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All you need to know - Cardiology part 1

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Summary

Join a 1/4 year medical student from UCLI for a captivating discussion on cardiorespiratory mechanisms. This comprehensive case study will help you navigate the difficult field of pharmacology, with personalized advice and detailed illustrations. You'll review anatomy, systems, and mechanisms such as the regulation of heart rate, blood pressure, and ventilation. The student will draw from his cardiovascular sciences background to elucidate complexities in heart and respiratory systems, and explain how common conditions like bronchiectasis and heart diseases arise from abnormalities. You'll also delve into autonomic nervous systems, exploring the roles of sympathetic and parasympathetic systems, and how their interactions affect bodily functions. Touching on pharmacology, the various types of adrenergic receptors and their effects on the body will be discussed. Lastly, the session will end with a thorough explanation of excitation-contraction coupling in cardiac muscle contraction. This teaching session promises to leave you with a strong foundation for future clinical scenarios.

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Description

All you need to know for your preclinical cardiology exams!

Cardioresp Mechanisms - 10am

Cardiac Cycle and ECGs - 11am

Heart Disease and Heart Failure - 12pm

Pharmacology of Cardiology - 1pm

Learning objectives

  1. Understand the anatomy of the cardiovascular system and associated electrical systems, with a particular emphasis on the pacemaker mechanisms and the functions of the SA and AV nodes.
  2. Understand and describe the anatomy of the respiratory system, including the layout and distinction between the right and left lung, and the implications these have in medical situations (like aspiration).
  3. Understand the function of the autonomic nervous system and how its two main branches, the sympathetic and parasympathetic systems, operate and contribute to key bodily functions.
  4. Understand how specific neurotransmitters, norepinephrine and epinephrine, influence various functions such as stimulation of the GS proteins or stimulating adenylyl cyclase to increase the formation of cAMP.
  5. Understand the different adrenergic receptors and their individual functions, as well as the implications these have in pharmacology, particularly in the development and application of selective and non-selective beta-blockers.
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The following transcript was generated automatically from the content and has not been checked or corrected manually.

Case series on cardio respiratory mechanisms. I'm 1/4 year medical student uh currently at U CLI hope everyone's having a good day so far today should be really interesting. Um You'll learn a lot. Uh And I'd encourage you to stick to the end because I know a lot of people, at least um people that I've spoken to and from personal experience, find pharmacology quite difficult. Um And I'm sure Ryan will give a lot of good advice with regards to pharmacology towards the end as well. And the other lecturers will have some really interesting stuff as well. So we're gonna start off by just going over the respiratory mechanisms, the cardio mechanisms. So sort of basics um a little background about who I am. So I've said I'm 1/4 year medical student at UCL at the minute. Uh I did my I BSE last year in cardiovascular sciences, which if anyone hears from UCL and a preclinical medical student, I'd highly recommend it. I actually really enjoyed it. There's a lot of free time as well for you to explore other things, other hobbies. And it's just a really interesting course overall with some great modules as well. And so just some topics that we're gonna cover today, uh We're gonna start off with uh just a little recap of anatomy and then to sort of more delve into the systems and mechanisms, including the regulation of heart rate, BP and ventilation. And there's just a couple of short questions at the end um that we'll go over if we have time. So hopefully that's ok with everyone. Um So yeah, just to start off with some cardiovascular anatomy. So we have various images here. And if you've already done your uh cardiology learning at medical school, you might realize that it's slightly different to what you were taught at a levels. The heart isn't perfectly sat with the atria next to each other and the ventricle just underneath, it's more sat with, it's sort of tilted and laterally rotated. So you can see um here that the base of the heart sort of points down rather than going perfectly down. And in the anatomical position, the r right ventricle and the right heart is slightly anterior to the left ventricle, which is more posterior and this middle image uh better highlights the electrical system of the cardiovascular anatomy. So I'm sure you've all heard about the SA node and the ABN and the A B node. Er, so it's important to know that the SA node spontaneously depolarizes at 100 BPM. However, the natural heartbeat is a lot less than this, it's like between 60 to 100 is normally considered normal. And this is because there's a lot of parasympathetic activity or vagal tone that regulates this. The A V node goes on, it goes from the SA node to the A V node and then down this bundle of his splits into the left and right bundle branches and then up these pini fibers. And it's also important to know that if the SA node does fail, these other areas do also spontaneously depolarize, but at slower rates. So that in normal conditions, when the SA node is working, these don't need to and it might be also um relevant to sort of know roughly those rates. So the A B node, people say it's around 60 BPM and the rest er is sort of 30 to 40. These are called the tertiary pacemakers and the A B node is known as the secondary. And this can be important to remember because if you