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Yeah. OK. Vince. Okay. Mhm Let's get rid of this. I'd be a pedal. Okay. Uh Can you see this? Yeah, that's great. Okay. Okay. So off you go so good afternoon. Um Just to remind those of you who have joined me for the first time, my name is Doctor John Bogle and I'm a relatively recently retired, any consultant in intensive care medicine and anaesthetics. And so we're going to talk today about a subject that's very close to the heart of intensive care doctors and especially given that we recently went through a COVID pandemic. This is something that's become I'd say almost uh mainstream news, this acute respiratory distress syndrome or what we call a R D s. And the reason I think it's worth talking about even to those who are not intensive care doctors, is that an extreme form of acute respiratory failure. And this will give us an opportunity to talk about some of the some of the physiology, normal and abnormal. And then we'll go into more specifics about ARDS without going into too much detail because it's a very, very big topic. So just to situate everybody, I've given a series of lectures and I'm trying to use a structure um that was introduced in the very first lecture I gave on oxygen delivery, which is the goal of everything we're trying to do. And as I said, you can break this down into its component parts, cardiac output, hemoglobin and saturation of oxygen. Um And that tells you basically those three components, tells you about auction delivery. And if those three components are okay, you're okay. And the reason below that you have sub factors, sub components to preload pump failure after the heart rate, etcetera. And under those subheadings, you have sub sub headings. So the the point of this is that when you get into the sort of the weeds of, of of medical problems, terminology, chaotic situations, whatnot and you're not sure what to do simplify, just go to the top of this pyramid if you like and just make sure that those three components are okay. And today, so we've talked quite a bit about cardiac output and various factors. Um So today we're gonna talk about one of the other three factors and that's gonna be saturation of oxygen and one of the sub factors is ventilation, profusion abnormalities. And we're gonna illustrate this with probably the most severe form, which is A R D s. So that kind of sits situated you in this sort of map of where we're going with these lectures, most of these lectures, not all. So today's talk, we're going to talk about, we're gonna introduce which have more or less just done. Um We're gonna go over some very essential respiratory physiology, which I think will be applied to almost any field, not just intensive care. We're gonna focus a little bit on it. Well, quite a bit on A R D S as an extreme example of acute respiratory failure. We're gonna tell you what it is. We're going to tell you how to help somebody who has us. We're going to show you what you mustn't do because that will harm you. And we're very good at that. Sadly, and how to focus and get your goals correct. It's very common that we mistake are actual goals and we go down the path of um improving something that we think is important. In fact, it may not be as important as we think, but you'll see what I'm getting at there and then we'll recap. Okay. So first we have to go through some basic respiratory physiology. So there's something called the ventilation profusion ratio and this is important. So what does this mean? It means that we're trying to marry in a lung unit? There's the alveolus and blue and there's your pulmonary capillaries, both your pulmonary arterial or artery and pulmonary vein. And we're trying to marry these two sort of perfect marriage. And so you want to ventilate your alveolus. And if you do that in this uh idealized schematic, your oxygen would be 13.3 killah past that's, that's normal. Uh, so to be 5.3, these are just, you know, normal values. Um, kind of ballpark figures, your blood coming from the returning from the body have delivered it's oxygen and, and picked up CO2 will go from the right heart through the lung circulation to the alveolus. And again, this idealized alveolus and it will then leave oxygen into having picked up oxygen. So it reflects exactly the same oxidants in the Alveolus and it will remove or um extrude the CO2, which is ventilated out into the atmosphere. So this is the absolutely ideal perfect marriage between the ventilation. That's the V and profusion of that alveolus, which is the Q. So ventilation profusion. This ratio is what's important is the marriage of the two. Now, if you have an extremely um misfunction, your dysfunctioning, I'll be your unit. I'll burkha pillar unit, you have what we call a high VQ. There's a lot of ventilation but very little if any flow. And so what you have there is what we call a dead space. So basically, you're, you're wasting your ventilation, you're ventilating something that's not picking up any blood. It's not transferring gas is, it's almost like if you breathe into a paper bag. So, um that's a dead space. On the other hand, the other extreme of this uh unbalanced ratio to a low V Q. So very little ventilation to a lot of profusion. That's a low V Q and that's where you have very little if any ventilation and you have lots of flow. So it's not picking up any of the oxygen or removing any of the CO2. And that's called a shunt in its most extreme form. Now, these are extreme, extremely abnormal values. Okay. So we said dead space is wasted ventilation and current is wasted perfusion. So those are two ends of a spectrum. So in the middle, you have the perfectly ventilated, perfused alveolus, that's a VQ of one on the other side. On the left hand side, you have dead space, you're wasting your ventilation. That's a very, very high VQ. And the other extreme, you have a very low VQ and its most extreme is called shunt, but you have everything in between those as well, obviously. So what happens if you have a hy vee cube? So dead space, you're wasting ventilation but it's well saturated. So you're not getting a lot of profusion but getting a lot of very good ventilation. So you have a dead space and don't forget when you have someone who has sick lungs, pneumonia or ARDS, you have um a large dispersion of the Alvie or units that are both the extreme dead space end of the spectrum and shunt end of the spectrum. And so if these two mixed together, what do you get? Well, you'll get a little, you got a very good profusion, uh sorry, very good ventilation and the blood coming from that well ventilated alveolus on top, the dead space