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Okay. Uh, I can't see why. That would be, um, mute is, um Damn, damn, damn. Yes. Beg your pardon? Um, if you like, I can start. Welcome, everyone. Uh, we're welcoming Doctor Vogel today. Who's going to speak to a throat? We've got a few technical issues, but hopefully they'll be ironed out. Um, that's better. I hope you can all hear me. You can. You can hear us now. Okay, That's good. Um, so we're going to Okay, then. That's good news. That means you'll be able to hear everything, but we're going to put questions and comments in the chat. Um, and we're going to be talking today about anesthetics. Um, and the title of the technical hitches and just the title of the lecture is often delivery a physiological approach. Um, and I'm gonna put some, uh, just some housekeeping that you need to be aware of, Uh, for this lecture is that we're going to put everyone should be put on mute, um, and try not to control the screen that needs to be controlled only by Dr Vogel. Um, uh, you're going to be on mute. So if you've got any questions or comments please put them in the chat. My name is Dr Sharon Raymond and the director of the Crisis Rescue Foundation and of this online medical school. Um, and I will be putting a feedback a link for feedback towards the end of the lecture, which we really urge you to fill in. We really are dependent on the feedback to continue. And that will be the last few minutes of the lecture. I'll put that link in, um and just really want to wish you a warm welcome. Please put your first name, your med school and what country you're in currently into the chat. Uh, and also any questions and you'll receive your certificates. If you've registered on event, right, you'll receive your certificate. Uh, once we have all the feedback. So without further ado, I'll pass on to Doctor Vogel. Um, and I think I've got Osama Kerry move, Appears to be taking over the screen. So if you just try and, uh, not control the screen somehow, if that's okay, uh, so that we can see a doctor. Vogel. Doctor Google. I would have liked to make you, uh, doctor, because I'd like to make your co host, but I've got a few technical issues, so I'll be working on that in the background. Okay, fine. I'll start. I'll get started on, Okay? Yes, please. Uh, it says I can't hear my screen because you haven't disabled participant screen caring. Uh, we can see you now. I'm trying to Yeah. Every time I try to share my screen, it says host, disabled participant, screen sharing. Yeah, but we can see, you know, I can see you at the center of the screen. So I think if you get started, and if there's any issues, we'll keep an eye on the chat. Yeah, I'm sorry. I'm not making myself clear when I try and scare the screen, which is what I've always done to be able to show the slides. It says the host, I believe that's you has disabled participant screen sharing. Okay, let me see if I can do something about that. And maybe is there any way that you can kick off without displaying these slides at the moment or not? Okay, I'll get I'll just give a preamble. Okay. Well, greetings to everybody. Um, I met many of you. I assume back in the spring. And so today I want to start a a series of lecture. Um, the majority of these will be, uh, first of all, I'm, uh, recently retired consultant, uh, in intensive care, medicine and anesthetics. And what I have always found is that we tend to learn physiological principles in medical school, as if something we have to get through to be able to pass our exams and then do what we really want to do is treat patients. And the problem with that is that when you actually get to treat patients, you really have to apply these physiological principles. They're important to make your decisions more, um, more accurate, your therapies better. And actually, they're quite fun. So what I'm trying to trying to illustrate today in the next few lectures is how you can apply. Um, this physiology that you learn to the bedside. So it's not just something for exams, it's not pure academia. You see, I can I still can't get my slides up. Um, So while we're waiting to get my slides up, Um, uh, what we're going to talk about today is a basic, um, framework on how you can actually, uh treat a patient using these physiological principles. And the most important thing for you is that quite often, uh, it's quite scary when you get into a chaotic or an unfamiliar situation and you're not sure what to do. And it's very easy to panic. And by applying the simplest, um, principles, you can get yourself out of trouble and give yourself some confidence. And we really saw this during the first wave of the coated epidemic that we went through here in the UK in London. And the point was that a lot of young doctors and not so young doctors were very scared because we weren't we weren't sure what to do. And a lot of the doctors were alone in a room because of because of the lack of PPE gear and the risk of it passing on the infection. So you're isolated. You've got a very sick patient. You're not sure what to do. And by many of these younger doctor's referring to this framework I'll talk to you about today. Hopefully, um, they told me afterwards, they felt a lot more confident. So this is what I'm gonna try and transmit to you today. Uh, Okay, We got it. Nope. Uh, okay. I think that's it. Okay, so here we go. So imagine yourself. You're now in a call down to the accent emergency department. Uh, I used to work in a trauma center, the second biggest trauma center in the United States. And believe me, this sort of seen was very, very common. So total chaos. People are screaming from blood tubes. Uh, drains. And what you want to do is put your thinking cap on, step back. Don't get your hands dirty and be the person who thinks What are you? What are you trying to achieve here? So what? So what are my priorities? So we're going to try and introduce today a physiological approach to the very sick page, and this is going to help you hopefully simplify a framework that gives you the confidence on how to think things through. So what is the outline of today's talk? We're going to talk about how you get out of trouble using very basic principles. That's the key thing. Keep it simple and basic. And if you do that everything else will fall into place. We're going to briefly talk about some basic cellular physiology. We're going to talk about some very basics of oxygen delivery, which is the key to this talk. We're going to talk about the components of oxygen delivery, what I call the magnificent 33 factors. And there's also one last sort of reserve. You can use the last reserve last ditch, and that is oxygen extraction. And that's useful. And they're gonna very briefly just mentioned some other causes of this Oxy because not everything is due to a lack of oxygen delivery. But that's the only thing we can deal with as far