come across an E CG where the heart uh rate's at about 45 you might think, oh maybe there's something wrong with the SA node. That means that um these areas are having to take over as a sort of escape rhythm. I'm sure that'll be covered later on in teachings. Um more specific to ECG S and stuff like that heart diseases. Um And this just shows a sort of basic anatomy of the coronary vessels, which are the vessels that supply the heart itself, the heart muscle. Uh And interestingly, uh the heart actually has the highest O2 consumption per tissue mass, which a lot of people might think it's the brain. But if you're going off just uh per mass, then it's the heart. Um Yeah, just a little bit of a recap on respiratory anatomy. So, as I'm sure you've come across the right lung has three lobes, the left lung has two. you have these weakened uh oblique and horizontal fissures which help demarcate the lines. Um And yeah, the trachea as well, the right trachea is more um vertical uh which is important um in clinical medicine as if you're gonna get a foreign object. For example, if a kid accidentally inhales a lego piece of marble, something like that, it's much more likely to end up in the right lung as well as aspiration. Uh If someone's vomiting and they um inhale some of that, it's m more likely to go down the right lung and potentially cause pneumonia, stuff like that. Um And yeah, it's also important to know that it's like an upside down tree. Almost a lot of people say. So there's a um massive trunk here and then as you go further down, it sort of branches out and gets smaller and narrower. And that's also relevant because in certain conditions like bronchiectasis, you might get pathological, widening of these distal um uh channels and that leads to recurrent infections. So it's important to have a basic understanding of anatomy and physiology even once you get to clinical medicine. So it's a good idea to sort of, um, get all of this into your knowledge now. Uh So we're gonna start off by just recapping about the autonomic nervous system. So it's important to know that it's not under voluntary control. It's not something that you control yourself. It's sort of just an automatic system that occurs in the body. Um So there's a two main branches first is sympathetic. I'm sure you've all heard of fight or flight before and maybe a biology covered this extensively about sort of what uh happens, the increase in heart rate, stuff like that. The mechanism of it is that it stimulates the er neurotransmitters, norepinephrine, epinephrine, they uh stimulate the GS protein S is stimulatory um which increases the activity of Adenylyl cyclase to increase er the formation of CAM P. Er, and then through that signaling pathway, this increases stuff like vasoconstriction that helps you when you need to have a fight or flight response or for example, an exercise or something like that. And you'll find a lot with these um mechanisms that when it comes to like sympathetic versus parasympathetic, it's pretty much just the complete opposite. Um So it's more of a rest and digest. So it's when you don't need that excess stimulation, it's main neurotransmitter is acetylcholine. Uh it causes pretty much opposite effects So vasodilation decrease in heart rate, um to gi so inhibitory protein that's activated, that pretty much just does the opposite. So it decreases the activity of ad cyclase, decreasing this formation. And, yeah, so we're just going to recap the adrenergic receptors now. So I'm sure you've seen this um a little bit before. Uh these just recap the sort of uh potencies of the neurotransmitters on each one, they're slightly different. Uh And if we just go of them one by one, so alpha one, so that mainly does vasoconstriction, it increases peripheral resistance um which has a direct relation on blood flow. We'll go over the formula for that later, uh increases BP, er has a few other minor effects. Um uh Alpha two, it inhibits norepinephrine release, it inhibits acetylcholine release and it inhibits insulin release. So it's more of an inhibitor when you're um dealing with that. And if we come into the betas, the beta one, it increases heart rate, increases the breakdown of fats, increases myocardial contractility and increases renin, we'll go over um the function of renin a bit later on. Um And we'll cover that uh beta two does vasodilation, decreases peripheral resistance, uh causes bronchodilation, aosis and some other things, it's important um to remember these sort of different functions, especially when it comes to pharmacology. So, certain drugs that target these can be selective or non selective and this essentially means that they're selected to one of the types or they can just er act on all sort of beta receptors. So for example, propranolol, which is a um beta blocker used in heart conditions. Uh it's actually nonselective. So a very important thing is you might be trying to block these actions here, but by using it, you would be preventing bronchodilation. So it's very important to uh be careful and make sure someone's not asthmatic stuff like that. So, understanding these underlying mechanisms is really important when it comes to clinical medicine. Um and just having a good uh foundation base and knowledge of this stuff will really help you er as you go through medical school. And so yeah, now we're gonna move on to something called excitation contraction coupling. So this is a sort of mechanism by which the cardiac muscle actually contracts. So an action potential like uh most things will initiate the contraction and it's mainly done through calcium signaling. So this great uh barrier that we see here is the what is called the sarcolemma, which is essentially just a cell membrane of skeletal muscle fibers or cardiac muscle cells. These little um gaps here that you see are essentially called t tubules. And what happens is the action potential travel down here down here and depolarization of the membrane causes calcium to go through these