will be very well perfused and hence very well saturated. So everything's working just not enough on the, on the low V Q on the front end of the spectrum, you're gonna have blood that's not really fully saturated. Now, the problem here is as most of the blood is going to be coming from the front end of the spectrum and they mixed together. It's not gonna be an arithmetic mean, it's not gonna be the difference between say 99 to 100 say and 80. So that'd be about 90 it's going to be much more closer to the uh the units that are contributing the most blood. So you're gonna have the end of the day, you're gonna have a saturation that's gonna be closer to 80. So 83. So that means that when you have this dispersion of these units, you're going to end up being quite hypoxic. Now, normally in our normal blood vessels, you and I, we have a degree of the shunt. So let's say about 2% 3%. And so you can see your starting point on the bottom. You're gonna have, if you're F I 02, that's F I 02 means the amount of the fraction of oxygen that we um we, we give somebody now from breathing air have about 21% oxygen in air. So it's about 21.21 or 21% and C F I 02. And you can see my P A 02 is normal on the bottom. That little dot Now, this diagram means that if I increase even slightly my F I 02, then my P 02, my arterial blood will go way up. So I'm very effective at giving oxygen and seeing the result, which is very positive. So with a little bit of shunt, you can see that I can rapidly and massively increase the oxygen in my arterial blood. But as I have more and more shunt as a percentage of the total flow, you can see my starting points lower. But when you give more and more oxygen, you're not getting the same increase in oxygen in the arterial blood. In other words, the lungs aren't as efficient of getting blood, getting oxygen from the gas, you're giving them into the arterial blood. And as you get to 50% which is say you might get with ARDS, you're starting a lot lower. But even if you give a lot of oxygen, you're not going to go very high. So this is the problem with a lot of these lung conditions, you're starting lower, but even giving oxygen, you don't get the same increase if any at all. But often you get some but not quite as uh as close to the normal where you get a very large increase in arterial oxygen in the, in the, in the arterial blood, even if you give a lot of oxygen in the gas. Why? So one of things you do get with someone who has sick lungs is you get hypoxic as we just saw. And if you get hypoxic, it drives your spirit e center. So you start breathing deeper and rectum and more rapidly but more, especially deeper. Now, the problem here is that so hypoxi will increase your ventilation. So you'll breathe more I/O with hypoxi that stimulates it. But by doing that, you'll notice if you're dealing with patients who have a high or abnormal, sorry, abnormal vehk us that they will lower their CO2. So they'll have a lower CO2, but they won't raise their oxygen by much if at all. Now, why would that be? It's because of the difference and shapes of the oxygen and CO2 dissociation curves. So you can see here the oxygen association Kervin read, once you get to a sort of a crest of a hill, there's a plateau plateau. So if you breathe even more and more, you're not going to get a much if any rise in oh two. But on the other hand, the CO2 curve is much more linear. So that means that the more I breathe I/O stimulated by hypoxia, I will lower my CO2, but I won't increase my oxygen by much. So you'll often get patient's who have abnormal ventilation, profusion abnormalities. Under words, acute respiratory failure, you'll see them with a low oxygen to the arterial. Uh blood is deoxygenated there, hypoxic or hypoxemic, but they're so too may be normal or even low. That's why. Okay. So let's look at an example of where this can come into play and this might explain something. So we know that if someone has a pulmonary embolism, uh you know, a significant pulmonary embolism, yes, they can have a right heart failure and that's maybe what kills them. But one of the signs of a pulmonary embolism is the patient will be hypoxemic. Now, you might ask yourself, why would they become hypoxemic? Well, let's look at something called a electron electronic impedance tomography. It's just a fancy way of looking at the lungs using electrical signals. And um, and then we'll also look at Andrio CT. So that's a classic CT having given a contrast. So you'll see in blue, it doesn't matter. This is just an example in blue. Those are areas that are dead space. In other words, wasted ventilation, you're ventilating, but you're not perfusing. And the problem is that when you have an embolism, it's a significant, you're blocking flow to that area of the lung. So you're getting ventilation going I/O, but you're not refusing it. Now, the thing is the blood has got to go somewhere. So where is it gonna go? It's going to spill over into those areas that are normal. And so it's gonna excessively perfuse those normal alveolar areas. So what's going to happen is you're going to get, um uh hi, sorry, low VQ. So a shunt which means that you're getting all that extra blood and the alveolus is overwhelmed. So the VQ um goes from high VQ so dead space to shunt because the blood just basically shifting to other ends of the lung. That's why you get hypoxi. Okay. So let's focus now on the acute respiratory distress syndrome as an example of uh an extreme form of acute respiratory failure. So here's the normal alveolus. Now, the normal alveolus is quite, it's quite interesting because a couple of probably haven't thought about. So for gas to passively diffuse along a concentration gradient, that's how it diffuses. It's gotta go from the alveolus, it's oxygen or from the capillaries of it's CO2 and it's going to diffuse based on the pressure differences and the this is physics, but the distance it has to, it has to traverse is vital to how much of that gas can move I/O. And in fact, it's so vital, it's the fourth power. So if I were to double the distance between the alveolar epithelium and the capillary endothelium, if I doubled, it would be too, that's double times two times, two times two, that's 16 times So even a slight increase has got a major impact on diffusion. Now, the other thing that people don't appreciate is that you have pressure, we all understand what pressure is, but there's something called curing forces and it's the sort of tangential pressures and flow because you're, you're, you're getting, if, if my body takes five liters a minute of cardiac output throughout my entire body, your lungs have got