as we know today. So getting out of trouble using basic principles. So we're here to go back to our chaotic scene, and this is a 38 year old male who has been hit by electric adjustable. But BP is low. Heart is fast, cold peripherally, so he's in shock. His respiratory is fast and sats are low at 90%. So where do you start with this guy? What are your priorities going to be? Well, you're going to do what everyone is taught when they do First aid or a L s acute life support, and that is your A b CS. So you're going to be saying abdominal A B CS. But also, let me just get rid of this. Uh, yeah. Okay, so you've done your a b CS, and you're now focusing on the one thing you can actually do to improve this person. And that's oxygen delivery. And what does that consist of? It consist of your cardiac output times your hemoglobin times your oxygen saturation. It's very simple. So you've you've kept your airway breathing in circulation. That's fine. But now you got to take the next step and that's you want to improve and optimal delivery. Cardiac. Put him a little bit of oxygen saturation. So let's look at these and see how you can actually break these down into their component parts and sub component parts. And in that very chaotic situation, you can actually forget all the details and simplify to keep the person alive, and then you can work out the details later. So if you look at each of these components individually, you've got cardiac output, which is composed of pre loads fulfilling, um, failure. So someone say cardio cardiogenic shock. Your heart muscle is dead. Uh, after load the aortic stenosis. Very, very high. Uh, sympathetic output, heart rate and rhythm anemia in case of hemoglobin. Hgb. Well, you haven't got enough of hemoglobin. You don't have the right kind of hemoglobin. Someone with thalassemia signal cell disease. Hemolysis The hemoglobin is not in its normal envelope of the red cell, so it can cause damage by being outside of the cell. And if there's too much hemoglobin, you get too viscous, sort of blood doesn't flow, and then oxygen saturation Well, you don't have enough. You're on the top of Mount Everest without an oxygen mask. You're hyperventilating. So someone, for example, who has obstructive sleep apnea or in the recovery room? The opiates that you received for your operation are starting to, uh, prevent you from responding to to You're hypoxic condition and most commonly is ventilation, profusion, abnormalities. But when you look at these pretty obvious sub components of the three factors, you can break them down into a sub sub components. And I wont read the multi here. But you can see almost all the medicines in this. So if you're in a really uncertain, confused situation, you're getting a bit panicky. Don't worry about the details. Just go right to the top of this pyramid and just think of Kartika hemoglobin, oxygen saturation. If they're okay, you're okay. And the details are underlined here and all that sort of sub subheadings you can work out later. So let's quickly talk about some basic cellular physiology. So what are we about? Were man versus machine. So it's all about energy. Everything that we're talking about today and for life is energy. So in a car you have a mechanical engineer. You provide fossil fuels, you give oxygen and you get an explosion. You get combustion. A man needs biochemical energy. He needs organic fuels. He needs oxygen again and again. There's in the cell. There's combustion on the motor of a car. It's near cell. And you need that, too, right? Work to provide heat and there'll be waste products. And it's quite it's really quite simple and very similar in many ways. And if you ever seen anybody who is in bio energetic failure, Well, um, you just go into the intensive care unit and look at someone in septic shock. Nothing works. They're swollen, their cells can't. They're vessels. Can't keep fluid in the right compartment. Their hearts are being adequately there. Oxygenation is not good because their lungs can't transfer oxygen to the to the blood. Their muscles and nerves aren't working their brain. They're delirious. Um, etcetera, etcetera. Kidneys are failing. Liver is failing. It's just nothing works because you're lacking in energy. So let's look how this works. So what I say is to create energy and why you need energy for membrane transport. So keeping the the electrolytes and the right compartment, um, the protein for protein synthesis, muscle contraction. And so here you can see a cell. It's membrane in the mitochondria. Mitochondria is where it's a sort of is the power house where you create energy mostly energy through oxidative phosphor relations. And again, you remember this from from your well, not even medical school, probably from high school. So we need a fuel. In this case, I'm just going to mention glucose, and it produces porotic acid and lactate. And just as, uh, we're going to talk about lactated the further electric. There's a lot of misunderstanding about lactated. But lactate, Um, probably actually, creating lactate is a very inefficient way of producing energy. in the form of a T. P, by the way, but it's very, very quick. It's about 100 times faster than oxidated than oxidated phosphorylation. So for a given period of time, you'll prove this is much ATP. Real active because a lot faster but efficient than you were going through the mitochondrial cell process, which is oxidated phosphorylation. So once we get acetylcholine into the mitochondria, which is the normal producing energy, it will produce 36 80 p s. You'll remember this probably and then produces waste in the form of CO2 water. When you're at rest, you need about 150 miles of aspirin per minute to basically keep the body functioning Normally. If you're not at risk, you need more, obviously. So how does this work? Let's put some numbers on this so cardiac output times. Hemoglobin times saturation. So three simple factors that determine auction delivery So five liters of cardiac output that's the normal at rest. Hemoglobin, A 150 g per liter, and there's a coefficient that determines the oxygen binding capacity of hemoglobin. It's about 1.34. It's a fixed coefficient, and then there's the saturation of oxygen if you're 100% saturated. So what do you get if you add these numbers together So 1 50 times 1.34 times 100% saturated. So you're fully saturated and you have a normal quantity of hemoglobin. You will get five liters a minute cardiac output and 200 mils of oxygen per liter. That means that if you have a normally a normal hemoglobin level in a liter of blood and the blood is fully saturated with oxygen, that blood that static, it's sitting on the table. Leader of it will carry 200 mL of oxygen in that leader. And because you're going to be circulating five liters a minute, that means you're going to be circulating five times 201 liter of oxygen per minute. So we said that at