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Okay. So let's get this up. Right. Uh Let's get rid of this. Hard. Hi. Good. Oh, okay. Ken. Good morning. Everybody. Can you hear me and see the first screen? Ok. Wonderful. Ok. Sorry. It's always a bit of a, uh, an exciting moment to see if my screen's up and running. Okay. So, good morning. I'm Doctor John Vogel still and uh recently retired consultant in intensive care medicine and anaesthetics. And today we're going to talk about a subject that sounds very, uh maybe a little bit basic and technical, but I think I'm gonna try bringing some clinical relevance to this and it's the control of breathing. I know a little bit about this because I did a year's research on this when I was going from Glasgow to Paris and uh using some of the tools that were available that we'll talk about briefly later. So, uh to start with, there's something called on Dean's curse. And if anybody knows anything about German um mythology, this was a story that was about a woman, uh woman, a knife who uh who was, who was treated on by her husband. I guess it happens. And even in German mythology. And so she put a curse on her husband, her unfaithful husband. And the curse was that if ever he falls asleep, he stops breathing. That would be really awkward, I think. Anyway, um, and there's actually a medical condition. It's central apnea. It's very severe central apnea. Basically means that if you fall asleep, you stop, well, you stop when you're breathing is greatly diminished. So, uh that was just a cute way to start. So on means curse. So what are we going to talk about today? We're going to briefly go over some of the anatomy and physiology of the respiratory control centers. Not too long, but just a recap. We're going to talk about how acute respiratory failure and respiratory control interact. We're going to talk about the relatively well known and often misunderstood dangers of uncontrolled oxygen therapy in COPD patients who are in acute respiratory failure. And I'll show you that there's a lot of mythology about that. We'll talk briefly about some of the drugs that affect respiration and how they impact on postoperative hypoxia and we'll briefly talk about sleep disorder breathing. So, uh first for the anatomy. So this is where your centers are, that your chemo receptors that um that control your, your minute, ventilation, your rhythm and your depth of breathing. And you can see that most of this takes place at the level of the brain stem, the ponds and the medulla. And that's where your respiratory center is. So we're going to look at the inputs the different limb of this what stimulates uh this receptor receptor center. So the central uh control area is the are the central chemo receptors that are very sensitive to CO2. And through CO2 P H P H is probably the final um messenger if you like because it transfers across the blood brain barrier. So, but CO2 and Ph are very strongly linked. So yeah, it's basically CO2. Then there are the peripheral chemo receptors that are located in the carotid body and the aortic art and I put the various nerves, the cranial nerves that are the conduits of these uh signals and the peripheral chemo receptors are mainly stimulated by hypoxia. So oxygen, but also to a degree by CO2 and peak, then there are mechanical receptors and these are in the nose, the lungs, the gi tract uh muscles and joints. So if you're going to exercise, you'll send signals up to your uh control center to start breathing in anticipation. If you like uh your nose, there's a tendency now for athletes to try and breathe more through their nose. There are a lot of receptors that release nitric oxide. So it's a bit complicated. But there are various other inputs other than just uh central and peripheral receptors of human receptors. There's a limbic system. So if you have someone who's afraid or in pain or anxious. You'll see, sometimes they'll go into what we call carpel pedal spasm because they'll adopt, reduce their CO2, the uh ionize CO2 because they're hyperventilating. And so they often fall, well, they can fall into uh into a briefly into uh unconscious. So I think that's kind of well known and there are voluntary uh centers in the cerebrum. So seeing music shouting, these are things that you can control voluntarily. And I put this bottle of wine here because I thought it was quite fascinating. I actually have this bottle of wine at homes at present. Uh The one of the main areas of the chemo receptor, the central chemoreceptor area is called the boxing or pre boxing or complex or it's be boot singer, B O M L0 T T Z I N G E R. And the reason the wine bottles there is to remind me to tell you you that this is, this is probably the only part of your body that's been named after an alcoholic beverage about singer was chosen because a group of anonymous and physiologists who are attending a conference in the west of Germany. I think they were from San Francisco or Stanford. Anyway, and they were trying to decide the night before they were going to make this presentation of their new discovery, what to call it after Mr A or Mister B. And they couldn't decide amongst themselves. So to be fair. They noticed on the bottle on the, on the table they were eating at a bottle of wine and decided to call it the boxing, er, after the bottle of wine. So that's a little bit of a fun fact for those who looked like fun facts. So what about the output? Once you've, you've had your reference about your reference and again, this is uh where your outputs look like. So if you look at the spinal column and the spinal cord, you have your motor nerves and your muscles that they will supply. So from the C one and C three, you have your accessory muscles. So if someone's say in respiratory distress, you can just tap along their neck and you can see them really struggling. That's a very good sign of there in respiratory distress and they're working very hard. C 323, C five is your diaphragm. So you won't remember. This is 345, keeps the body alive. Uh That's important. So for example, if you're going to be doing a block, a nerve block of the scaling nerve to try and put someone shoulder or arm to sleep, you can often block the 345 and you can knock one of your diaphragms out for, for, for a short period of time or for the duration of your block. That's important in some cases, uh your intercostal muscles that will pull your rib ribcage up. Uh 62 L1 of your abdominal muscles, if you see someone's abdominal muscles, call them to play. Usually on expiration. What they're doing is they're tensing their muscles and pushing their diaphragms up to increase the next breaths, tidal volume. So they're