one above each kidney and they are responsible for releasing mineralocorticoids, glucor, et cetera. So, aldosterone is a mineralocorticoid. What it does is it has its effects over hours and days and it basically acts on sodium potassium channels in the distal coated tubule. So, aldosterone is responsible for sodium reabsorption and potassium and H plus iron excretion. So, a simple principle to understand uh when it comes to the activity of nephrons is uh water follows sodium. So if sodium is being reabsorbed, water is also going to be reabsorbed. And as a result, you're preserving body volume, body, uh body fluid volume and therefore helping increase the BP so quickly, the aldosterone is released. It's a miner allocor acts upon the D CT, the distal tubule and is responsible for sodium water reabsorption and potassium H plus excretion. So, ideally, if a person uh had elevated aldosterone levels, what would happen is they would have an excess of sodium reabsorption. So, hypernatremia, hypernatremia and hypokalemia because they're excreting potassium uh aldosterone also, then again, because it's reabsorbing water helps uh in increasing blood volume and consequently, BP. Uh Another fact about angiotensin two is that it is a very potent vasoconstrictor uh and it helps increase uh peripheral resistance. And as a result, BP on the right here, we have a graph. Uh We've got the dye imploded um in the X axis in minutes and we've got arterial pressure on the y axis. You see that if a person's hemorrhaging, um in the absence of the renin angiotensin system, their BP does not seem to improve drastically. But in the presence of the sudden angiotensin system, the BP is connected almost instantaneously, I would say. Uh and then we've got a key factor in the bottom left corner that angiotensin two is four times more potent than no adrenaline or epinephrine or adrenaline. Um and increase in BP. This then quickly just summarizes all of the effects of angiotensin two. First one is arterial or vasoconstriction. So, angiotensin two binds to 81 receptors which leads to vasoconstriction and therefore increase in BP. It stimulates secretion of aldosterone which is a mineral corticoid acting upon the DCT to increase sodium and water reabsorption and potassium excretion, it acts then to, to further release or rather secrete ADH. So ADH is anti dietic hormone. And this is secreted from the posterior pituitary gland. What ADH does is it acts upon the collecting tubules and it simply uh facilitates water reabsorption. It does not act upon any of the electrolytes which just ay in water reabsorption, preventing uresis. I'm sorry, preventing diuresis and uh helping preserve body volume. Therefore, to increase BP, the angiotensin to also stimulate sympathetic response. So it enhances the release of norepinephrine uh which will then lead to sympathetic stimulation of toxo glomer cells to further increase concentration or dine production actually. And then finally, this is an, this is an independent action of Adjutants. Two. It increases sodium and water reabsorption in the PCT of the proximal con tube. And the similar function is performed by aldosterone in the DCT. This then just summarizes all of it. What I mentioned the last slide in just a picture here, a flow chart. Uh arterial invasive constriction by binding to a one receptors. It increases secretion of ADH antidiuretic hormone which acts upon the collecting tubules just to absorb or reabsorb water. Uh We've got increase in sympathetic uh stimulation, increase in allo secretion, mineralocorticoid helps in sodium pota water reabsorption and potassium excretion. And then finally, we've got increased sodium and water reabsorption in the PCT. Here, we've got the second question. Now, which of these is the primary effect of angiotensin two on blood vessels. Keep in mind the question properly. It says blood vessels. So you'd be able to eliminate a few of them naturally. All right. So far the answers have been correct. It is vasoconstriction via the A one receptors. So, angiotensin tends to bind to these 81 receptors and then um lead to vasoconstriction which helps increase BP. We've then got the third question here. Which of the following is not an action of angiotensin two. I think a good way to do this question is by eliminating the other options. Cos if you know the actions of angiotensin two, you can just um just cancel out some of the options here. So there is somewhat of a split here but it's not too drastic. The correct answer is promoting vasodilatation of the renal afi arterioles. It does not do that because um it's, it's whole purpose, the whole purpose of angiotensin two and the rash is to increase BP, promoting vasodilatation would lead to a decrease in BP. The fourth question here, a patient with hypervolemia has found up elevated plasma and aldosterone levels. Which of the following is a direct effect of aldosterone in this patient. This will require you to think a little bit. OK. So currently it's a 5050 split, but it is leaning more. OK. Now, now it's a 66 we've got, we've got a few different answers here. I'm just gonna go over this question here. A patient with hypervolemia has found to have elevated plasma renin and aldosterone levels. Now, if you guys remember, aldosterone is a mineralocorticoid. It helps in sodium and water reabsorption and potassium and H plus iron excretion. And so I think the the correct answer is the very first option here to increase potassium secretion by the principal cells which then leads to that excretion. We move on to the fifth question here. A 65 year old woman presents with severe vomiting and diarrhea for two days. Her BP is 85/50 she has low urine output. 