rest you need 250 miles. But we're delivering one leader, so four times as much as you need, so we have a lot of reserve. So let's talk about the individual factors of the magnificent magnificent three. Those are your three factors again. So this is important to remember because we often think in terms of silos. We think of one factor of the cardiac output slow. He's in shock where he's anemic or he's hypoxic. We want to think in the way these three factors are interconnected. If one variables have in itself, that is not necessarily very dangerous. Of course you want to know what the cause is. That's really important. But if one variable itself is not, you've got half of your delivery of oxygen, your maximum delivery of oxygen a minute, and you can probably live with that. So you're flying an airplane and 11 of the three engines is out. You probably keep going to your destination if you If you have two variables now, your delivery is now one quarter one half times one half and three variables that are have you're getting 1 61 8th Sorry. 1/8 1 half times, one half times one half the delivery of oxygen so you can see that is not going to be enough to keep you alive. So that's why you want to think in terms of how do these three variables interact? You don't want to just think of, you know, looking at one side or one factor. You want to look at all the three together and to determine is my auction delivery going to be adequate? So here's a clinical case. Um, and this is I think it's a good illustration of what we're talking about here. So you've just had a lady who's 69 years old. He's had a total hip replacement in the operating room that day and because they gave her fluid and a little bit of blood. But they're replacing the volume and you go to visit her in the evening. And because of that volume loss and mainly the volume replacement, you're deluding a lot of the hemoglobin. He's gone from a normal hemoglobin before the operation to 7.5. So, um, we're 75 so I'm using, um, Dexa liters, as opposed to leaders the old fashioned. But he looks well. Her BP is normal and she's smiling at you and she's about to eat your dinner. You look at her, she's not. She's not sweaty, not diaphoretic. She's pink, and she's very pleasant. Talk to you. So you're thinking there's no need for transfusion. We'll just wait. Okay, that's great. You go home to have your dinner and you're thinking there's no there's no there's no urgency. There's no just hear. Everything is fine. This is a very classic case now, not that night. When you're in bed, he's given nonsteroidal anti inflammatories for POSTOP pain. The next morning you come and do a war brown and you see her. She's confused, he's breathless and he's passing moderate quantities of black tarry stool. That smells terrible. And that's Molina. So the question is, what are your main concerns? If you want to try and answer the question I was going to ask you is Are you worried about her? Um, bleeding? Are you worried about her oxygenation? Are you worried about her being anemic? What are your main concerns? Does anybody want to try and take a guess? Yes, you're going to see the response. Is Dr Vogel in the chat? Because it might be too much because we've got over 100 people, So it'll be a bit much for people to, um, you know, but the majority of saying bleeding, stomach bleeding. That's the response. We've got quite a few responses saying bleeding. Okay, well, those are all correct answers, but they're not really right. The reason I say that is because what are the concerns? The real concerns. I'm just going to stop your doctor, Vogel. We've got one. We've got one student saying anemia is a concern. Anemia. Okay, well, I think you're You're right, but you're not complete. So what I'm trying to get you to do is to think in terms of not in silos. It's the in terms of how the three factors inter. So this lady last night, her hemoglobin was low. She was anemic, but she was fine. Probably because her cardiac output had increased to compensate for her anemia. So okay, you're not worried about her to get this all the time On awards, patients will be seen with low hemoglobins, and nobody gets excited excited about that if they're looking fine. But what happened to her overnight? He's lost volume. So now. So yesterday here her hemoglobin was low, but her cardiocap it was adequate, and he was probably delivering. She's lost one of the three engines. Her He's delivering about 500 mils of oxygen a minute. So it's oxygen delivery we're talking about. I don't think in terms of the specific physiological parameters. It's the the conglomeration of the three together Oxygen delivery. Okay, now, what happened was that overnight he went from a 7.5 hemoglobin, but her cardiac output has dropped. So now if you connect the dots, the three factors together, they're saturation was probably okay, then. Now he's delivering 250 minutes and she's really, really, um, in a very dangerous position. So the first thing I would be doing is giving her some volume because you can do that rapidly. And And then, of course, I'd be asking for blood and I'll be asking for an endoscopy is to see where the cause of the bleeding is, which is probably the stomach. So the point I'm trying to make with this illustration this clinical case is you want to think about in terms of individual silos, just cardiac output, or is it just saturation of the hemoglobin? I want to connect the three together, and you realize that you've got a medical emergency on your hands because this woman will not tolerate that low that low up delivery for very long. You want to quickly start improving the cardiac output and eventually hemoglo so thinking Silos. See how these I always think of the three together. So let's look at the factors one at a time. So cardiac output. Normally you have the famous starling curve. You have feeling pressure on the Xanax and the out cardiac outflow out of the heart on the Y axis. And normally you see that curve is kind of steep, and then it gets flat. Well, everybody who is listening to this talk, if you're healthy, ought to be where that red dot is. So that means that if I fill you cardiac up, just stress future lecture. That's without being stimulated. So you you can improve your cardiac output by about 2 2.5 times, just from filling. If, after having adequately filled the heart, you still find that the cardiac output and the delivery is not optimized is not adequate. Adequate? The word I want to use. Then you may stimulate the heart with various drugs. Or you may stimulate yourself your sympathetic nervous system. And so you alter your starling curve. It's called the starting curve, where your cardiac function curb same thing. And so now, for the same feeling you get a lot more cardiac album. Okay, so feeling first and then you can stimulate the heart. Either you do that giving a cardiac stimulant benign, a trump, or you