basically like an accordion. They're squeezing the accordion. So that the next time they pull it apart, you get more gas going in and that's a sign of someone who's really starting to struggle. Um So what about the physiology of this? Now, how about the ventilator response to progressive hypoxia at a normal CO2? That's important. So, we've normalized the CO2 and we're going to make you progressively more hypoxic. And as you can see, so this is on the x axis. This is traditionally, you're going from the higher to the lower, from left to right, not the other way around. So 16 to 5.3. So you're getting more and more hypoxic progressively hypoxic. And we're gonna look at how your minute ventilation will um will react to that progressive hypoxia. And as you can see, it stays pretty flat until you get to about eight and then suddenly it gets very steep. So you're very reactive to hypoxia. Now, eight is about a 90% saturation. So why? Eight? Well, uh oh yes. And one more thing I forgot to mention that in health, you what drives your respiration is mainly CO2 P 02. Only if it's very severe. So we're much more driven by the uh regulation of breathing through C O, too much less through oxygen unless we're very hypoxic. So, going back to the question, why eight, why 90% saturation does it, why is, why is that a sort of turning point where you get more reactive to, to hypoxia? Well, it's because if you look at the oxygen dissociation curve, you can see our gentleman is breathing nicely than P 02 of 13 and he's on the flat part of the curve. So he's got a bit of reserve before he gets into the difficult the cliff of the cliff edge if you like. And as he gets that cliff edge, that's eight, that's about A P 02 of 90 sorry, saturation of 90. Now, if you drop it further, you're going to get a very, a large drop in oxygen saturation. So your, your response to hypoxemia kicks in just as a steep part of the association curve is reached. So that's why there's a logic to this. What about hypercapnia on your events where your response to hypoxia? So we just talked about how you respond to hypoxia if your CO2 is kept normal. What about if you have a high CO2? How does your response to hypoxia differ? Well, that's what it was. If you have a normal P CO2, if I make you hyper Kapnick, the too often do go together, we just talked about that. You'll see. So I've just doubled your seo two. So that's about 75 millimeters of mercury. For those that think in millimeters of mercury, you can shift your curve to the left. So that means that for a given level of P 02, you're going to get a much greater minute ventilation than if you had a normal CO2. So, hi, hypercarbia will shift your curve to the left and when it's combined with hypoxemia, it will strongly increase your spirited to drive. So these two are, are uh will submit there, sorry there, synergistic. They don't submit their synergistic. So one will increase the sensitivity of the other. So what about CO2? We said CO2 is the main driver for your respiration. So we're going to focus on this a bit. And so if you're awake and it's very important to differentiate awake and asleep or sedated. If you're awake, you can see it at a normal P C oh two of 5.3, you've got a very steep response curve with a very, very steep slope. So that means that for a slight increase in C 02, you're going to get a very marked increase in ventilation. But the curve actually has uh got this sort of biphasic uh what some people call it a hockey stick uh appearance. What does that mean? It means that as your CO2 gets below normal, you become much less responsive and so you don't respond, it's not a straight line all the way down. And in fact, if you look carefully all the way down to 1.3, you're still, you still have been a ventilation. What does that mean? It means as long as you're awake, your cortical centres will keep you breathing. So even if you have very, very little CO2, hence, you shouldn't need to breathe, being awake will keep you breathing. You will not become ethnic. The next curve that you have to know is something called the CO2 excretion, hyperbole, hyperbole to. What does that mean? It's basically looking at how many ventilation impacts on your CO2. So it's like the flip side of this. How does if I suddenly start hyperventilating? Um what will happen to my CO2? And as you can see if you go to the top left hand corner, if you're really hyperventilating, say 25 liters a minute, your seo two will drop and it gets, it's quite steep until it gets to about 5.3 and then it flattens out. And what you can see that, what does that mean? It means that if I breathe a little bit less but you know, say I'm at 5.3 and I breathe a little bit less in terms of minute ventilation. I'm going to get a very large increase in C 02. So I'm very sensitive to slight changes and minute ventilation in terms of my CO2. And there's a point where those two curves are in a steady state. So how much ventilation do you require to maintain a uh normal CO2? And for that matter, acid base balance, because the two are, you know, as you learn from the last or one of the last lectures, CO2, an acid base balance are uh closely linked. So that's your sort of your, your balancing point where how much ventilation you have to uh provide to get to remove CO2. And how much do you need to keep yourself breathing? That's if you're awake now, if you're asleep or sedated, the curve is less steep. So for a given increase in C 02, you're going to get less of an increase in, in ventilation. But in this case, you can reach something called the apneic threshold. What does that mean? It means that if you're asleep, you're sedated, we'll give you a very practical example. If I was uh anesthetizing somebody very the beginnings of an anesthetic, they're not paralyzed, they're still able to breathe. And I were to put an oxygen mask or a, a mask with a non rebreather thing, um bag on so I can like an Ambu bag and I start ventilating them, I can hyperventilate them to a point where they stop breathing. I couldn't do that with you if you were awake, but you can do that with someone who's sedated or asleep. So, there's a little bit of a difference there. What about the effects of hypoxia on the ventilator response to CO2? So as my P 02, that's normal, that's your slope. So it's a slope that tells you how you're going to respond to changes in C 02. If it goes, if your CO2 goes up, your arterial CO2 goes up, you're gonna respond by an increase in the uh ventilation. What if my P 02 becomes uh become more and more hypoxic? Well, you can see the slope of my response to raised CO2 becomes more dramatic and more uh more effective. So I will have for the same CO2, I'll