channels here called L type calcium channels. And once inside the um sarco once through the sarcolemma, it can bind onto the sarcoplasmic reticulum onto these R yr two receptors, they're called ryanodine receptors. And this leads to a massive release of calcium which is being stored in the sarcoplasmic reticulum. Now that all this calcium is free uh and released here, it can go on and allow contraction. Now how it does this is in a normal um complex er up here with Actin Tropomyosin which are the binding sites and a troponin complex. Now what happens is calcium will go and bind to something called troponin C which causes a conformational change which moves this Tropomyosin out the way allowing these binding sites to now be free. So the actin can now bind onto the myosin and walk along it using APA S and essentially causing the muscle contraction pulling together and you can cause relaxation er in two different ways from this. Um So you can either through here e flux it through this calcium er sodium exchanger in the sarcolemma. However, you could also reuptake it into this to store for the next um contraction. And here we can sort of see the er sympathetic stimulation. Er so that would be the normal situation but say you need excess. So how the sympathetic nervous system would handle that is it would send these catecholamines, norepinephrine, epinephrine, which would bind to the g stimulatory proteins that we talked about, which would increase the cam P uh activating protein kinase A to go and increase this sort of um depolarization activation. Uh and increase the signaling pathway. So I hope that all makes sense if anyone has any questions throughout just uh, pop it in the chat and um, we'll uh try and cover it uh to the best of our abilities. Um, and I'm gonna talk about chronotropy. It's a term that you might have heard of. Uh chronotropy. I'm trying to remember it like a chronograph watch. It relates to times to the heart rate, er positive chronotropy at least to an increase in heart rate. Or is it a term used to describe an increase in heart rate and negative would just be a decrease in heart rate. So again, this is mainly um done through, it can be done through various things. It can be done through uh the sympathetic nervous system, the parasympathetic nervous system. Um and uh also here is just some drugs that interfere with it. So you have propranolol which um talks about it binds the beta adrenoceptor, stopping the positive chronotropy, er an atropine blocks negative chronotropy by binding to the muscarinic receptors. So this is very useful in, for example, bradycardia where you might have a slow heart rate, you're trying to uh get it back up. So you're stopping the parasympathetic um tone on the heart, allowing the heart rate to rise back up. And then another term is inotropy. Now, this refers to the force of contraction. So if there was to be positive inotropy, this would be an increased force of the muscular contraction or the cardiac contraction of the heart. And a negative inotropy would be a decreased uh fossa muscular contraction on the heart. And, and a law that is, that comes up quite a lot is the Frank Starling law, um which essentially states that an increase in enddiastolic volume. So that's when the heart's filling up with blood. If there's more heart, if there's more blood filling up in the heart, this leads to a greater contraction due to the increased tension on the muscle cells, uh which leads to a greater um sort of contraction. So, here's a nice little screenshot from osmosis, which shows you the graph for it. So down here, we have ventricular enddiastolic volume, er and on the otherwise, since we have stroke volume, so that's essentially how much uh blood is getting pumped out of the heart with every contraction or every heartbeat. And in the purple line, you see the normal relationship and with the green, you see the positive inotropic effect that can be done by the para the sympathetic nervous system, sorry, drugs such as digoxin and the negative is pretty much the opposite. So it's uh parasympathetic nervous system or beta blockers. And so it's important to realize that there is a limit to this and that limit is essentially the maximum tension on the heart before it gets overworked. Um And you can always think of this relationship like any of you who've done bicep curls before, if you're doing a bicep curl with just the air, there's only so much force that you can put into that because you're not pushing against much. However, if you've got a dumbbell, um, you create a much greater force due to the tension on the muscle that allows you to create this greater force. So that's just the way that you can think of it. Um, I hope all that makes sense. You might uh know a bit of this or remember it from physics G CSE S or if any of you did it at a levels or anything like that. Uh And it's also important to know that the the the sort of main uh goal of the mechanisms or the systems is to match perfusion with ventilation. That's why cardiology and the spirit have a lot of overlap, especially with their uh conditions. For example, loads of heart conditions can lead to pulmonary problems or loads of pulmonary problems can lead to heart conditions. Um So these mechanisms do work together a lot of the time and we've talked about how stroke volume will respond to. That's just basically uh the stroke volume will change in order to try and meet the metabolic demand. So if you're exercising something like that, your heart will react to try and pump more blood out. Um And we use the increased force of contraction to do this. So I hope that all makes sense to everybody Um So we're just gonna go on to cardiodynamics now. So these are a few equations on the screen. They're not extensive, they're not all the equations you need to know, but they're sort of the basics for cardiodynamics. So we know that cardio cardiac output is the heart rate times the stroke volume. Er And if you just think about it, like the heart rate is