do that yourself. So, um, when you go for a run, you suddenly get an outpouring of sympathetic nerves. So if you normally are a non super athlete, that's And as you get older, your cardiac output will drop your maximum cardiocap. It'll drop. Um, but if you're young and relatively healthy, um, you can normally increase your cardiac output by about five times. So from, say, five liters a minute, go up to 25 liters a minute or so. An athlete say a marathon runner can go up to say 30 35 liters a day. So why is cardiac output so important? And some would say, maybe even the most important factor. Now you need the other two factors. Hemoglobin, oxygen saturation. But cardiac output may be the most important. And why would I say that? There's a man I'm a climber? I used to be anyway, when I was younger and I've been all over the world, climb Himalayas included. Why is it so important? Because when you climb, you are in an environment that's low in oxygen, so you have to acclimatize and to acclimatize. There's several things that happened, but one of the most important is you produce more hemoglobin to carry more oxygen. And so what happens is that hemoglobin takes a while. It takes about five days to a week at altitude to increase. So what happens is it's unlike hemoglobin increasing to compensate. Cardiac output is fast. So if you get on a bike because I used to. When I used to go to work and I cycle to work and look behind me and there's a bus behind me, I'm pedaling like mad. My cardiac output, which is five liters a minute. Arrest isn't going to take, you know, a week to suddenly increase to 25 liters a minute. It's going to go up immediately, so cardiac output, unlike hemoglobin, for example, is very fast. Secondly, unlike oxygen saturation, once your cardiac output sorry, once your oxygen saturation is 100%. Given the flat part of your actions association curve, you can't really increase it, uh, measurably much so it's basically unlike oxygen saturation. It's linear in the clinical range. So going from, say, five years a minute to $25 a minute, that's pretty linear. So unlike oxygen saturation it's not. You don't reach a plateau until you get to the very high levels, so it's rapid and linear. So let's look at this. If you take someone who's hematocrit is normal and you progressively dilute them so your hematocrit drops, so your normal polemic. But your hematocrit is dropping, so you're becoming progressively more anemic. What happens in terms of your cardiac output? Well, there's your normal hematocrit, let's say and as your chemo dilute so you're basically normal polemic again, but you're becoming more and more progressively more anemic. You'll see that your hematocrit drops, but your cardiac output goes up and it goes up a lot more than Humana hematocrit drops. So, in terms of its impact on oxygen delivery up to a point by reducing your hematocrit, you'll increase your cardiac output. And the reason is you're getting less viscosity. And if you remember, what size equation about flow for a given pressure difference of viscosity is the lower the viscosity, the greater the flow. Plus, there's something else that a lot of people don't appreciate is blood is a non Newtonian liquid. What does that mean? Well, if you've ever had gone for a meal and you think a bottle of catch up, which you all have done, catch up and you turn it upside down to put on your french fries and nothing comes out, nothing comes out. Suddenly, it all pours out. It's because catch up, like blood or non drip paint, is a non Newtonian liquid. That means the faster it flows, the lower viscosity becomes so the faster it goes, the faster it goes. Okay, so those are the reasons that your cardiac output and your flow through the vessels increases dramatically when your hematocrit drops. But again, up to a point. No chemo globe. So as we said you, when you get to altitude, you can produce more hemoglobin to compensate or inadequate same thing to compensate for the lack of oxygen in the air, your breathing. And if you look at oxygen delivery on the Y axis, you see as your humanity improves, you're going to get your degree of oxygen, but you get to a point where you don't want to keep improving your hematocrit. Because what's then gonna happen is your oxygen delivery is gonna start dropping. Why? Because your blood getting too thick. Have you ever seen someone with Polycythemia Rubra? Vera? Um, that's a problem if you go to altitude again and again, that's something I used to be very involved in. Um, if you're sitting in a tent because there's a storm high up and you can't really move for a couple of days, one of the risks is getting a deep vein thrombosis and pulmonary emboli because your your legs your your blood is very thick. Your D you're always dehydrated, so it's even thicker. And you're not moving your legs, You're not pumping the blood around, and so you're gonna very let me very susceptible to getting blood clots. So, yes, you want more hematocrit to compensate up to a point. But then it gets becomes, uh it reduces your oxygen delivery if you get too too much, uh, an oxygen saturation. So you all know the Oxford in Hemoglobin association curve. You have initially, um, a low pickup of oxygen because hemoglobin is a bit reluctant to pick it up. But then once you start picking up you get something called cooperative itchy, and suddenly, as you increase your peer to you get a steep rise in the oxygen saturation. So, uh, hemoglobin is absolutely picking up oxygen, and then you get to the top one's fully saturated for hemoglobin, a one for oxygen molecules to one hemoglobin molecule and then starts to flatten out. But you can modify that curve to either release more hemoglobin. So, for example, if your tissue is hot temperature all impacted low. PH uh 23 p d p. G. That will release hemoglobin. So if you have exercising muscles, which is hot and acid, that will cause global to be released, that's what you want. On the other hand, you want to uptake hemoglobin in certain circumstances and what we'll do that well, a low temperature high peak and a low CO2. And those two are important. You'll see why, in a second so alcoholic and a low CO2 and the two go together, you'll have a much greater uptake of oxygen. You'll hear your curve to the left. So as you can see in this small diagram, if your P 02 is illustrated with that blue dot and the saturation that's a that's equivalent is there. Then if you put your curve to the left, you're going to get for the same p 02 a lot higher saturation. So how does this work? Let's look at what happened to a group of doctors who went to the top of Mount Everest and believe it or not, they dropped their trousers. Some of them did, and they had someone stick a needle into their femoral artery to take an arterial blood sample at 8400 m on Mount Everest, and that that that place the 8848 m the F I 02 is 7%. It's one third of