have a higher minute ventilation. So hypoxi will increase your sensitivity to see. Oh two. That's a good thing. I think. So, if I suddenly make my CO2 a little bit higher, my P CO2 increases. How am I going to respond? Well, if my P 02 is normal, I'll increase my ventilation somewhat. If it's on the other hand, I'm a hypoxic and I have, it's the same increase in C 02. I'm gonna get a much greater increase in the uh ventilation. So, as you see, again, the two are synergistic. What about age? This isn't common, common problem because someone like your age, I presume will have a nice, vigorously response to see. Oh, too. So you can see the slope is quite, quite steep. So you're gonna be very responsive to a race in C 02 by increasing your minute ventilation. But if I have someone who say 64 to 73 so an elderly person, what we call elderly today. And I wish I didn't use that term because I'm in that range myself. You can see the slope is about 50% less. So for the same increase in C 02, you're going to get much, much lower increase in minute inflation. And by the way, for some reason, diabetics seem to hear the same reduced slope as elderly people do. So you can see again the difference in your response by increasing the ventilation to a given CO2. Okay. So what about acute respiratory failure and ventilatory control? And some of this, I'm going to have to bring back some of the basic concepts that we talked about when I talk to you about A R D s. So I do apologize if this has been uh it has been if you remember this from last one of the last lectures. So that's no problem with that. It's good to have recall every now and again. So what are the types of respiratory failure? And I personally do not like um uh terms that are not logical, but that's the way it is. So we can talk about uh type one respiratory failure, which is lung dysfunction. So say pulmonary edema or pulmonary embolism, but let's say pulmonary edema, that's a very good model. And what you get there is hypoxemia with either a normal or more commonly a low CO2. That's interesting. And the second form is what we call type two respiratory failure. And that is a dysfunction of the muscle pump, the, the actual bellows the lungs. In other words, are not uh pumping enough gas I/O. In that case, you're going to get a ratio to and often with hypoxemia unless you add a supplementary oxygen, which is quite easy to correct in this case in type two. So type one, you have uh you're in type one, you're mainly hypoxemia, you're mainly hypoxic ischemic and you have a normal or often Alosi 02 and type two. By definition, you're not breathing enough. So you're gonna have a raised co two and often an accompanying hypoxemia unless you give an extra oxygen. But why the difference? Well, so to understand the difference, you have to understand something about what we used called. Last time we talked about ARDS, ventilation profusion ratios. What does that mean? It means that you have a unit in your lungs and Alvie Alveolus where the gas comes I/O and you have capillaries from the pulmonary circulation that will um will sweep by this alveolus and we'll um, allow CO2 to be extruded into the atmosphere and we'll pick up the oxygen that you breathe in and then it carries on to the left heart and then that goes through the body and supplies oxygen. So normally you'd like the ideal ventilation profusion ratio. That means the ideal amount of ventilation to the ideal amount of profusion and their marriage. Beautifully. In this case, you can see this is the perfect what we call VQ ventilation profusion a ratio. Okay. So that would be the ideal uh lung unit and everything's working fine. You're getting rid of CO2 and you're picking up oxygen because you're ventilating your alveolus beautifully. On the other hand, if you have somebody who has what we call a high VQ, so lots of ventilation relative to low perfusion. So it doesn't mean you have a lot of ventilation this. So it means you have a low perfusion relative to the ventilation that you're receiving. In this example, you can see you have good ventilation, but that very thin arrow which shows you have very poor profusion. And so the blood going past is going to be um basically uh what we call a dead space. It's basically you're ventilating an area that's not really contributing to gasic streak. On the other hand, you have areas of low VQ, so very little ventilation, but lots of perfusion and that means that that blood is not picking up oxygen as, as efficiently as it ought to. So you can see very little, very narrow, narrow, very little ventilation, but lots of profusion. And so, um, you're not going to be getting a lot of oxygen rich blood mixing with all the other areas. So, ideally in someone who's healthy, you're going to have most of your units will be like the one on top of those are healthy units. So good VQ ratio is 1 to 1. Some of the areas of your lung will have what's called high dead space. That's the bit on the lower left and some of the areas will be low VQ. Now, if someone is very sick, say with pneumonia or ARDS, you're going to get many more units that have high dead space and or low V Q, the low VQ and it's extreme form is called a shunt. That's a shunt means there's absolutely no pick up of oxygen or uh elimination of CO2 from those units. So dead space basically is wasted ventilation and shunt is wasted profusion. And the more of those abnormal VQ areas you have, the more your blood gases are going to be perturbed and disturbed. So that's the sicker you are, the more you're going to have those dead space interim areas. So let's go back to the question why with type one respiratory failure where you're going to have a lot of uh low V Q and why do you have a normal or low CO2. And the reason is, and this is seen in type one respiratory failure because severe hypoxia that would be uh consequent to having uh Elizabeth Suntan and Lovie Q will you respond by increasing your minute ventilation that will reduce your seo two more than it will increase your 02. Why? Because of the different shapes in the oxygen dissociation curves? One has got a plateau and one's linear in the rain trip. We're often we're working in. So let's see what that looks like. So this is going to show you what the oxygen association curve on the red on the bottom and the CO2 curve on the blue on the top, which is much more linear than the 02 curve. And you can see that as you increase your ventilation, your 02 is not going to go up by much because the curve is pretty, pretty much on a plateau. Where's your CO2 by hyperventilating because of the hypoxic drive is going to drop because you're on a steep part of your curve. So you tend to