how many BPM stroke volume is, how much you're ejecting per beat. So it's a nice little formula. Uh BP is cardiac output times total peripheral resistance. And the mean arterial pressure is the diastolic BP plus a third of the pulse pressure. So a lot of people will say a normal BP is like 1 20/80. So uh the mean arterial pressure of that would be 80 plus a third of the pulse pressure. The pulse pressure is the difference between the systolic and the diastolic BP. The difference here is 43rd of that's like 13.3. So you do 80 plus 13.3 get like 93.3. Uh and that would be your mean arterial pressure. And it's also important to note that um a lot of people talk about 1 20/80 is the systemic BP, but your pulmonary system actually has a separate BP. Now, the normal values for that is 25/8. Now, the reason it's such a low pressure is that it's a low pressure system. Your heart needs to pump blood from uh your left heart has to pump blood from the heart to all the way to your feet, to the extremities of your hands. So it needs a lot of pressure in order to create that large pressure gradient. However, your right ventricle is only really pushing it to the lungs, which is very close to it. It's not too far. So it doesn't need that much pressure to overcome this and therefore has a low pressure and just physiologically, it's good to sort of understand this because when there's a hole in the heart, for example, like a ventricular septal defect, um uh you can al without having to like sort of memorize it, you can almost just try and think about it and think, well, the left ventricle's got a higher pressure than the right ventricle. So blood's gonna go from the left ventricle to the right ventricle. And so that's another good thing that uh I particularly like about the physiological side of medicine is that it's not really like you have to memorize something, but if you just understand the basic system, you can almost sort of figure a lot of stuff out, um especially when it comes to like physiological questions or stuff like that. And uh interestingly enough when that left to right shunt shunt does happen, er, the right ventricle can hypertrophy so much over time that by the time that person, like if they were bored with this, by the time they were a teenager, the right ventricle has got such high pressure in it that the shunt switches direction uh causing deoxygenated blood to be spread around, which then brings on the symptoms. So it's diagnosed much later on uh in that particular scenario, another law. So there's a lot of physics when it comes to dy dynamics, a lot of these um equations you might have seen before. So um yeah, so flow is equal to the pressure gradient over resistance. So this is the same for the cardiac uh system. So blood flow is determined by the pressure gradient. So if you're trying to push from your heart to your feet, so that would be the pressure in your heart minus the pressure in your feet over the resistance and the resistance is all um due to like the uh blood vessels. So whether they're constricted, expanded how elastic they are um stuff like that, whether they're sclerosed stiffened, stuff like that. And yeah. Um So here's a little nice diagram of the systemic uh synthetic activity. Sorry. Er And sometimes these diagrams can be quite confusing, especially if there's like a broad one, there's loads of different things going on. But the easiest way to probably tackle these are just to sort of follow them around once then go the other way and just sort of think about it like logically. So here we can see that an increased sympathetic activity we know causes vasoconstriction by acting on those adrenergic receptors. We see here down here, basal constriction and what this vasoconstriction does is it increases venous return. Now, why does it do this? Well, if you were to constrict the um veins in your foot, for example, this would cause an increase in pressure. Now, this creates a massive pressure gradient between your veins or um your blood vessels and your right atrium where blood returns to. So because of this increasing gradient, it pushes more blood back to the heart. Uh by vasoconstricting, this increases the venous, return the blood to the heart. And we've talked about how er if you fill up the heart more, it leads to a greater force of contraction. So that's what's meant by preload. So just in definition, so preload or an increased preload is that increased filling of the heart in diastole and afterload refers to the resistance. So for example, if you were to have vasoconstriction er in your um peripheries, that would be an increased afterload. So, afterload is the force that you're pushing against to get heart out of, to get blood out of the heart. And preload is the force that is created when filling the heart. So having that access return to the heart creates an increase in preload. This as we know from the Frank Starling law increases the force of ventricular contraction or uh and this increased force increases the stroke volume increase in cardiac output. So this just sort of goes through it step by step. And the sympathetic activity can also have a direct er increased force of ventricular contracture and can also have an effect on the slope of the pacemaker potential by increasing the um the funny current which is basically increasing the activation of the essay node uh that we talked about which increases heart rate, which thanks to this formula, we know that just increasing the heart rate will simply increase the cardiac output as well and increased parasympathetic activity uh sort of has as we talked about they have often opposite effects. So the increased parasympathetic activity will decrease the slope of the pacemaker potential, decrease the heart rate and thus cardiac output and increased parasympathetic activity can also decrease the force of contraction, decreasing preload. Um stuff like that, decreasing force of atrial contraction, sorry. Um And yeah, so it's, it's often good to try and think