to pump out that same five liters a minute. So if I go for a run and I go from 5 to 15 or 20 liters a minute, that 20 liters a minute, it's gonna be a heck of a lot of force going through those capillaries. And what separates the endothelium and the epithelium from the alveolus to the capillary is a very fine memory and that membrane is gonna be like Kevlar because it's got to be um thin enough to allow the gas is to, to defuse cause it's gonna be very, very thin. It's 0.2 of a micron as you saw, but it also has to be incredibly robust to withstand those forces of the blood passing through it. And in fact, interestingly enough, if you did a study and there were studies done where they took horses, race horses, thoroughbred, race, race horses and they ran around the track because their, their bread to do one thing that's run like the wind and they did. Bronchoscopy is on these horses. What did they find that the Al Viola were flooded with blood because those membranes are being damaged and the membrane being so unique type for uh sorry, it's still like Kevlar, it's called type four college three. And the other part of your body where you have that is your Nephron because has the same, the um contradictory needs no words very thin but very robust. And in fact, there's a disease called Goodpasture syndrome, which is antibodies against a specific type for collagen. So you can get Alvey or hemorrhage and you get Lamy or nephritis. So it's all kind of makes sense. Now, what about ARDS? Let's look at what that looks like. Now, I don't think I have to go into too much detail here, but you can see the thickness of this sort of inflammatory soup that's going to separate the capillary from the elbows. And you can imagine that lungs will be very stiff with this inflammatory liquid. And the distance between the various components is going to be massively increased. So you're gonna get hypoxic and get thrombosis. It's just a real nightmare. So I want to go into detail, but you can see very correctly the differences. So one of things that often um strikes people is this is what a normal lung looks like. When I was a medical student, we used to have the pleasure if you like. It was interesting of going to autopsies every afternoon. I used to bring my sandwich to the apathy occur and watch autopsies being done. And you'd see this classically, this is someone who have their lungs taken out of their thorax after they had passed away after they died. And that's what a normal lung would look like. It's about 808 100 g or so, this is what ARDS lung looks like in someone who has died of the ideas. It looks like a piece of liver. It's at least 2 to 3, even four times the weight of the normal lung. And I recall very well how they used to squeeze the lung and then just fluid all over the floor when they used to do this. So this is what you're trying to breathe through when you have severe ARDS and this is something you don't want to forget. Um So if you have someone with uh pneumonitis, in this case, it was ARDS due to take one. And what this is a true case we had, this is what they looked like when they came in on their chest X ray. And they were actually not too well, but the X ray was not perfect, but it wasn't that dramatic compared to how they look, they look terrible. Well, something about ARDS is there often is a lag face. So don't be fooled by an X ray that looks relatively normal 24 hours later. That's what they looked like. And if you look at the CT, which gives you a lot more information. Um This is what a, you know, classic ARDS case would look like. So you have a normal normally inflated lung that's in the dark areas you have overinflation, which is just above that. Now, it's very hard to see overinflation on a CT. There are ways of checking it, but it's not easy on the CT you have airway collapse as you get this heavy lung waited down by this edema is gonna start collapsing airways and then it's going to collapse out of your life. And some of that, those Alvey oil will be flooded with inflammatory fluid. So you're gonna go from overinflation to normal inflation to airway collapse to Alvey or collapsed consolidation. So if you have ARDS, there are three important parameters, you'll measure, they tend to be related to outcomes. One is oxygenation that seems obvious. I interestingly enough many studies and I'd say most studies have found that oxygenation per se is not necessarily closely related to outcome. What is the oh, is dead space? So that wasted ventilation we talked about now, dead space is not easy to measure. That's why we tend to ignore it a little bit. But there are formula that we can use. I won't go into those today, but they're not difficult. Um uh Something called the ventilator ventilator E ratio, which we use more and more because that's very closely related to mortality and then the mechanics, your lungs, how do they actually work. Are they stiff? Um There's a lot to the mechanics and we'll talk a little bit about that in a second. So, first of all oxygenation, how do we, how do we assess and how do we classify oxygenation? But we use something that we call the P F ratio and you'll hear a lot about this. If you follow the subject, it's absolutely central. So what is the P F ratio? So if you look at the X axis, you have the pa oh two in the arterial blood. So if you take an arterial sample from say the radial artery, you'll see what the arterial P 02 is. And on the Y axis, you have the oxygen saturation. That's what you get. If you put a oxygen a pulse oximeter on somebody and very often we use the oxygen saturation as the monitor. Are they okay or not? In terms of hypoxemia. Now, is that is the oxygen saturation that's very easy to obtain on a saturation monitor? Is that really appropriate to determine if someone is very hypoxic or not? Well, not really why, because if you have somebody who's got normal lungs, they'll have a uh this is again, this is a ballpark figure they'll have a P 02 of around 88. Now, the P F ratio is your PA 02 divided by the amount of oxygen you're giving as described by the F I 02. So if I'm breathing air. She said earlier it's my F I 02 is 20.21 or 21%. If I'm breathing 100% oxygen, then it's one or 100%. So you divide your P 02 by your amount of oxygen you're giving. So obviously, if I'm giving a lot of oxygen, my P 02 should go up uh concomitantly. So in this person, he's got a P F ratio, 88. That will be the same whether I'm giving 21% oxygen or 100% oxygen because it's a ratio. So one goes up, the other one should go up equipped an equivalent manner. And what is my saturation? In this case, it's 100%. So everything's fine. So you