what your breathing right now, so they're in a breathing. A hypoxic. Make sure they weren't carrying. They weren't breathing oxygen when they had the blood sample taken. And don't forget, I said they drop your trousers or can I find amazing? But that's what they did. So what did they find? What do their blood gases show on the summit of Mount Everest or near the Summit 2488? That's pretty high. So if you look at the blue, uh, values, those are normal values, just in case you are not aware. And the green ones are what they found on the summit of manners. So the p 02 that is your normal value. About 13 13 or so of, uh, killers. Pascal's of your P 02. The arterial bloods containing oxygen pressure p 02. On the summit of Mount Everest, it was 3.27. That's unbelievably low content. A box street 197, we said earlier, was 200. So roughly 200 of a leader of fully oxygenated fully, uh, normal hemoglobin containing blood. A leader sitting on the table top will contain 200 mils of oxygen per leader. So here they found, it was 1 97 pretty close to 200 the content of oxygen in the people who are breathing that very low mixture of oxygen. In the summertime, I never had 1 46. That's not too far off normal and oxygen saturation. Normally, it's about 197 months, and there's was 54 so you can see that the P 02 is very, very low. But the content and saturations weren't as dramatically impacted. And by the way, they all were fine. Blood tests were normal. Um, all had high hemoglobin is about 50% higher than normal because they were compensating. They were climatized. Yeah, and one. So this is a drop 75% of your p 02, you're content dropped by 25%. So a lot less. And your saturation? Um well, it dropped about 50% but 11 of the volunteers had what was the lowest saturation ever recorded in a healthy person. And that was 34%. So that's pretty dramatic. He was fine. By the way. He wasn't going to real failure. Know hyper lactacidemia know lactic acidosis. So they were all tolerating this well, they were commenting. They were young, young and healthy, and obviously so why was the P. 02 solo with the content preserved? It's because of something called the boar effect. And this is just a sort of biochemical explanation of what those shifting curves. So those are sort of the equilibrium you see with C o. C 02 h plus an +02 and hemoglobin and there's the other biochemical formula. And if you hyperventilate, which is what you do on the top of Mount Everest, if you hyperventilate, you drop your CO2 and you drop. You become alcoholic. So what happens is those values become small. You shift your curve, your equations left so your hemoglobin with oxygen is much more prevalent. So you're able for the same P 02 to get a lot more content of oxygen. And that's exactly what they saw on top of an effort. So it's physiology in action. Therefore, greater oxygen content forgiven P 02. So this is interesting. So during the coated, I thought I'd bring Cove it up because Coated was new territory for everybody, and it was because it was brand new. We had to work out what to do, and you had to work out some basic. We should have worked on some basic physiological principles, and we did a mistake for made because people didn't always refer back to the physiology. So the question was, how low can you go? What does that mean? Well, if someone came in to the to the hospital and they're saturations were 88. Everyone is getting very, very excited. And they said, Oh, we must intubate these people. No, intubation is not in ventilation, Not a normal way of breathing for you and me. We spent most of our lives, I presume, breathing spontaneously. And there are some really important physiological, um, cost to pay by ventilating some positive pressure. And we'll talk about that in the future. A lecture? Um, So maybe we maybe we were a bit fast off the mark by getting by intubating and Ventolin everybody. Because unless you're struggling to breathe, a lot of these patients were not struggling to breathe. They were called happy hypoxic. They weren't looking like they were in distress. They weren't working hard. They just had a saturation. So everybody by New York reflex started putting tubes into patients and ventilating them. And this team in San Francisco spend years working on, um, an animal and human models. How low? How low can your oxygen be before you start suffering? They found that the real the real parameter you want to measure was your cardio vascular compensation. Because the degree of hypoxemia per se was rarely because of harm. It was the lack of your cardiovascular system able to compensate for that degree of hypoxemia. So this will take you right back to what we said in the beginning. It's those factors, those three factors compensating each other, which determines oxygen delivery. If your oxygen delivery is okay, then you might be all right, and you may not have to suddenly panic and start doing things that can cause harm themselves. And that was one of the lessons that was learned in the first wave of coated. Not to jump to intubation in ventilation on everybody, especially if you're not struggling, breathing if the work of breathing isn't too hard. So again, this is a very nice illustration how your different factors can compensate each other and that oxygen delivery is the ultimate determine whether you need to worry or not. So we talked about the factors, but they're not all created equal. So here's a clinical case. 55 year old male, um, pedestrians hit by a car. He's taken to the hospital and the department. They do an ultrasound scan of his abdomen fast scan, and they see lots of free fluid in the abdomen. Undoubtedly, it's blood, probably a ruptured spleen, maybe a liver. He's also got a community fracture of his femoral shaft, so he's got a couple of liters of blood into the muscle of his femur. He's taken to the operating room and after being resuscitated with three liters of keloids, so the blood he's already lost. It's going to be even further dilute by the A cellular fluid because there's no red cells in colloid and blood on the way, because that makes sense because he's lost blood. But while they're waiting, the hematocrit adequate is 15%. That's low. The oxygen saturation is 80% despite 75% of oxygen. So those two factors are not normal. CCP is for BP is about okay, and heart rate's a little bit fast. Now the question is regards to oxygen delivery, and this is a purely theoretical case. What do I worry about most in this case, the low, low hemoglobin, low hematocrit or the low oxygen saturation? Does anybody want to take a guess of the two? Which would you worry about the most because based on physiology? Well, let's let's look at this. We said you wanted to read it out. We've got his saturations hemoglobin. It's gonna be a mixed bag. I think I'll just, uh, go through this because I think time's running out. So? So we said that if you have a