85/50 is quite hypotensive. So that's low BP. Blood tests reveal hyponatremia. That is a decrease in sodium concentration and hyperkalemia, which is an increase in potassium concentration, which hormone is primarily responsible for collecting her sodium imbalance in this situation. Gonna give you guys a few minutes here because this might require you to. Well, I mean, I've echoed the point a few times now. So hopefully everyone gets this correct. And I, yeah, so most of us have got this correct, correct. Uh The answer is aldosterone. Once again, mineralocorticoid helps in sodium reabsorption and potassium excretion. In this particular case, we see that the person has low levels of sodium and high levels of potassium. And what all serum does is because it stimulates the absorption of pota of sodium. We're gonna reach uh a normal level of sodium and because it helps in excretion of uh potassium, we're gonna reach a normal potassium level as well. Uh six question here. These questions are very UK ML based. So you can do these um drops to you. A 70 year old man with chronic heart failure is started on spironolactone. One week later, he develops generalized weakness, blood test re potassium levels of 6.2 millimoles per liter. Uh that is an elevated level, the normal levels of potassium in a human being or in, in an individual, which should be around 3.5 to 5.2. So this person is hyperkalemic. What is the mechanism of action of the drug most likely responsible for this for this finding? So, if you guys haven't done your pharmacology yet, um it's not gonna be too difficult as long as you know, the different enzymes that we spoke about, the different hormones that we spoke about and that affects spironolactone is a drug that affects one of these, one of, one of the mechanisms of, of these enzymes or the of these hormones. Ok. So, so far all the ultras have been correct um gonna give you guys just one more minute if you wanna give it a shot. All right then. So the correct answer for this question is blocking the mineralocorticoid receptor in the distal nephron. That is where aldosterone acts. Once again, aldosterone is responsible for sodium reabsorption, potassium excretion. If you block that particular receptor, aldosterone cannot impose its actions. And as a result, it will, it will not be able to excl potassium leading to potassium conservation within the body and a hyperkalemic state which is 6.2 in this case. So spironolactone is uh an aldosterone receptor antagonist. Uh Aldosterone again is a miner allocor. So the first answer or the first option a is the correct option. We're now gonna focus on specialized circulations. We're gonna look into the fetal circulation. So I appreciate that this is a very heavy or packed slide, But most of our learning can be done from the, from the image that we've got on the right there. So the fetal circulation, what's important for us to know is that babies don't have the lungs well developed or rather they don't even use their lungs to oxygenate blood. Um They get oxygenated blood from the placenta. So from the placenta, uh oxygenated blood goes up to the baby's heart via the sorry, once again. Oh, sorry, it goes via the umbilical vein and then via a particular or a specialized structure is the doctor's stenosis. It bypasses the liver and then enters the IVC and then is drained into the right atrium. So the oxygenated drug from the from the placenta is taken by the umbilical vein to the IVC via the doctor's stenosis to bypass the liver train in the right atrium. Now, usually what happens in adults is that the right atrium pumps this blood to the pulmonary vein and then to the lungs for oxygenation. Uh But because we know that babies don't have this capability. We've got a specialized uh modification within the fetal heart. Uh If you guys have done the anatomy lectures before this, you would have known of the fossa valis that is seen in adults. Uh but in babies or other in, in fetuses, it's referred to as the Foramen valet, that is simply a hole between the right atrium and the left atrium, which allows for this oxygenated blood to enter from the right atrium to the left atrium and subsequently bypass or consequently bypass uh the lungs. So once again, umbilical vein, oxygenated blood from the placenta passes the liver via the duct