about these systems just to try and get an understanding of what's going in on in the body, how things go normally and how things um maybe going wrong in a patient's situation. And there's just a little recap about the Adreno receptors. Um So now we're gonna go on to a bit of the regulation um aspects. So the regulation of BP, uh it's mainly done by this thing called baroreceptors which detect changes in pressure. So, a decrease in the pressure would cause decreased activation of these baroreceptors. And this would s send a signal to increase sympathetic activation in order to try and rectify this. So a lot of it is like almost homeostasis. It's trying to just rectify it. Uh it's trying to maintain normal values and try and rectify it when it goes outside of these normal values, the ability to sort of compensate decreases with age, which is why hypertension is very prevalent as um in the elderly population, as you get older, you're not really able to uh sort of decrease your BP as well or respond to high BP. So you have sort of chronically er higher blood pressures. Here's a nice little diagram from geeky medics. Um I didn't really use it in preclinical medicine. I didn't really know about it, but like once you get to clinical medicine, it's a lifesaver. It's generally so good. Um So they might have some good resources like this for preclinical medicine. But I definitely keep it in mind for when you guys get to clinical medicine or if any of you are clinical medics, ACY CP SAS, they, they're so good for that. They've got videos explaining everything. They have videos that even like show you the different uh heart murmurs. So you um if you, if you learn about the different heart murmurs in preclinical medicine and you're overwhelmed thinking, oh, what does that sound like? What does that sound like you should go to Kiki medics, they have videos for all of that, uh should help you sort of differentiate the different types of conditions and they have checklists and stuff for like examination if you need to know the cardio respiratory examination for your uh preclinical exams or anything like that. Uh And it's just a sort of nice flow chart. So as BP increases this, we said it increases the activity of the baroreceptors, increasing the um activation of it, which causes a increase in parasympathetic and a decrease in sympathetic activity which causes the effects that we've talked about. Uh that happens in those two systems. Um And then here's just another diagram sort of uh showing exactly what activities it has. So uh decreased cardiac simulation increases the rate of the essay node um and stuff like that. So we, we said we mentioned Renin earlier as um something that can cause or regulate BP. So how that works is um this is the full name of it, the Renin angiotensin aldosterone system. Uh you might just see it called grass. Um Some people call it Russ system, but like that's all signs for system. So, um yeah, if you wanna be pedantic then yeah, that's that, but it's just the rash. Um So Rennin is released by the kidneys. Um and it actually goes on the end of the system, aldosterone acts on the kidney. So it's a nice little circular thing. So, renin is er released by the kidneys. Uh and the liver releases something called angiotensinogen, which basically the renin converts angiotensinogen to angiotensin one ace in the lungs, which stands for angiotensin converting enzyme converts angiotensin 1 to 2, which acts on the adrenal gland to release a hormone called aldosterone, which essentially works on the kidneys to increase the reabsorption of sodium. Now, through osmosis, I'm sure you're very aware that if you're pulling in sodium, water's gonna follow that. So, uh it also pulls in water with it. And this increased volume in the blood vessels causes an increase in BP. So, running causes an increase in BP. Angiotensin two can actually also cause vasoconstriction itself. So it doesn't need to get all the way to aldosterone to have a sort of sympathetic effect. Um And this system is actually a, a massive target for hypertension medication. So, you might have heard of ace inhibitors, which basically inhibit this ace here. And you might have also heard of Arbs or Aldosterone receptor blockers, which essentially just block the receptor sites for aldosterone on the kidneys. Um And I'm sure you'll go over all of this in the pharmacology sort of aspects of your lectures. Um Yeah. So that's the regulation of BP, sort of overview. Uh There's various factors that can actually influence vascular, smooth muscle tone. So you've got a lot of extrinsic control. So the nervous system we've talked about extensively the humoral system, which is more like the hormonal size. So you've got your adrenaline angiotensin two. You've got vasopressin, vasopressin is also known as a anti diuretic hormone. So you might have heard they called that A DH. And that essentially um deposits more aquaporin receptors in the kidney to take up more water. Um which sort of increases BP. Again, you've also got these things called NAIC peptides. So you might have heard of A NP and BNP. So what happens is when the atria get too uh filled up or get stretched, I guess they release something called uh A NP. Now, this signals in both an endocrine and paracrine way to decrease the BP. So it's noticed that the volume is a bit too large, blood pressure's quite high and it does this in order to try and prevent um cardiac hypertrophy. Uh and it inhibits the sodium and water reabsorption in the kidneys. So, it's a sort of cardioprotective mechanism is in the fact that it's trying to prevent any cardiac hypertrophy or damage. And BNP is similar. A lot of you might have heard of BNP and heart failure. So it's a good um indicator on blood tests. You might look for pro NT type BNP. Uh And that is essentially something that's released from the ventricles when it's similarly stretched and it acts locally in the ventricles to prevent fibrosis causes by vasodilation and it also decreases renin and