fully oxygenated, uh, leader of blood with normal hemoglobin so you can see hemoglobin. This this diagram is 1550 grasper leader, and the P 02 is 12. That's normal. You'll have, as we said earlier, 200 mils of blood in the static, calm blood sitting on the table top. It's not moving, so there's no oxygen delivery auction content, 200 mils of oxygen content per liter of blood. Now let's look at the different scenarios. If I were to make, uh, p 02 half of normal, that's equivalent to an oxygen saturation of 80%. You will get 80% of 200 so you're gonna have an oxygen content of 160 mills Now, what if I were to do the opposite or further, we were to make the hemoglobin half 75 we keep the p 02 normal. So persons got a normal saturation. You're gonna have a half 50% 75 of the oxygen capacity. Uh, that leader of blood. So the hypoxemic patron who's got half of the normal p 02 is going to go from 200 to 1 60. That's 80% of normal. And the next person who's going to have half the normal, uh, hemoglobin is going to have half the 200. That's 100. So from a purely physiological point of view, you're probably worse being anemic than you hypoxemic. Now, please do not leave this lecture saying that I think it's okay to leave some more. The saturation. 80%. I'm just trying to get to sort of start Googling these different physiological parameters around to think of it, as we said earlier. But as I said earlier, uh, a low saturation that would have triggered what could be a harmful. It wasn't harmful in many cases. Um uh, therapy, like intubation ventilation. If they thought about it. If they looked at the overall oxygen delivery, they have found that in fact, they were okay and they were tolerating. So let's look at this graphically. How does this work? Sorry. This is Yeah. This is not the right track. This is another graph. That's this illustrates as well. This is a really I found this a very fascinating subject because 1974 there was a famous study that was conducted in Stanford by a Swiss professor who was my boss, actually, many years later. And he was looking at ways of improving, um, a sick lungs ability to carry oxygen. So basically, they use something called peep positive experience Any pressure. So it's basically like this is very simplest. You have a an alveolus in your lungs that's full of fluid from a d more from pneumonia. And you wanna try and open up some of the Aveeno like putting positive pressure into the lungs and that positive pressure will, um, one will expand the LDL line. You're hoping it will improve the oxygenation so your oxygen saturation ought to improve, and it will help you remove CO2. So you're dead. Space will hopefully reduce and and basically prove the compliance of the lungs. The lungs will become much more supple. And so people have for years and decades and decades and decades been studying ways of optimizing the pressure they put in the lungs when they have some with sick lungs in the intensive care unit, and it's only recently I'm talking about the last year or so many of the world's greatest experts on this subject have come back to the literature of 1974 and said, You know, we think the most important thing now is not, you know, improving oxygenation. It's important. It's not the most important. What's most important is your oxygen delivery, because why? So let's look at this if you've got somebody and this is something classical, and this is one of the big dangers of using physiology inappropriately, imagine you have someone who's got very bad pneumonia. You intubate them. You take them to the intensive care unit. This is a very common scenario. You've got them on a ventilator. You've got a monitor on them. You've got a pulse oximeter on their finger, so it's not invasive, and you've got the saturation on the screen, and it says 80% and the nursing staff next to you are getting very worried. They don't like that number because it's not normal. Everyone assumes you want a normal number, which is not necessarily appropriate, by the way. So what you do is you're going to turn the the ventilators pressure up a peep to try and pop open those alveola and improve those numbers. And you do and guess what happens. You increase the pressure from 5 to 10 to 15 to 20 whatever the number is. And on the screen in front of your eyes, you see the saturation going from 80 to 85 to 90. 95 96. Everybody's got a smile on their face and you're going. Wow, that's great. Okay, trust me, this is a very common scenario and a very common mistake we make. So what happens as you increase the tape we call the PF ratio? I won't go into that right now. It's just a way of giving a crude number of your saturation. Okay, it's getting better. So your PF ratio is getting better. You're transferring more oxygen from the gas. You're giving the patient into his arterial blood. So your saturation on the screen is immediately going up. Wow. Wonderful. You couldn't ask for anything better, right? And you're ready to, you know, open the champagne, but what you haven't done, you haven't measured the cardiac output. And that's why you must always do this in a sick patient who is being ventilated. What's happened to the cardiac output? It's going down and you won't necessarily see a drop in blood pressure, by the way, so you can have a normal BP, but a cardiocap it's dropping. So overall, what do we say? The goal was, Was it saturation? Know it's oxygen delivery. So what happens to your oxygen delivery? It's gone down. So what appears to you to be a success, in fact, is a failure. So that's why you have to take these factors into account. And so today there's certainly realizing that maybe we've been focusing on the wrong thing. It's only taking 40 years, but we've got that last oxygen extraction. That's the last chance glass. So what happens with an extraction? Simple. There's a capillary. There's a cell. There's your arterial blood flowing into the capillary, and it's got hemoglobin. One hemoglobin molecule. It's got four oxygen molecules attached to it, so it is 100% saturated. The oxygen will be required to produce energy in the cell, so one of the molecules of oxygen snipped off and the blood flowing out of the venous side back to the right heart has got three of the four molecules of oxygen sites occupied. So the hemoglobin, the central saturation, is 75% 46, 75. So that's normal. And so one of the things you can do is you can measure blood going back to the right heart using a central catheter, centrally placed central venous catheter. And you can measure blood. Um, in the super vena cava, the right atrium. And it could be the order of 70% or so. 65 to 70 72%. Something on that order of magnitude. Very low. It's 50%. That means you are basically absorbing more oxygen as it passes the cells. That's your last gasp. You like it's your cells. Uh, last mechanism to try and keep the cells turning over with enough oxygen. But you