compensate in terms of CO2 by blowing off more CO2 because of the steep part of your curve. Whereas the flat part of your oxygen association curve isn't going to really help you a lot because you're already at the top of your curve. And this was important because um during COVID and I like using COVID because it brought up a lot of physiology, um very interesting from a physiological point of view. Uh Sadly, but one of the things that people notice in the beginning of the COVID pandemic were patient's coming to hospital and what they called. Hi, happy hypoxic. And what you'd see on the ward, for example, are literally people talking on their telephones and looking fine. They didn't look that they were in distress. And yet when you measure their oxygen saturation, they were very, very hypoxic. So that if you like that paradox created this group called the Happy hypoxic. So why do you get Happy hypoxic? Well, it's the same story. So you have your, um, your response to progressive Aisa Kapnick hypoxia. So you show that earlier, that same curve that if you become more and more hypoxic, you're gonna, you're gonna suddenly get an extreme increase in your response to hypoxia when you get to around eight kill Pascal's or 90% saturation, we showed that earlier. So with a severe hypoxia. So you're getting very hypoxic, which these patient's were, you will increase your better ventilation that um increasing the ventilation due to hunt and Lovie Qs. Well, as we just said, lower your seo two more than it will raise your 02 because of the difference in the oxygen curves that we just talked about. So you're going to get a very low 02 that will not be really compensated for by increasing your ventilation, but it will reduce your SEO two. Because your CO2 curve is more a linear, has a more linear appearance compared to 02. The respiratory centers are exquisitely sensitive to CO2, as we said. And so hypocapnia can completely abolish the response to a very low S P 02. So basically, we're saying is that your response to the hypoxia will mean that you will be blowing off. So to effectively, because of the steep uh CO2 response curve, unlike the oxygen association curve, it will lower your CO2. And as your centers are very sensitive to see, oh to, they basically will lose their drive to breathe that they would normally have if you were so hypoxic. And so you look relatively comfortable, you don't look like you're gasping for air even though you're very blue. So Hipaa hipaa car bic suppression of dyspnea was the main reason for the phenomenon that we all saw of the happy hypoxi. Now, this is another subject we're going to talk about and this is something everybody seems to know about. And that is if you have somebody with COPD, usually sit here COPD and they come into the hospital because they're in a bit of respiratory distress, they're probably hypoxemic as well. And we all know you must not give them uncontrolled oxygen. So you don't just plop an oxygen mask on and turn up six liters a minute or 40% whatever your type of oxygen mask you're using in the ward, because the danger is you're afraid that you may stop them breathing or you'll cause severe hypercarbia. And this has been taught to everybody from junior nurses to senior doctors. And the problem with this is, is the reasoning behind. It may not be 100% correct and definitely the cause of this is definitely not correct. Uh So let's go into this. It's actually a little bit interesting. So why, why does this occur? So, as I just said, traditionally, you're taught that giving ex ex excess oxygen, what do you mean by excess oxygen is, what would you would consider normal amounts of oxygen to somebody who is in the ward who's got pneumonia, for example, but for the chronic obstructive pulmonary disease patient's, that could be dangerous because the idea that was proposed was that by breathing oxygen, you're going to be removing their drive to hypoxia because the belief was that COPD patient's have lost for some reason. They never explained why they spoke for years and years. We've decades, we've been taught that they have lost their ability to respond to see. Oh, too. So what keeps them breathing is the response to hypoxia? That's all that's left. And so if you give them that oxygen, they don't have the CO2 response anymore. And so you take, you give them oxygen excess oxygen, you remove that desire to breathe because they no longer have to because they're no longer hypoxic. So leave them hypoxic, which is kind of, well, maybe dangerous in its own way. So, is this true? Well, let's look at this. So how do we before we can actually say, is this true or not? It might be a good idea to see how do you measure the spirit you drive? Because we're talking about respiratory driving. And I can tell you from personal experience, I did a year's research using these tools. So how do we do this? One of the best ways to do this is something called mouth occlusion pressure or P 0.1. Now, I don't want to go into too much detail because it's a little bit complex but not that complex really. So what is it? It's, we used a circuit that would have a mouthpiece and that would connect you connect through that mouthpiece to a circuit, circular circuit that would allow you to breathe out in one direction and in the other. So there are valves. And what that does is that because you're breathing into the circuit, which has got uh a small uh tube allowing you to trickle in oxygen. So you don't get hypoxic, but you do increase your CO2 because you're breathing in your own CEO too. So over time as you breathe I/O and I/O your CO2 goes up and up and up and up. It's exactly the same as if you had a paper bag. Okay. And what you do is you have a, a sugar that comes down as you expire. So you've expired, your sugar comes down and your next breath you're going to take a breath in. But because the shutter is down, there's no flow, you can't breathe. So it's like someone stopping you from taking a breath in, but it only lasts that sugar only is down for 100 of a millisecond. And it was discovered that if you're um if you're not able to breathe in for only 100 of a millisecond, your brain doesn't even recognize the fact that you can't breathe in. So you're not, your breathing is not perturbed. It stays nice and smooth. So 100 millisecond. What happens is the sugar comes up. But before it comes up, there's a small tube that measures the amount of negative pressure that you generate. So basically, the harder you're trying to breathe in the morn egg acttive, the pressure is as the CO2 goes up. So see you two goes up because you're re breathing, you're trying to breathe harder and harder because you're responding