spinosus, uh enters the IBC, the right atrium. Then from the right atrium, it skips over to the left atrium via that hole known as the Foramen of valley. From the left atrium, it goes down to the left ventricle from where it is pumped to the AORTA and then the rest of the body. Now, some of this blood does not, does not manage to make it into the left atrium and falls down to the right ventricle itself. Uh Here is where we talk about the second modification when uh so the second modification in the fetal circulation. So when the right ventricle pumps this blood to the pulmonary vein, there's an attachment between the pulmonary vein and the AORTA referred to as a doctor's arteriosis. So, any oxygenated blood that came via the IVC, the right atrium and then into the left atrium, uh that didn't make it to the left, sorry, that went down to the right ventricle and didn't make it up to the left atrium gets pumped out to the pulmonary vein. But because the pulmonary vein is attached to the aorta, it simply just falls back into the aorta and enters the fetal circulation once again. So there's three key shots that we need to focus on the doctor's stenosis which helps in bypassing the liver. We've got the Foramen ovale which helps in bypassing the lungs. And it's basically a shot between the right atrium and the left atrium. And then finally, we've got the ductus arteriosis which is between the pulmonary vein and the aorta. Uh Shortly after birth, we get closure of these structures and they're known as different things. So the, the fossa ovalis uh sorry, the Foramen ovale is then known as the fossa ovalis, which is seen as a light membranous structure, um a thin membranous structure and the doctor's arteriosis is then known as a ligamentum arteriosum looking into them in a bit more detail here. The Foraminal valley, the Foramen of valet is a shunt which allows blood to flow oxygenated blood to flow from the right atrium to the left atrium, effectively bypassing the lungs. And shortly after birth or at birth, actually, uh because of increased left atrial pressure, we get a closure of this Foramen Valley and then once it's close it stays close forever. Uh And then we, we get the structure known as the fossa valis, which may be seen in an adult heart as for the doctor's arteriosis, um it helps in attaching the pulmonary vein to the aorta to assist blood in the right ventricle to return to the aortic circulation. And shortly after birth, within a few days because of increased oxygen levels. Now that the baby's breathing on its own uh and reduced prostaglandin levels, the doctor's arteriosis closes and is now known as the ligamentum arteriosum. So, prostaglandins are simply vasodilators. So, in the absence of vasodilators, that is the prostaglandin. In this case, it leads to closure of the ducts arteriosus leading it to form the ligamentum arteriosum. So the foramen ovale becomes the fossa ovalis, the duct's arteriosus becomes the ligamentum arteriosum. Now, this is another question in the fetal circulation. What is the primary function of the foramen ovale? Ok. So far every single answer has been correct. That's great. So the answer to this question is to allow oxygenated blood to flow from the right atrium to bypass the lungs and flow into the left atrium. And once uh the child is born, uh it closes immediately due to increase in left atrial pressure to lead that than from the fossa or valis? Uh The eighth question, you know, I think this is the last question for the day. I'm not too sure, but which of the following features of fetal circulation ensures that the oxygen rich blood bypasses the liver. Perfect. So again, this is also quite a straightforward question. The answer to this is see doctor's stenosis because we know that doctor's arteriosis helps in connecting the pulmonary vein to the aorta. The Foramen O Valley is the hole between the right and the left atrium. And then the doctor's stenosis helps in bypassing the liver and then attaching to the IVC and then helping drain blood oxy oxygen rich blood into the right atrium. Uh That is it from my side today guys. Uh If you've got any questions, pop them in the chat. Uh And alternatively, you can also send any questions via email, that's my email ID there. Uh And I can help you with any of the questions from today's lecture or just cardiac physiology in general. Um I'm gonna stick it on for a few minutes if you guys have got any questions. And I think there should also be a feedback form because that helps you guys get your certificates. Thank you very much for a wonderful presentation. I'm sure we've all uh been well covered on cardiac physiology and cardiovascular physiology now. Um So if anyone's having trouble accessing the feedback, I will put the link in the chat as well and that's us. Thank you very much. Thank you everyone for sticking it on. Um I hope you guys have a good evening. If you guys have got any questions, what Yep. All right, perfect. Thank you very much, guys. Have a good night.