aldosterone production. So, again, it's uh it's a sort of cardioprotective mechanism trying to protect itself. Um And again, as we said, B MP is very highly raised in heart failure. Um Another factor you might have heard of Cox, uh which produces prostaglandins that can cause a rise in C A NP and cause relaxation. Um And then you've also got local factors, so you've got endothelium derived factors. Er So one of them, you might have heard of nitrous oxide. Er this is released which stimulates something called soluble Guanylyl cyclase to produce C GMP which produces relaxation. And we talked about various stretch receptors and stuff like that, uh which all basically affect arteriolar smooth muscle. And here's just a little diagram splitting it showing vasoconstriction and dilation. Um And yeah, just recapping a lot of stuff we said. So, autonomic nervous system, your local metabolic O2 demand. So if something's hypoxic, you might try and increase blood flow to that area. You've also got these prosys Breiner endothelium derived relaxation factor, nitric oxide um and various other factors. So we're just gonna move on to gas exchange now. Um So there are various factors that affect gas exchange. Um One of these is the diffusion capacity, which we'll talk about a little bit later, decreased concentrations of oxygen leading to a different er lower gradient. We talked about how gradients are important. Uh Some simply hyperventilating because um they've got a blocker, something blocking their. Um they've swallowed an object or something that's preventing them from breathing as much. Or for example, uh uh pharmacological depressant causing hyperventilation will cover that as well. Later. Um, shunts we talked about and VQ mismatch comes up quite a bit. It's quite important these sort of the ventilation, uh cures the blood flow. Um These are the sort of normal concentrations. Um So when it says mixed venous blood, it means the venous blood from the body, not um venous blood from the lung. So, for example, once blood's gone through your body been used, uh it's O2 concentration is only about 40 then the alveolite, it's 100 from the inhaled air, creating a massive gradient of about 60 with carbon dioxide, it's smaller gradient. So, uh your body dumps CO2 into the venous blood, the alveolite, it's about 40. So that pushes carbon dioxide uh from your blood into the alveoli to be breathed out. And there's very, er, there's a way that we can measure gas exchange that's used quite a lot, which is called TLC O. You might have heard it DLC O which is total along carbon monoxide absorbance. There are various things that can affect it. For example, the surface area for gas exchange, the surface area of the alveoli, the partial pressures of the gasses which are here and the thickness of the barrier that it needs to diffuse across stuff like that. And from this test, you essentially get a value called the transfer factor or the diffusing capacity. There's various things that can affect this. For example, hemoglobin. If you have anemia, you might have a reduced diffusing capacity, cos you don't have enough hemoglobin to carry the oxygen. Um you can have alveola alveolar hemorrhage, which you might think a loss of blood would actually decrease your diffusing capacity. But um interestingly enough, it actually increases it because all of the blood that's being um lost is still in the alveoli and still able to take off, take up the carbon monoxide that's used in the test. Um And yeah, so we're just gonna move on to the delivery of oxygen. I'm sure you've seen this guy plenty of times throughout a levels or like uh even your lectures so far. Uh And you know that things sort of shift uh release of oxygen to tissues to the right. Um For example, an acidosis, an increased P CO2, an increase in temperature, for example, when you're exercising and stuff like that, and people often say that an ideal oxygen saturation is above 90%. Now, if you've ever tested it on yourself, using an oximeter or something, it's probably like 9899 really high. It's not 90. Um However, if someone's desaturated in a clinical setting in a hospital, then you'd normally want to target 94 to 98 for them to recover AC O PD. Uh the targets are actually lower and this is because people with CO PD, they chronically are hypoxic and this sort of changes their drive. So it changes that homeostatic balance where if you were to over, if they're chronically low, if you were to overcorrect and send them up to 96 then their brain might think. Oh, we've got way more oxygen than we normally have and it will shut off the sort of ventilation, um, drive and they'll start actually hyperventilating, retaining CO2, not breathing it out, which is very dangerous. So you wanna sort of target their saa little bit lower. Um six, they can us much more clinical years. Um uh there's very slight different different diagnose um definitions. So, hypoxia is a deficiency in the amount of oxygen reaching your tissues. Whereas hypoxemia is the uh the oxygen content in the blood is actually low. So there can be slight differences. Um However, here you can see that there is a type where it's both. So there's low concentration of o in the blood hyperventilation, um hyperventilation because there's not enough oxygen in the blood. And uh consequently, there's also not enough reach in the tissue. So it's both uh anemic. Again, we talked about how hemoglobin can affect the carrying capacity of blood stagnant hypoxia. That's when there's not enough blood flow. So the blood isn't actually moving enough. Uh This could be due to a severe pee. So a blood clot, uh which is a pea is a pulmonary embolism it's a blood clot in the lungs. You also just get blood clots in your leg, I guess, like deep vein thrombosis. Um And yeah, so there's also two types of failure. So you can, you've probably heard about respiratory failure. Now, the main difference is it's not that um uh difficult. It's just type one is just hypoxia on its own. So the person will