to see oh two, that's what you normally would do. And the pressure that you're generating against that closed treader will be more and more negative as your CO2 goes up and you can plot that out and that's a, this is actually quite interesting because it's becoming a, it was a research tool, but now it's becoming much more mainstream because people are looking at um the deleterious effects of patient's who have very, very high respiratory drives that will cause harm to your lungs. We know that now most ventilators, for example, have on their ventilator circuit of the ability to measure P 01. So it's gone from a laboratory tool. That's what I used it for. Uh Now it's become mainstream and we see the importance of this in trying to avoid patient's harming themselves, are breathing in too hard, too much, too much respiratory effort. Okay. So what we say with A P 01 is, as I said, as the CO2 increases through your re breathing just like a paper bag, but it's a circuit as the negative pressure that you're generating by sucking in harder and harder uh increases progressively with an increase in C 02, you're actually measuring indirectly the neural output from the Medullary Centers. And this is considered a measure of respiratory drive. It's your effort. It's your desire to breathe. Okay. Now, it's not the same as your respiratory work. It's because so for example, if I have an asthmatic who's got a severe attack, if you look at them, you can see they're desperate to breathe, their, their eyes are bulging. But if you actually measure the amount of gas going I/O, it's a lot less than their actual desire. So on one hand, you have the desire to breathe if you want to consider potential energy and the actual ability to do that work because they've got a very heavy load and that is the respiratory um system is so bronchi is so constricted that they can't get that gas I/O. So we're just focusing now on your desire to breathe your respiratory drive. So do these, we've been taught to these patients with COPD who are very, very sensitive to oxygen, not all but those that are very, especially those that are very hypoxemic have, have no no CO2 response. And so now we have a tool to look at this as I just explained to you. The po one is a way of seeing how you, what your respiratory drive is when you're given excess amounts of CO2. So if this theory is true, then you could have absolutely no response. No P 01 to an increase in C 02. So let's see what that looks like. So this was the respiratory drive mentored with the PO one. And that would uh that's what a normal person would look like. You'd be between one and two doesn't, the numbers don't matter, but that's what healthy, healthy person would look like. You put them on the circuit and you get them breathing more and more CO2 and you you draw a line as the CO2 goes up. You can see the pressure that you generated against that closed sugar will be more and more and more negative. So basically, you're sucking harder. There's somebody with COPD who's not a CO2 retainer. So he doesn't have a problem with uh with responding to see. Oh, too. But the guy who does, supposedly according to the theory that we were taught for decades, well, guess what? Their CO2 response curve is also high. It's not low. So that was nonsense. And this is proof that that was nonsense. And in fact, what's interesting if you were to take a healthy person. So the person that you see in brown on the left and you were to give them the same respiratory drive of one of the two that you see on the right, you'd be breathing not five liters in a minute of, you know, air I/O or gas I/O, you'd be breathing something like 50 liters a minute if you had that drive. So that's not the answer. That's not why people um don't are sensitive, may be sensitive to Oxford copds. So there's no difference in P 01 values between the copds with CO2 and the non C O T CO two retainers both exhibited higher, not lower drops than healthy individuals. So they have high drives, not low. So that's nonsense. So what's the new evidence. The new evidence says that oxygen worsens your ventilation perfusion, mismatch and, and you're dead space. So, remember we talked about the two lung units, either you have wasted ventilation that's dead space or you have wasted perfusion. That's V Q mismatch or a shunt if you like. And the problem is this, that when you have a unit, especially a low V Q unit or a shunt where you're wasting your perfusion, your body has a wonderful um self correcting mechanism. And that's called hypoxic pulmonary vasoconstrictions. So, the low oxygen in that L V or unit is going to cause you to turn off the tap. Would that mean by that is it's going to make you that strongly vasoconstrict, the pulmonary arterial blood going to that unit, you want to waste blood, going to a unit that's not going to be um uh picking up oxygen. So what happens is you turn that tap off and you basically isolated that unit. So it's not gonna be contributing hypoxic blood anymore. The problem is when you give oxygen, you're going to give, there will be little small volumes of gas going into that alveolus, but they'll be very rich with oxygen. So they will open up, they will reverse the very important hypoxic pulmonary vessel constriction effect. So basically, they're going to allow you to suddenly start perfusing this alveolus. That's got a, you know, adequate amount of oxygen now, but the problem is an oxygen CO2. So we're saying is that oxygen induced hypercapnia is not due to reduction in respiratory drive and P 02 may increase but the PCO to may increase to dangerous levels. So how does this work? So just to this is just sorry about this, but this is just exactly what I showed you a few minutes ago. There's your normal ventilation profusion unit. We just talked about this to really cement this in. That's a normal V Q one and one, this is what might happen with someone who has hypercapnia. So there's your unit, you can see that there's not a lot of gas going in and there's not a lot of perfusion because you've, you've caused hypoxic pulmonary vasoconstrictions. You give somebody, you give somebody a high concentration of oxen degrees. So the volume of gasoline, you know, is still very low, but it's got a very high concentration of oxygen relative to air. So now the alveolus has got a lot of oxygen in it and that will attenuate your protective hypoxic pulmonary visor construction. So now you've got lots of blood going past. The problem is that blood now is going to be dumping CO2 into the alveolus. But because a lot of gas isn't going back and forth, you're going to have very little amount of co two to be extruded. Normally you breathe that