can't go. So here's a case. True story. This I was just stop you. Sorry, doctor. Because, uh, can you hear me? Doctor? Lola is asking. Is there a difference in oxygen saturation and oxygen delivery? Oh, yes. Great difference. Yes. Yes, yes, Yes. As we just said in the previous slide, you can do something that will improve oxygen saturation dramatically even. But because you're reducing cardiac output, uh, you may not think you always will, but you may reduce cardiac output with the pressure you put in the in the thorax. You may actually improve one, but reduce the other. And because oxygen saturation can only go so far, it's only 100% saturated and the cardiac output such an important variable. You may not realize that your saturation is getting better, but your cardiac output is dropping, and hence overall, your oxygen delivery is being reduced. And that is that is the new It's not new at all. It's very old. This is something that some of the world's experts are suddenly suddenly after 40 45 years. Realizing the mistakes we've made, we focused on the wrong on the wrong. We looked at the wrong end of the telescope. We're looking at the fine detail and not looking at the overall picture. The overall picture is oxygen delivered. Okay, so going back to this patient that had a ruptured spleen, they had a hemothorax that was drained to blood in the chest. They were taken to the operating room, had a laparotomy had there spleen repaired, and they were then taken to the intensive care unit where I was the consultant on call. The BP was a bit low, the heart rate was a bit fast. Saturation was not great. And the PF ratio was low. So the oxygenation of the lungs was was the lungs were not fully oxygen in the blood. So this man has got low cardiac output. That's pretty sure, but most importantly, we got the first results back. The harmonic was 9%. That means he's got a hemoglobin of about three. So that's really low. You don't want to go any lower than that, because you will. You may well die. I've seen that several times with little trauma in my lifetime. So this man is on a knife edge. You get blood, right? Everyone agree. You must get blood. But this is the problem. He's a Jehovah's Witness. And, um, this is probably the only time in my life I was ever involved in the sun newspaper. Um, and this guy So they made nonsense stories about this, by the way They said he died in this nonsense, but anyway, he was a guy who was witness and we cannot give him blood. He desperately needs blood. So this is the dilemma. His cardiac output is low. We know that. And we're talking about oxygen delivery. We want to improve the cardiac output, but if we give him fluids, we can give him blood. We'd ideally like to give him blood. If we can't give him blood, If we get him clear a cellular fluid like keloids, then the problem is it's going to dilute. The hemoglobin is already there, so it'll drop the hemoglobin even further. And if we do that, that could cause great harm. So we're trying to do a balancing act here of trying to improve his cardiac output, but not drop his hemoglobin, and we're not sure what to do. Do we fill it or not? So what did we do? We want to know. What would the effect of filling be on his most important factor? Oxygen delivery. That's the key to everything we're talking about today. So what do we do? And how we know of oxygen delivery in this man was adequate or not? Any ideas? So does this man have an adequate oxygen delivery Yeah. Uh, sorry. I hit my button by accident, so we kept the central venous saturation. Remember, we said we normally lose one oxygen molecule in this case. And if it's if you if you're in trouble, if your oxygen delivery is inadequate for yourselves will take two oxygen molecules and your central venous saturation will be very low, Which means you and that will not be something you can maintain for a long time. So you're gonna have to do something about that. But we want to see this is this is our his cell suffering. So what do we do? Look at the center in saturation. It came back at 73%. That's great. That means that he has got enough oxygen delivery to keep his cells happy. So we didn't have to fill him. We didn't have to do anything. We just waited. Gave him him and the Knicks we gave him. You know, Iron gave him, uh, erythropoietin. You eaten. And, uh, over time, quite quickly he increases hemoglobin, and he got better. He went home and he thanked us, came back, and thanks for taking care of him and not giving him blood. So That was one of many ways of measuring if someone's oxygen delivery is adequate for their needs. And interestingly enough for decades now, we have try to guess, When do you need to transfuse somebody from the point of view of anemia? And it used to be based on animal studies they used to make the magic number was 10 10 10 g, or 100 g per liter, or 10 g per deciliter. So 10 was 100 was the magic number, but it was really not based on a lot of evidence. So then then further studies were done about 20 years 30 years ago, and they found that people could drop the hemoglobin to 7.5 and they were fine as long as it didn't have cardiac conditions and as long as they were normal bulimia. Okay, don't confuse anemia and normal bulimia because those are totally different subjects. So as long as they were normal limit and they didn't have cardiac issues, their hemoglobin could be 7.5, and they looked okay. They didn't need any transfusion and just let them improve their hemoglobin with, you know, with iron, and, uh, this time well, recently, just hot off the press came this paper, which I thought was very satisfying because these numbers are all kind of indirect. They're made, they're not made up, but they're more or less guess it. And what we find with this new study was that if you actually use a central venous oxygen saturation, this is just what we talked about with this Jehovah's Witness to assess oxygen delivery instead of just some magic, um, arbitrary hemoglobin target. You can improve your transfusion triggers. So they're saying now, instead of just magically saying, Oh, the hemoglobin was 7.5 or 10 or whatever they say if you can get a central new saturation if it's okay and your oxygen delivery is okay, you're okay. So it's exactly were just talking about a second ago. In fact, if you remember the lady who had the hip replacement, he was fine with a hemoglobin of 7.5 and you see that all the time? Okay, just to try and put some a bit more Doctor Vogel, I'm just gonna add a question here that we've got from Ilya, who said if a person has a constant anemia, hemoglobin is around 75 to 90. Is that a livable state? Uh, is there any way to return to the normal level without permanent medical care? I've also texted you the questions. You can see it on your phone. Okay, um, if someone's got a chronic anemia of five and if their clinically well, I mean, you're not gonna I don't