can describe me as having normal lungs in terms of oxygenation. What if I have someone who's got pretty bad ARDS? Well, here my PF issue is 27. So it's about, I would say it's exactly a quarter, but close to a quarter of what the normal would be. And so what because of the oxygen association curve, what is my saturation you'd see on oxygen post oximetry, it's 100%. And the difference between the pho too and the P F ratios as you can see is quite considerable. So if I just looked at the set, the pulse oximeter, both of those cases would say 100%. But in fact, the P F ratio is uh is very different. So it's the pho to that you get from an arterial sample divided by the F I 02, which is a fraction of what you're giving. So I give 50% oxygen. My P F ratio, my, my F I 02 is 20.5. Okay. What about dead space? Well, as I said, dead space is wasted ventilation and what you can see here is it's very closely related to mortality. So if you look at something called the dead space fraction, which is just a way of quantifying dead space, you can see that the more the dead space fraction increases. So the more ventilation you're wasting because you're not getting uh the perfect marriage between the ventilation and the profusion, your mortality goes up, uh equivalently goes up severely and that's one of the better monitors of uh of mortality. And it was a very closely related to a risk of hospital mortality. So that's a very good marker that we probably haven't used enough because it's not that easy. It's not as easy to, to measure as say the PFA influence. So here's the clinical case. This is a true story. I remember this like yesterday. This is very sad story. This was a woman who was 49 years old and he was very healthy, previously healthy. She came in having had uh what was the previous pandemic, which was swine flu or H one N one flu. She had been with us for eight days being ventilated with very, very sick lungs and she had a very high F I 02. So I think it was about 20.9, so 90% Oxford, which is high, maybe even 100% I can't recall, but it was very high. I had just taken over her care from the previous consultant. The title volumes they were using to ventilate. Her were the classic title volumes that many people were using about 500 mils per breath. There was no improvement and her oxygen saturations were deteriorating were getting worse and I thought this girl is going to die. Now, at the time, we have something called ECMO, which is extracorporeal membrane oxygenation. It's a way it's like a cardiopulmonary bypass machine. You take the blood out of the body, you oxygenate it and you remove CO2 to different degrees sometimes. But that's essentially what you do. You're replacing the lungs outside the body and then you pump the blood back in, you also can help the circulation. So, ECMO is something that's being used more and more uh as an artificial way of keeping you alive until your lungs hopefully get better or you get transplanted, for example. And at the time in the city of Leicester, there was a study going on a very important study called the Caesar study. And they were looking to see if ECMO actually helped in these cases. And they were very very desperate for volunteers or patient's to investigate. So I knew about this and I called them up and I said we have this lady, she's young, she's healthy. If she makes a recovery should be, ought to be fine afterwards. Um, would you take her for your study? And I think this was a no brainer, aren't it? There's no way they're going to say no. And they refused. And I, I was amazed. now, do you know why they might refuse? Anything? Tells you why this might be the case? Uh Well, uh yeah. Uh ventilating F I 02 and the flu. She has the distress flu. She has. Uh huh. Well, that's a good try. The reason was, was because the title volumes that were being used were classic tidal volumes that we use all the time and at that point in time, but they're not good title lines we know today, those are very harmful title volumes. And they were, their logic was that if you're using those title Lyme's for about a week, you will have destroyed her lungs. So there's no chance of her recovering on if we put it on the machine. If you won't recover on her own, under her own, uh on her own accord, you have destroyed her lungs. Basically, you've made it impossible for her to come back. So let's talk briefly about some of the big breakthroughs in management of ARDS and any sort of a ventilation in fact. So what do we know about ventilation? This is a famous painting that's in the Tate Gallery in London. Take modern, sorry, take uh Tate Britain. And it's a famous painting in 19th century of a doctor who's doing all he can for a very sick challenge. It's basically just watching her and that's not necessarily a bad thing in some cases because eventually, sorry, I beg your pardon? I think it's Edward Gen. Yeah. No, it's not. It's, um, fill this his name was anyway. Um, so when we ventilate you to everyone's surprise, we don't cure you of anything. We just by Tom, that's what we do. We buy time until you decide your body is signed, you're gonna get better or you're not, we can't cure you with a ventilator. But one thing we know for sure today, we definitely can make you a lot worse. So ventilators at best is just buying time at worse. If we do it badly, we can definitely kill you. And that's been one of the major breakthroughs. Sadly, in our management of intensive care, patient's being ventilated. So we knew we now know we've killed a lot of people because we did it back. So let's look at this. What happens if you over stretch a normal loan? This is a rabbit lung. Okay. And you can see as you start with control and you ventilate it five minutes, 20 minutes, you convert that normally pink looking lung. Remember the autopsy, you saw a second ago and look at it on the right. It looks like a piece of liver, just like the sick lung you saw earlier at the autopsy, but this is not a sick lung. This wasn't a sick lung. This is an over ventilated lung. The stretch you put too much ventilatory volume into that lung. And we know of today for sure that if you over stretch that lung, you will cause damage locally to the lung, but also outside the lung. So basically, we talked, we talked today about what we call protective lung ventilation. And we were definitely, we're not doing that. And that's why the Leicester team refused to take our patient because they knew that doing what we did for that eight days, um probably damaged her lung to the point where there was no point in trying to save her because it was not going to achieve anything. So today, that's one of the