out, you know, fully remove that CO2, but very little is breathed out because you haven't got a lot of gas going back and forth. But what does happen is the CO2. Now, it gets so high in the alveolus that it actually gets higher. It's higher than the concentration of the blood coming past it. So it now reverses flow. So it basically dumps it CO2 into the alveolus and then back into the blood and that high CO2 concentration, we'll raise your seo two. Now, the problem with COPD patient's, if you ever, you ever seen one is they are hyperinflated. Have, you know, look at that, we'll just examine them. You can see their, their chests are very big. Their, um their cry co fibroid membranes, uh cry co uh sternal notch is very, very narrow. If you look at an X ray, their diaphragms are very flat, their lungs are very large, they're hyper inflated. And the problem with that is that if you have, uh you have your arm stretched out, fully stretched out and you put a weight on it and you try and flex your arm, you'd find that very difficult if you're almost slightly flexed and you try to lift the same weight. So say your weight lifting a bit, you'll see that it's a lot easier. So your muscle length will determine whether you're at a mechanical advantage or disadvantage. And the COPD patient's lots of reasons usually due to loss of elastic tissue and your lungs for whatever reason, they are very hyper inflated and their diaphragms are very flat. And so what happens is there at a very uh strong mechanical disadvantage. And so just like the guy who's arm is totally outstretched with a weight on it, they have a hard time lifting it. And so that means that extra CO2 that suddenly is being dumped from this, uh the sequence that you've just seen, they're having a lot to do a lot more work. And the problem is they're at such a mechanical disadvantage. They can't get rid of that, that extra gas. And so they just say, you know, I'm exhausted, I'm going to let it go and they just become uncontrollably hyper Catholic. So that's the reason it's a bit more complicated, but it's more interesting. So the upshot of this is what do you do about this? And the key today is if you ever have somebody who's got COPD, do not do what I've seen quite often happening. And that is um they'll say, oh no oxygen and you'll see the person getting very hypoxemic. You want to titrate your oxygen just to the point where they give a saturation between 88 say 90 92. So you don't want to go for a normal, a normal oxygen level, say 97 98 99 you don't want to go through that, just go for 88 to 92 you'll be safe anyway, that was interesting. So, here's another clinical case. Um Now this is uh from uh a talk I gave on venous return physiology. What happens if someone comes in with a fractured femur and a ruptured spleen and they're, you know, lost a lot of blood internally. And the point I was trying to make was, you know, if you give them, this is the story, um your resuscitating, you're starting resuscitation and they're in agony and you give them morphine. And I say to everybody, what's what might happen if you give morphine? And what amazes me is absolutely everybody in these talks I give and not just two, you say the same thing. They don't say you might crash your BP. This is the story of venous return. Know they say he'll stop breathing. Well, that's a really interesting point because it's almost impossible to stop somebody breathing. If you titrate your morphine to pain, a quick story. I remember once this happened to me twice. In fact, I was uh well known for being a dabbler in regional anesthesia. And I was, I think I was relatively good at it. And I remember one case, in particular, young man came out of surgery with a fractured ankle that was fixed. He was a strong guy and he was in the recovery room, he was screaming in agony and the nursing staff added in addition to what he received intraoperatively, they gave him 37 mg of morphine um incrementally and it didn't touch, he was screaming. And they asked me eventually, can you please come in and do something about this man's pain? And I said, yeah. So I said, turn him on and over and I gave him what we call a sciatic nerve block. So basically, I put a needle next to his sciatic nerve which will um block the sensation from his leg and remove the pain. And as I was literally, as I was starting to indirect, he stopped breathing. And the nurse said to me, oh your, your block is uh somehow stop this breathing. I said that's nonsense. But I realized he was right. And the reason is, is because I had taken a man who was in agony and 37 mg on top of everything else he'd received, didn't touch him. And now I've totally removed his pain. So he's become like a volunteer. And if I gave you as a volunteer, 37 mg of morphine, I'd probably stop you breathing. So you've got to titrate to pain. That's all I'm saying. So, pains are very, very good stimulus. So what about the effects of drugs and respiration, opioids, depressed the respiratory effects of low oxygen, but especially CO2. So here's again, this curve we saw earlier awake. And if we look at someone that's the CO2 excretion, hyperbole what you talked about. But if you have somebody who's getting an opiate their, their slope. It's mainly the slope after opiates that is reduced about 50%. Now, if you look carefully, that's quite a marked reduction of the slope. But the new steady state where you start to ventilate enough to get rid of that CO2 you're producing is shifted a little bit to the right, but it's not that dramatic. So what we're saying basically is you can have a very severe uh respiratory depression uh in response to see oh two. So 50% less than you would if you're normal without opiates, but the actual increase in C 02 is not that great. So, and the drop in minute ventilation isn't that great. The danger is if you add a second drug that may have some respiratory depressant effects, then you're gonna get something that's additive and then you may be in trouble. So, um so this is we're saying is that CO2 minute ventilation may seem mildly abnormal, but in fact, your responses so too is fairly uh impressively diminished. So be careful, you give a second, a second respiratory depressant that could be dangerous. Now, if you look at the post operative period, when people are coming out of there anesthetic, what have they received? Will they received opiates that will be just said, reduce your seo two response. You may have some residual volatile agents. So you're high subfloor in some of the volatile gasses you breathe in. Those don't act on CO2 so much, they act very, very strongly on your peripheral chemo receptors uh and the response to hypoxia and even