have low oxygen and type two respiratory failure is where they're hypoxic and hypercapnic. So that means they have low O2 and high CO2. So you'll be able to see this on an arterial blood gas and I'm sure you'll come about um of course, acid base disorders and all of that in future lectures as well. Um So we briefly talked about VQ. This is more a more detailed slide on it. So V stands for the gas flow or ventilation. Q is the blood flow or perfusion and a normal, the overall normal BQ of the lung is about 0.8 and that figure er comes because they say that a normal person will breathe in about 4 L of air a minute and there'll be about 5 L of blood flow a minute in the body which 4/5 is 0.8. Here are some various definitions of um areas in the lungs, the conducting zone. This is where part of your lung that conducts gas down to the terminal bronchioles can also be known as dead space as respiratory exchange does not occur. Um So this is like a trachea, stuff like that where like um air's going through it, but there's no gas exchange going on. There's a respiratory zone where gas exchange occurs, your alveoli and dead space, um which is areas that don't encounter a fused areas. Um So alveolar ventilation is not even the lower areas receive more due to that, as we said, it spreads out as you go down. So there's more alveolar at the bottom. Um And luckily, there's also greater blood flow towards the base of the lungs. So it sort of balances out. Uh And you can have various responses. We talked about um sort of homeostasis, they're trying to maintain the balance your body. So in a hypoxic situation, you might get hypoxic vasal constriction. So this is where the pulmonary arterioles constrict blood away from an area with no ventilation and towards more ventilated areas to sort of get more blood from those, get more oxygen from those ventilated areas by having more blood there and taking it away from areas that aren't really getting useful exchange of gas. You can also get hypercapnic co hypercapnic means high O2 co2 sorry, carbon dioxide bronchoconstriction, whether the bronchioles divert away from dead space or poor poorly perfused areas. Um And so we talked about regulation of BP and heart rate. We're gonna just quickly go over the regulation of ventilation. So the objective as we've talked about is to maintain the homeostasis of the body. So, in this case, we're talking about oxygen and carbon dioxide. And uh the overall er aim is to match ventilation to the meta metabolic activity of the body. So, we have these things called central chemo receptors, which are very important. We'll go on to a while later. So these are located in the brain. So central is the brain, the ventral medulla, its main stimulus is the concentration of hydrogen. And so carbon dioxide can actually enter the CO CSF um which is here on the diagram CSF the capillaries in the brain so it can cross the blood brain barrier um and it affects the ph by the normal er sort of equations that you see that affect Ph and stuff like that. Er and this increased hydrogen will be picked up by the central chemo receptors here. Um uh I said they're very important and that's because they're very sensitive. So a one meta uh not uh rise in P CO2 leads to an increase in ventilation by 2 to 3 L a minute. So we talked about how they say a normal person's 4 L a minute. It's probably a bit more, to be honest. Um but again, 2 to 3 L is a massive change. If you suddenly start breathing in 2 to 3 L more, you would notice it and it's a very small rise. We talked about how the normal value was about 4540. Um, oh no, that's kind of change. Uh, the normal value is about um, like the uh late, er, high twenties. So it's a very small change that needs to cause this massive change in your breathing. Er, however, we'll get onto it later, the peripheral receptors aren't that good at changing. Uh various effects can have an effect on this ventilatory drive. So sleep, er, the drives, depressed depressants we talked about. So for example, alcohol benzos opioids, they can all decrease the drive and we talked about earlier CO PD. So in chronic conditions, er excess, uh HC 03 can be transported into the C ASF acting as a buffer and reducing this sort of um detection of uh high CO2. And this leads to someone chronically being hypoxic, uh hypercapnic and not really having that drive to sort of get rid of it. Uh And this is what we're seeing in the CO PD patients. And so I mentioned the peripheral receptors. So here, um we see that the stimulus is more the oxygen concentration rather than the uh hydrogen iron concentration. Uh it also has a quick response. So both the central and chemoreceptor will have very quick responses in this case. However, we can see here that P AO two has to decrease 50 mg milli um of mercury before there was appreciable effect on ventilation. So the normal amount is actually only 75 to 100. So it needs to decrease by about 50 which is quite a lot before there's even like a response by the, um, receptors to sort of, uh, change your breathing. Uh, so you're much more reliant on your central ones if, um, and you really don't want them to sort of be damaged or not working, uh, cos otherwise, uh, you'd be in trouble probably. Um, and yeah, I talked about earlier about the acid base stuff. So essentially, if you're breathing too much, you're blowing off a lot of CO2. So this decrease in CO2 which is acidic, increases your Ph and causes an alkalosis. And again, when we talk about opposites, too little ventilation will be the exact opposite high Co2 uh Acier acidosis. Um because of that excess co 02 pia, you also have various other um things that regulate ventilation. For example, the carotid body chemo receptors. So here you saw um the peripheral chromic receptors, uh carotid is one of them. So it's in your carotid arch. Um they detect oxygen concentration as well. You have the pulmonary stretch receptors. So even in your pulmonary system, you do have stretch receptors. Um basically how much