major things we've learned. So what happens if you overstretch your lung? Well, you just saw what happens locally. You saw that the lung looks like a piece of liver, but it's not just the lung. We know that you can cause what we call bio trauma. So as you, as you stretch the lung and damage the lung, you will get with high tidal volumes, an increased release of cytokines which spill over into the systemic circulation. And if you look at one of the side of kinds that we know it's called terminal crosis factor. You can see with low tidal volumes, you'll get that increase with high tidal volumes, get a much greater increase. So just by stretching the lung, you don't just damage lung, you damage the whole body. And so same thing with I L six, which is another well known uh cytokine. So this is quite compelling. And if you want to see what it looks like, you're a microscope, this is what non injurious ventilation looks like compared to imperious. So if you look at the lungs, um I'm not a pathologist, but on the right hand side, you can see there's a much greater influx of, of white cells and macrophages on the kidney. The same thing. So you can sing histological slices like lung, the kidney and even the intestine are being damaged by overstretching the lung. So this is a systemic problem. So, uh in the year 2000, there was a famous study called the Arts Net study. And this study was basically comparing, well, at the time was considered normal tidal volumes, at least that normal in terms of what we would ventilate someone with versus what they called low tidal volumes and low title lines. As you'll see in a second is a misnomer. These were not low tidal volumes, these were normal tidal volumes. So what you could see is that if you looked at people that survived and those that didn't if you used traditional high tidal volumes. Those are the people that survived if you used what they called lower, lower title volumes is the right word, but they weren't low. They were normal title volumes for the person's size. You got a survival benefit. And in fact, the mortality with higher title lines, they use 12 mils per kilo of predicted body weight. You'll see why we use predicted body weight in the second was 40%. If used, what would be a normal person's pretty estimated title line, given the estimated size of their lung, it reduced uh by a quarter. So 30% instead of 40% but was really interesting in this study. And it wasn't often cited, it was a really, really important part of this study was that if you were to look at oxygenation, so your, your Ventolin some with either high or lower lower title volumes, okay. And you look at the oxygen that's in their blood. You think that's what you want someone to hire oxygenation, right? But you'll see with the lower title volumes, that's what you got in terms of oxygenation, looking at the P F ratio, but it was much better with higher tidal volumes. Now, why is that important? Because if you have, if you're at the bedside and you have someone who has just been intubated for ventilation because they've got sick lungs and you have a pulse oximeter on, for example, and the nurses are in your, you know, younger doctors or even your older doctors are saying, oh yeah, let's get a big time of line and you see the oxygen saturation getting better with a big title line. You're gonna say, yeah, that's great. And you're going to keep doing that. And this is an example of where you've got to have faith in the sciences because yes, you will have a better oxygenation right in front of you on the screen, on the monitor. And you think that's wonderful, that physiological parameter is more closer to normal. But if you believe the science, that means that in about a week, that patient may well be dead because you're satisfying your false idea that a better oxygenation means the patient's more likely to survive. And in this case, this example, it's the opposite. So don't be fooled by picking the wrong physiological parameter. And this is a trap that a lot of people fell into because even after the study was published, and it was very widely uh cited a large percentage of, of hospitals throughout the world, in fact, still gave high tidal volumes because they just the temptation to look for a better oxygenation was so, so great. So be careful what you're, you know what you think you're aiming for. Now, when I said what we started to do, we're using, we're using initially really large kind of volumes. So say 500 mils now the tidal volume the amount of gas you put into someone on each breath is going to be a percentage of your total lung volume. So, if you have big lungs, you're going to need more of a breath, then if you have smaller lungs. So how do you determine, how do you estimate someone's lung size? Now, we're not going to do radioisotope scans and everybody. So the best way you can do it is to estimate it. And how do you estimate it? You estimate it based on your predicted body weight. Now, everyone would assume predicted body weight means your weight or part of your weight, right? Well, has nothing to do with your weight. That's the trap. It's got to do with your gender, your sex and your height. Okay. So let's look at two uh, scans here and the, and the green, the green rectangles are the size of someone's lung that's a woman and those are the size of her lungs and her lung volume is 3.2 liters. This is another woman, same height, but obviously a lot thinner, a lot less heavy, less obese and those are the size of her lungs and her lungs are 3.3 liters. So you can see they have the same height, the same sex, but their weight's, their actual weights are a lot different. And this is one of the traps. You get someone who's in a bed and they look like they're, you know, say I don't know, 200 kg, you're thinking they're going to get really, really big volumes, know has nothing to do with your weight. That's why you want to measure their height when they come in and you wanna know their sexes and their formula you can use to estimate with someone's lung volume is. So those, those volumes you see on the bottom, the lung volumes, 3.2 and 3.3 liters, we'll give you say, I'll take 10% of that, for example. So 3.2 liters give per breath, say 320 mils instead of 500 mils. Okay. Now, those are normal sized lungs. And so we're going from high volumes, abnormally high volumes to marrying the breath to a normal lung, how much you give to a normal person breathing per breath. But that might not be a good, a good idea. So we're going from high to normal and now we're going to go to the reality of the rds because when you have a R D s, um, on the left hand side, you can