a very, very minimal residual of these gasses. So when you're in the POSTOP area, you're awake, but you may have some volatile gasses still available, they will respond, they will diminish significant your response to hypoxia. And if you have any neuromuscular blockers, and this is not someone who's paralyzed or even partially paralyzed, the neuromuscular blocker itself, it could through the nicotinic receptors will actually reduce your chemo receptors, your peripheral chemo receptors and the response to hypoxia. So you add all this stuff together and you can see you're going to get into what could potentially be a dangerous situation. Does this matter? Well, there was a really interesting study where patients who have gone from recovery where they have loads of nurses, loads of doctors, oxygen saturation probes, everything's very tightly controlled, everyone's happy because your saturation is 98% or above that. Then they looked at them, these patient's measuring through telemetry. So the nursing staff don't know what you know they're saying. They looked at the, the S P 02. This is after major noncardiac inpatient surgery. So not people going home in an hour's time or two hours time. And what do they find? They found loads of patient's over the next two days and they only measured for two days. It could be even worse on day, three or four or five. But for the next two days, they found that the saturations were really low and they lasted a long time. And most importantly, it was common, it was prolonged. But most importantly, nurses missed 90% of these quick pox emmick episodes because they didn't have the, the continuous data that was transmitted, telemetric Lee. So, what we're saying basically is that you see someone in the recovery room and thinking, hey, they're great. You set up in the ward, you can almost guarantee a large, at least a third of them will spend an hour or more uh very low saturations to lower than you'd ever tolerate in the recovery room. You'd never accept that. And as we know, patient's postoperative, we have a much higher rate of dime than they do intra in the inter operative period where you're being very closely monitored. Could this be one of the causes? I don't know, but it's worth looking at and one of things that's very important is that you'll see people putting a pulse oximeter on patients' and saying um it's a good monitor of your ventilation. It's not unless you have breathing air. So you have some, you see this all the time someone's on with an oxygen mask, they've got a saturation of 98% or 99%. And nursing staff for happy you're thinking, oh, they're ventilating beautifully. Well, no, because why? Because by giving oxygen but because of the shape of the oxygen dissociation curve, you could be right at the cliff edge and you'll be a 99% saturated. Okay. Or you could be on the steep part. But if I give you a bit of oxygen, you're ventilation maybe poor, but the oxygen will basically artificially raise your saturation. So you see someone and they say, oh, he looks fine, but in fact, they're hypoventilating. It's the oxygen that stops them from getting um hypoxic. So the point I'm trying to make is that the, the uh pulse oximeter is a poor monitor of your ventilation. It's a monitor of your oxygenation, not your ventilation unless you have that person breathing room air. So when I used to go in the recovery room, I'd say to the nurses before you send the patient up, I wanna see that saturation without oxygen. If it's okay, then he's probably ventilating enough. If it's, if he takes it off and it suddenly drops, that means he's going to be um hyperventilating. And this is this true. Well, here's someone who's getting 30% oxygen. There's US P 02. It's perfect. And here's your entitled CO2 as a marker of your ventilation. And you can see um it's going up. So pulse oximetry with oxygen is not a good monitor is not a good monitor of ventilation. Ok. Quickly sleep disorder breathing something very common. It's a real public health. Uh I'd say dramatic with obesity and the like. So what does, how does this work? Do you have receptors, including your chemo receptors? Which tend to, how can I put this when you breathe in? You're generating negative pressure to suck air in, in and the two bleeding from your larynx into your mouth and nose is a muscular funnel. And if you were to suck card, if that muscle was flaccid, it would just collapse. Like you imagine something on a, on a balloon, it would just collapse. And so you're gonna be unable to shift gas. So what happens is that you need a uh a tonic tensing of those pharyngeal muscles to keep that tube patent. And so we have various receptors, including your chemo receptors and your mechanic receptors that will, as you breathe in, they will tense the muscles in your pharynx. So they don't collapse and then stop gas moving I/O. So what happens is that you get, um you get fair into your muscle forces increased when you breathe in, you're closed airway becomes an open airway and you have a good title volume. So your breathing it nicely because your resistance to breathing in is low. Now, on the other hand, if you have, for some reason, heart a suction and your parents doesn't, doesn't open adequately, you're gonna close your airway because it's going to collapse the pharyngeal tunnel. If you like or funnel and there, you're gonna have a lot of resistance and therefore you're going to get periodic or apneic breed. So you're not gonna be able to shift the gas I/O. You know what's gonna happen is you're going to suddenly get hypoxic and hypercapnic and you're gonna, that arouses you and you wake up, but it also causes a marked stimulation of your respiratory season. I'm sorry if your cardiovascular center. So you get hypertension and the whole concept heart probe. So let's look at this. So you're sleeps, you start sleeping, you're dilator to your pharynx is reduced. In some cases, you get narrowing of your airway. You become apneic or hypopnic. So you're not drifting as much gas as you would. Normally, you might snore, you then become as a consequence of not ventilating enough. You become hypercapnic and hypoxic that caused you to make an increased effort to breathe. Thanks to your receptors, your chemo receptors, you start to wake up. Your sleep is disturbed, your airway then opens as you wake up and you restore your breathing. But the hypercapnia hypoxia well, and the arousal will cause you to have an adrenergic surge. So you're sympathetic system kicks in and that causes people that have sleep apnea. You have hypertension, ischemic heart disease, heart failure, obesity, it makes you obesity worse, your sleep is disturbed. So it's, you