air is getting in. Um you also have airway irritant detectors. So for example, noxious agents, like if you have allergies or something, it's bronchoconstriction, hyperventilation, coughing, and gag reflex to help protect you by getting rid of foreign bodies or anything that detects as irregular uh that could also have an effect on ventilation by causing hyperventilation. So for example, if you're in a toxic environment, your body's thinking I don't wanna breathe this in. I wanna hyperventilate, protect myself, stuff like that. And your pulmonary also has the vascular receptors um that uh detects problems in the blood flow. So we talked about pulmonary embolism. So that causes a decreased blood perfusion, um stuff like that. So that's just the slides mainly done. Are there any questions at the minute from anyone? Doesn't look like there's any questions at the moment? Um, I'm just looking up very quickly and then, um, I'll give you guys a bit of a break between your next one. As I know you've probably got a lot of lectures today. Um, but just quickly, um, there's just gonna be two questions. Very, um, brief, er, stuff we should have covered. So, does anyone want to have a go at putting an answer in the chat or something for this one? Mhm. I have to let you know what responses come to come through when they come? Ok. Mhm. Mhm. No. Looks like you've got them stumped. So it says which of the, right? So this is actually quite, um, it's, it's, it's not a massively hard question but it does try and trick you out a lot. So, especially in an exam setting, you might be, um, thrown off. Um, so let's go over them. So extrinsic regulation of stroke volume is determined by the structure of the myoc myocardial fibers um at the end of diastole. So I think that's more just trying to get out there. It's more of an intrinsic thing. Um um and so here for me, the typical end diastolic volume is around 70. So you might think to yourself. Oh, yeah, that sounds er familiar. So it must be that however, uh it's actually the end systolic volume, it's around 70 the end diastolic is about 120. Um, so that's how much your heart fills up with Frank Starling Law of the heart explains how the heart can adjust its contact unity according to preload. Er, so that is the right answer. Um, that's the law that we talked about. Um, here afterload is the amount of active tension in the myocardial fibers just prior to ejection, that's actually preload. So, again, all of these statements are technically right. It's just like the slight words that like are wrong which might throw you off cos you might think. Oh, I've heard of that before. Uh, it must be that one and you don't even read the rest of the options. However, it's important to know that they're probably gonna try and trick you out. Uh, cos it is single best answer as well. So sometimes two answers might even be right in a saying. But, uh, in the question, they'll make it, see, they'll make it, um, obvious which one or they'll make it. So that one of them is more right than the other. If that makes sense. An a um a negative inotropic effect is a decrease in the rate of contraction for a giving, given resting fiber, that one's wrong as well. So the right answer for this one was C um and I'll just talk you through the second one. So which of the following statements er concerning ventilation and perfusion is the most accurate. So the ideal VQ ratio in humans is 0.8. Uh So this is actually really um this, this is really trying to trick you cos I did say that the overall VQ ratio in humans is 0.8. But the ideal, an ideal VQ would always be one where ventilation is matched to perfusion. But in the real situation in real life, your, your body just can't get that. There is a point in the lungs where it probably is perfectly one, but the overall is 0.8. But the ideal would always be one because in an ideal world in a perfect world, that's what the ratio would be. And B ventilation and alveolar zyme one is the greatest. We talked about how uh ventilation increases down you go. So that one's wrong. Um And in response to hypercapnic areas of the lung, the pulmonary arterial is constricted. But by the way we talked about that happens in hypercapnic situations where there's too much CO2. Um And then, so D is the right answer in this one where a person is lying flat, the differences in B and Q between the apex and the base of the lungs are abolished. So the actual difference as you're going down, that gets removed when a person's lying down just because of the difference in gravity, the forces of the lungs and stuff like that. So that's us done for today. Thank you for listening. Um If there's any questions, put it in the chat, if you think of anything later on, that's my email. If you wanted to ask me something and this is the feedback form for be Mr er for today's talks, um feel free to send some feedback. You're really help improve how we run these events. Um It's for you guys. So knowing what you think will be best, what sort of content you wanna go over, how you want it, structure that sort of stuff. I think that'd be really useful for everyone. Great. Thank you so much for presenting today. Um for everyone who's watching the lecture, can you please fill in the feedback form? It really helps um both on the QR code and I've posted one in the chat as well. There are two different feedback forms for two different things. So if you fill them both in, then you'll get access to the notes after all the lecture series is done, which is I'm sure all of you want. Um So if you want a note back, please fill in the feedback form. Um But otherwise we're gonna take about a 10 minute break and then start the next lecture. Thank you Rishi for presenting today. And um I will stop this for now. Ok, so thank you. See you later. Thanks, lady. No worries. Yeah, yeah, that's fine. Thank you. Just let me know um uh email or whatever I thought. Oh, I could put my email for you in the shot as well. Uh ok, thanks everyone. I'll see you guys later. Bye.