see that's the size of a normal lung. Okay. So you'd say you'd say the person was one of the patient's of one of the scans you saw a minute ago, that person would say have 3.2 liters. So I'd give say 320 miles per breath, I will overstretch your lungs and hence Dammika. But in fact, if you look at someone who has a R D S. A lot of that lung tissue is turned off. It shut down its full of inflammatory fluid or is crushed by the weight of the edema of the fluid above it. So you're going to lose a lot of that normal sized lung and you're gonna get what we call baby lung. So that volume is 3.6 liters and this one's 800 liters, you can see that a lot of the normal lung is, is completely collapsed. So we've gone from ventilating you with really big volumes which were totally abnormal. And that was probably killing a lot of people to now tailoring your volume to a normal sized lung, which is better but not perfect because we're not tailoring it to the size of a sick baby lung, which is a lot smaller than a normal lung. So, how do you estimate the size of a baby lung? Well, one of the things you can do is measure, we call driving pressure. And I don't want to go too much into detail of this, but it's a very quick and easy way of determining on a ventilator whether you have scaled the size of your breath to the size of not a normal lung. That's, that's less bad than a very high volume of gas, but to a baby lung. And it's a pretty good proxy for lung size. And so here's a scan of someone who's got uh a lung that's not too bad. And you can see that they have a normal, relatively normal sized lung and the driving pressure is about eight, that's, that's good. And someone who's got a baby lung that's, you can see there that there's a lot of lung tissue that's been lost because of the full of a dumb, a fluid inflammatory fluid and, and collapse. And here you're basically going to use that If you use the same volume into that appropriate volume into that normal lung on the left, use that same volume into a much smaller reduced size lung. You're gonna overstretch it and you're gonna create a lot more pressure and that's going to increase your driving pressure. And you can see that's 19 and that's not good because overstretching a normal small lung will still cause damage. So, we've gone from when we eventually, we have now realized that going from a very big tidal volume, which may improve oxygenation but will kill you to tailoring it to a normal sized lung which we estimate looking at your sex and your height, not your weight. And then going even further, we look at the driving pressure, how much pressure is generated. So we're trying to basically scale the breath to the size of that small, abnormally small loan. So we've gone from very high to normal to best. Now, the other thing about ventilation, you want to avoid what they call recruitment and deer recruit. And what does that mean? We use? Very simple analogies here. So you have something called the pressure volume curve. And this is, again, this is some basic physiology you can see on the X axis, you have the pressure, you have to uh do you have to uh apply to blow up the alveolus? It's been like a balloon if you like. It's not exactly that, but it's good enough analogy. And on your y axis you have the volume. So imagine you have a brand new balloon brand news, just come out of the packet. You're gonna celebrate someone's birthday and the balloons completely collapsed and you have to blow into it. What you have to do is blow really hard and the balloon doesn't boot. But budget all you're really using a lot of pressure and nothing seems to happen and then suddenly it seems to, with a lot of pressure applied, it suddenly gets easier. And so by what we call recruiting or adding positive and experimented pressure, that's peep, you're trying to pop the balloon over it. Then when you get into that steep part of that blue line, that, that's steep, part of that curve. You're in the sort of sweet spot and you're going to be ventilating going from just like the balloon you blow. Now you have your balloon pops open and you just take a little bit of pressure to make it bigger and let a bit of gas and get smaller, bigger and smaller. It doesn't take a lot of pressure. So it took a lot to get it open. But once it's open it's a lot easier to blow into. And then you keep blowing. If you were to keep on blowing, then it's going to get bigger and stretch and it's going to distend until it pops. And so that's so you've got on the left hand side, it's relatively the blue lines, relatively flat. That's what we call low compliance. So you've got a lot of pressure, very little change in volume. On the extreme right hand side, you've got a lot of pressure and very little change in volume until it pops. And between the two is where you want to be. So a little bit of pressure and a big change in volume, okay. That's the safest place to be. Now, the problem with. So you want to recruit the lung, it's like blowing into that balloon. So it just pops open. But what you don't want happening is letting all the gas out. So it becomes just like the brand new balloon out of the packet. You have to use a lot of pressure again. Do you want to keep it in that middle zone? And the way we do that is first we recruit by popping on the balloon open and then we use what we call positive and expiry pressure. So that means in steady letting all the gas out, keep a little bit of pressure so all the gas can't get out. So you're keeping yourself going all the way back down to the base of that blue line again. So you're keeping in the middle and that's called peep, it's called recruitment to pop it open and peep is to keep it from going all the way down uh to completely deflating again because that damages the loan. This is what we're doing. Okay. This is a video that shows you exactly we're trying to do. So you're recruiting alone, you can see the alveolar popping open, letting all the gas out, which is not good, keeping them alveolar popping open again. You see they're popping open if you ever do um lung surgery and they collapse a lung during the operation and they ask you to, to blow the lung up. This is exactly what you say. It's very dramatic. You can see the, oh, you're just like little balloons popping open. So that's, that's recruiting a lung and you don't want the guest to roll out. So you're putting a bit of people. Now, the other thing you can do and this has been quite spectacular. It's quite amusing because it seemed such a simple technique and it was used a lot during the COVID um pandemic and that's something called prone position. And in fact, if you look