know, nothing but bad, nothing but bad and very common. Second. Okay to recap. So this is the uh we talked about the anatomy and the various centers and the bottle of wine. The Boat Singer complex for those who want to impress it parties. Uh your response, your ventilator response to carbon dioxide. Why if somebody breathes with, with uh inefficient lungs, so they're sick lungs with type one respiratory failure, they may have a low P 02, but they'll have a normal or even low CO2 because of the difference in the association curves. Once linear one's flat, um COPD patient's, if they are sensitive to oxygen, it's not because they don't have respiratory drive, they have too much respiratory drive. So it's the opposite of what we were taught. But still the the lesson is care with the oxygen titrate to 88 to 92% saturation but don't deprive them of oxygen. Um Does the accumulation of various respiratory depressant drugs matter in the POSTOP period? Yeah, it's common. It's prolonged and it's mostly missed. And we talked about oh essay and how you had the cycle where you reduced your dilator um that keeps your airways open when you're asleep and that causes a rise in your CO2 and drop in your P 02 and that causes a disturbed sleep cycle and another nerd surge and lots of uh lots of problems animate from that. Okay. So that's really quick summary of a fairly complex subject and I hope I make it too confusing. But if you have any questions that he delighted to try and answer them. Yeah, thank you dot So I have a question. Um It's about you said when um there is um in case of uh instant when oxygen is being given to the patient and the it causes uh because it's previously um brother constricted vessels to dilate and I don't understand the oven for oxide expert of it. He said it will be exiled and it will come back to the blood. I don't together. But okay. Yeah, I can understand. Would that be a little bit confusing? So if you have a unit that's not getting a lot of gas going into it. Okay. So it has a low ventilation profusion ratio. So lots of blood, not a lot of gas. That means as you're breathing air, for example, the alveolus not getting enough gas going in will become more and more hypoxic that low oxygen in the alveolus will cause a reflex. That's a protective reflex and which makes perfect sense is you'll basically turn the tap off of blood going to the alveolus. So you'll get fazio constriction. So that's hypoxic pulmonary veins, constriction and that's good. That's defends or protects your body from perfusing areas of lung that aren't able to contribute to gas. Extreme. Now, if you give somebody high concentrations of oxygen debris, even though the total volume of gas going into that alveolar is low, it's got a lot of oxygen. And so that extra oxygen will now reverse that protective reflex and it will open up the profusion to that alveolus. So now you're getting blood going past the alveolus, but it's still not being ventilated very well, but it's getting a lot of oxygen because it's so enriched with oxygen that you've given. But the problem is the CO2 that's building up inside because this blood is dumping CO2 into that alveolus. It can't get rid of it as, as efficiently as it ought to because it's got such poor ventilation and that's CO2 will start building up and building up and building up until it gets so high. It's spelled like breathing into a paper bag again, gets so high, it will be higher than the blood coming past it. And so it will, it will reverse the flow and it will start flowing CEO to just like a paper bag as you breathe into a paper bag. The CO2 will now be reversing flow. It'll dump into the blood. So it will not be picking up blood and blowing it out. It'll get, be increasing the CO2 to a point where it starts, um, uh dumping CO2 into the blood passing that alveolus. So your CO2 will increase and as your CO2 increases in someone who's already at a great mechanical um disadvantage, they just can't, they can't breathe anymore. They try really hard as you saw they have a very high uh respiratory effort. If you measure it with a P 01, the inclusion pressure. But they just basically have to give up because it's just too much roads. They can't sustain that. But I agree. It's, it's not uh I think if the, if you wanna remember one message, if you have somebody like this and they say, oh, you mustn't give oxygen, know you titrate to 88 to 92%. That will keep you safe. Okay, good. Anybody else? So what you see in essence is that the safe oxygen concentrations were giving to patient should be between 88 to 92. So what I'm saying is that so the reason I'm saying all this is because there have been many instances that I've seen where doctors are told um you must or nurses a spectrum, you must not give oxygen to these people and they're so afraid to give you oxygen, they leave them hypoxic. And the reason this happens is if you like it's more of a theoretical interest, but the result is the same. You want to be careful with the auction you give because you can uh remove hypoxic pulmoni vessel constriction. But that's the theory. The practice is you put just enough oxygen on to look at and put a, you put a pulse oximeter on them, say they're saturations 80 you just give them just enough oxygen so that the saturation now is 88 90 but you don't aim for 97 98%. You don't aim for a normal value. 88 to 90 or 92 let's say 88 to 92 is more than enough. And that way you won't fall into the danger of making them hyper Kartik and, and going into hyper kept Harvard coma okay. So you remember nothing else about less of it. 88 to 92. That's you titrate the oxygen you give more or less auction till you get to 88%. And then once you get to that where you can stop giving more oxygen, but you're not going to try to go for a normal value. That's the key. Any other questions? Okay. Well, there's no more questions. Yeah. Ask you one more question, a question. Um Do you have to give like a baby or like see a new friends child that has a or is that broke you light? Is which 92% oxygen? Those statues still need oxygen? Yeah. Well, be careful. Now. I'm not talking about everybody. I'm talking about COPD chronic obstructive obstructive Pulmonary Disease. Patient's not talking about Children or anybody who's healthy if I have pneumonia and I'm hypoxic, you can give me as much oxygen as I need. Um I'm talking specifically about people who have chronic obstructive Pulmonary disease. They're the ones that are classically. Everyone's afraid to give oxygen too. So be careful. I'm not talking about everybody. I'm talking specific category. Patient's okay. Was that useful? Yes, it was. Thank you. Okay. Okay. Well, you all take care.