at, um, if you look at survival, um someone who's supine so on their back and they have acute respiratory distress syndrome or someone who's been put in a prone position, you'll see survival is much greater for those that are prone. And this has been interesting because prone ing has a survival advantage. And going back to what I said earlier about oxygenation, many studies show that the oxygen oxygenation doesn't have to get better for you to have that survival advantage. So pro ning itself seems to help and this was done a lot of COVID and there was even something called awake prone in people that were not ventilated, didn't have an endotracheal tube in their lungs. They were being ventilated with machine. They just told the person, please lie on your tummy and they found that they seem to uh many of them seem to get better, so prone ing seems to work. And why does it work? Well, it's a little bit complex. I haven't got time today to go into the details of how it works. It's quite interesting entry. But if you want a simple explanation, there's someone who's supine and you can see that their, their heart is slightly to the left and there's a lot of that sort of whiteish tissue underneath that's collapsed lung. And if you've turned them prone, now the heart is against the sternum and all that white tissue has become dark. So it's basically opening up bits of lung that we're not open before. That's a simplistic way of looking at it. But that it works to keep it at that. So, here's a clinical case for you. 21 year old female, she's an acute respect to distress following flu like symptoms. These are all true stories, by the way, she needs intubation. And as soon as she's intubated, her oxygen saturations dropped from 87 which is low 2 78 on 100% oxygen. This is scary. This is a 21 year old female and you wouldn't expect your oxygen to go down with 100% oxygen, but it was going down and we're thinking something terrible is happening here. So we tried to recruit her. So we basically tried to do what you saw a second ago with the balloon. We tried to use a bit of pressure to pop open those balloons and hopefully get more gas going into alveoli to get some more oxygen into her blood. And we used a peep of 20 and the auction saturations improved to 94%. So that's pretty good, isn't it? Everybody happy with that? I don't know whether 94 is. I think that's very good. Yeah, I mean, everyone thinks that's good. Yeah, that's the normal thing to say. And I think that's absolutely a very appropriate answer. Very normally appropriate expected answer. Okay. Let's think about this. What is our goal? This is what I'm trying to focus on in this talk. What is our goal? So this is her P F ratio which is, as I told you before, it's a measure of how effective your lungs are oxygenating. Taking into account the arterial oxygen saturation versus the amount of oxygen you're giving in the F I 02. And that's not good. So that's what her lung looked like. It was collapsed. Okay. So we use peep and we're trying to increase the pressure. So her lung will pop open and there'll be more Alvey oil open to uh accept oxygen if you like and hence improve the oxygenation. So we did that and guess what the PFA she got better and now her lung looks like uh exactly as you saw in that video a second ago. That's great. But is that really what we're left? We're after, well, our ultimate goal is to have a survivor, right? And if you look at something else we didn't bother talking about and that's something you really, really, really have to look at. That's the cardiac output because let's go right back to the beginning of this talk. We said the goal is oxygen delivery and oxygen delivery depends on three factors, cardiac output, hemoglobin, which hasn't changed in this case and saturation. We improved our saturation. But what do we do? The cardiac output in this case, we dropped the cardiac output. And so what happened to oxygen delivery? It dropped. So, yes, we have a much improved oxygen saturation and the nurses and the doctors are clapping their hands and very happy because on the screen right in front of you, you have a pulse oximeter with the results showing the oxygen saturation went from 78% to 94%. And that's the thing you're seeing right in front of you. And you're thinking, wow, wonderful. But we didn't measure is the cardiac output and that dropped and that we calculated the oxygen delivery drop. So we haven't one here. This is not the way to go. Now. It doesn't always happen, but it may happen. And the reason is as you increase the pressure to open up those lungs, you're squeezing the heart and you're reducing venous return. And we talked about that in one of our previous lectures. But by, by doing a valsalva maneuver, for example, if you do it long enough, you'll pass out because you're squeezing your heart, your, if you look at your neck veins, when you do that in the mirror, you'll see the veins stand out, that's stopping blood from getting back to your right heart. So you're dropping your cardiac output and of the two factors cardiac out. But in this case, is going to be more important than saturation. So, so yes, you look like you're getting a better oxygen. You are getting a better oxygen saturation, but that's not the ultimate goal. The ultimate goal is delivery of oxygen, the D 02. And in this example, we weren't paying attention and the auction delivery was going down because we were reducing the cardiac output with the extra pressure we're putting in the thorax to improve the saturation. So don't forget what your goal is. That's the whole point of this. So to recap, we talked about the normal and abnormal ventilation profusion ratios and how the sicker you are, the more you are, um the more you are likely to have zones of lungs that are either dead space or shunt. So you're further away from the normal. So it's a spectrum if you like and spectrum is larger, we saw what uh ARDS lung looks like compared to a normal lung. We remember we talked about ventilation, it doesn't cure you, it just buys time and we can definitely make you a lot worse. We can't make you better with the ventilator, but we can definitely make you worse. We talked about the important study showing that if you go from a high tidal volume, abnormally high tidal volume and go to a normal title volume for normal person's lungs, um, you'll improve mortality even if it means that you don't improve oxygenation as much. So, be careful what you wish for. That was important point that in fact, the ideal would be not to a normal lung volume but to an abnormally small lung volume. The baby lung that's associated with ARDS. So you want to tailor that to the, you tell your, the breath you put into somebody to their uh small law, you might want to tailor it using driving pressure as a, as a way of estimating the size of the baby lump. You want to avoid the balloon that collapses or over distends. So you don't want it to be too small because it collapses and it takes a lot of pressure to open it up, that damages the alveolus. On the other hand, you don't want to over distend it either because that damages the alveolus as well and has effects on the Kartik output in the right heart. So you want to be in the middle of the zone, you saw that steep it and you want to make sure that your, you get your goals correct. Don't forget the ultimate goal isn't saturation, it's oxygen delivery and don't forget at the end of the day, as we said, we are in the oxygen delivery business, not in the oxygenation business. Okay. And those three factors are what you're waiting for and that's it. So if you have any questions, I'll be delighted to answer them for you or try to at least. So, in a simple words, uh at a while ARDS increasing a tidal volume for the sake of oxygen increasing the saturation is a full size idea. It was a false idea. Full side. Yeah, fool's idea like we're trying to, as you said, go by the book, increase the saturation. But it's true because we know today thanks to several studies, but the most famous study was this famous are genet study that if you were to take a normal uh normal size loan, not, not a sick lung, a normal size loan, forgetting Guardia's. If I take your lungs and for a period of time, I use big tidal volumes and I were to look at the um damage done to your lungs, I can damage them. That's the point. And this is the point. If you use big tidal volumes bigger than the normal sized lung is requiring, you will damage lung and you will cause cytokine release, which means you will not just damage your lungs, but as you saw, you will damage your kidneys, you'll damage your gut, you'll damage a lot of things. So we know today that a ventilator that's giving a breath that's too big compared to the normal size of your lung is going to damage your, your lung and your body. On the other hand, if you have the ARDS, your normal lungs are smaller, they have what's called baby lung because of the Dema and all the, the, you know, the, the L V or that are flooded with the d, uh, inflammatory fluid. So you're normal sized lung becomes even smaller. So you want to marry the ventilation, the title volume of the gas you're putting in per breath to the size of that lung don't want to over basically stretching. You don't want to stretch them. That's what we're saying. Anything else? Yeah. Hi doctor. Could you please um, expend the, the partial oxygen and F I 02 again, I'm not sure I get that concept. Okay. So if I were to look, if I take a sample of your arterial blood from your radio artery and it's safe, for example, um your lungs are normal. Okay. And the, the oxygen uh the P 02 in your arterial blood is let's say arguments say let's take round numbers, let's say it's 80. Okay. 80. Kill a Pascal's that's close to normal and your breathing um 100% oxygen. So that's F I 02 is one that would be 80. That's your killer Pascal's of oxygen divided by one. So your P F ratio is one. It's sorry it's 80 80 80 divide by one. Great. Yeah. Yeah. Okay. Now if I turn the uh F I 02, if I give you not 100% oxygen, I give you 50% oxygen. Theoretically, your P 02 should drop to about 40. That's half because I'm giving you half the oxygen and because the auction is no longer 100% not 1.0, it's 0.5 50% 500.5. Okay. It's not taking percent. I didn't take the decimal points 0.5 40 divided by 400.5 is 80. So the ratio theoretically doesn't change. Now let's say you have sick lungs and instead of having giving you 100% oxygen instead of having uh 80 killer Pascal's in your arterial blood sample, you have 40 killer pascal's. That means 40 divided by one. That's 100% oxygen I'm giving you, that's 40. Your, your P F ratio is 40. Now, it was 80 when it was normal and now that you have sick lungs, it's 40 that's not good. Now, if I give you 50% of oxygen, that's an F I 2.5 40 you're 40 can go down to 20 because you're giving half the amount of oxygen. So 20 divided by 200.5 is 40. So the ratio doesn't change. That's the whole point. But I think, I think what's important is, is just that you understand that there is a term called the P F ratio. And it's a way of um, crudely assessing how effective your lungs are transferring oxygen with differing F I 02 because people give, you know, give 20% oxygen or 30 or 40 or 50 or 100. And I guess lets you adjust for that otherwise would be very, very, very complicated. Try and figure out every time you change the F I 02. Anything else? I have a question. Uh If we have our patient is a racing athlete as they know they have bigger long capacity. Yes. So should we increase the title volume for this person or not? That's a really, that's a very, very good question. Um You know, I honestly, well, first of all. Don't forget if you have a, let's say you have an athlete and they have, let's say the big lungs, as you say, but they have ARDS, they're normally bigger sized lung because they're athletic is going to be smaller because of the illness, the disease. So, I don't know what their size of the lung is. You could do very fancy, you know, isotopes studies, but we don't do that. What, what you'd have to do is try and do a sort of, um, uh, how do I put it? You try and estimate what they are by looking at the driving pressure. What basically saying is that if I knew what your normal sized lungs are and I put in a normal volume of gas into your lungs, the pressure required would be, I don't know, let's say X 10, say okay or eight. If I suddenly make your lung half of the size and I try and put the same title volume in, you're gonna need double the pressure. So by using that driving pressure, I'm kind of indirectly estimating the size of your lungs, but I understand your point and it's a good one. I can't really, I don't know the answer to, you know, how much volume you put into an athlete who has big lungs. But what's really important. And this is the key thing is don't fall into the trap to think someone who's really, really obese needs big tidal volumes they don't. It's got nothing to do with your, it's an estimate of how big your lungs are normally and it's got nothing to do with your weight. We call it ideal or predicted body weight, but it has nothing to do with your weight. It's your sex and your height. That's it. Thanks. Okay. Anybody else? Okay. Well, I wish you a happy good afternoon.