assume you're not going to put a central venous catheter into their right atrium. But if there were clinically Well, um, I would want to know most of all. Why is it that way? Probably do some sort of chronic inflammatory disease. That's the kind of thing that would give you a low hemoglobin if they have a chronic bleed and say an ulcer of some sort or or cancer of the colon, That's another thing. So I don't forget is what we're talking about today is how you how you were able to tolerate these physiological problems, these physiological abnormalities. But the most important thing in some ways is that why, you know, when I said you could tolerate a low oxygen saturation up to a point. But the real question I want to know is, why is that saturation low. Maybe they've got a pneumonia. Uh, ongoing. So? So the hemoglobin being low I want to know are they can tolerate it clinically. If they look fine. They're eating dinner there, joking. They're not diaphoretic not sweet there, you know, they look okay. Their mentation is good. They're passing urine. Uh, I probably think, you know, I don't know why that hemoglobin so low. So I've been looking at, you know, things like the eye bleeds or chronic inflammation and that sort of thing, I do a further further tests on that. So, um, so this is just to do some of the some numbers and all this. So on the x axis on this graph, you have hematocrit. So we're going to take a normal hematocrit were going to continually dilute the person, so they're, um they're normal glycemic, but they're progressively more anemic. Uh, we're going to show him the various, um, parameters how they people react to this. So we're gonna progressively make you anemic by him. Uh, so your normal limits, but you're becoming progressively more anemic. So what happens? Let's look at what they call d 02. That's delivery of oxygen to the teachers. That's what we're talking about today. Oxygen delivery and as you someone more dilute. The oxygen delivery will be pretty much the same because as you become more dilute, as we said earlier, your cardiac output and your flow through your capillaries is improving. It's more than compensating. You're low hematocrit, so that's good. Compensating your oxygen extraction. Remember, we said that was like your last guess. That's your last reserve to keep enough oxygen flowing to the cell so they can keep functioning. That's normal. You're not gonna extract more oxygen. So just like that, Jehovah's Witness was very, very anemic. The extraction was normal, so the delivery was probably normal. Their V 02 is the actual usage of oxygen in the cells. So do your cells have enough oxygen to keep on functioning and producing a T p E energy to keep your body functioning normally? Yes, so everything is fine so far, and as a marker of self hypoxia is lactic acid, and that's normal again. So everything's fine. You're more and more dilute, but obviously your flow is improving. To compensate for that low hematocrit that low hemoglobin. Now we're going to carry on diluting that person. So now your delivery is starting to drop. And what's the compensate? Very mechanism now, and you can no longer maintain the improvement of cardiac output is not able to maintain this lowering of hemoglobin further, you're going to start extracting more. So about 50%. So now if you were to put a central venous catheter into someone's right atrium and you suck out blood and analyze it now is that you'll go from, say, 70% to 50%. Okay, so that's a sign that your cells are suffering well, they're not suffering. They're needing to suck up more oxygen from the blood that's passing by that So you're extracting. It's like something that you can do temporarily. It's like, uh, I don't know. It's like a pump pumping water out of a boat. It's temporary, but it's just to keep you afloat. So oxygen extraction is now starting to kick in. Your V 02 is okay, so your cells are still getting enough oxygen to produce the energy they need to keep your body functioning, and your lactic acid is okay. I will make you even more dilute so more anemic your deliveries, even going down further. But you can extract more than two out of the four molecules of oxygen and so you can't extract anymore. So now your cells are not getting that extra oxygen it needs because your deliveries is too low and now your cells are no longer able to function to produce energy, and your body is starting to fail. And now you're going to see signs of lactic acidosis. And that point where you know longer can compensate at all, is we call a critical oxygen delivery critical d 02. Some people call it the an aerobic threshold. Quickly. Other causes of disassociation Everything we've talked about is something you can do to improve the person's, um, delivering oxygen and hence production of energy in the cells. Is still your biopsy the only cause of inadequate auction delivery or oxygen utilization? I should say no. There are other causes, one is impaired microvascular delivery, and we'll talk about this at a further lecture. So your micro vascular system is one of these systems that tend to be ignored. So we look at growth, things like BP and heart rate, but we don't actually look at the microvascular, which is where you can get a lot of trouble being caused. And so the cells don't get the oxygen because the blood is not getting to the cells because the micro vascular system is not working and the other is something we used to call the six cell syndrome. And basically your cells, for some reason, are not able to pick up oxygen. So one very good example, which is never, ever, ever forget, because I've seen twice I've seen people's lives were saved. One of the things you can get is someone is lacking in vitamin B. One is called Berry Berry or Wet Berry Berry or Treasuries Beriberi you give me. I mean, I've seen two people who are on death store with septic shock. We didn't know why they were not gonna, uh, able to use oxygen. Why they were about to do died and we gave them. In fact, it was a medical student. The first time you said, you know, you thought about beriberi and we thought we hadn't and we gave me, and at the end of your syringe, the person got better twice. I've seen that in my career so because the cells to actually use oxygen. Yeah. Doctor Vogel, I'm going to try and close the meeting. Now, I know there's lots more to say, but I'm just conscious that we've just Can you give me 10 seconds? I'm just done. Okay. So forget this. This is not important. So forget this as well. Uh, I just want to conclude, because I literally it's the most important thing. Forget this is not really Okay, So this is the ending of this. It's just to say that don't forget. If you're in a crazy situation where you're not sure what to do, you're not confident what you're dealing with. Remember that when you get crazy, simplify. Do your A B CS after you've done a B CS. Just think it's cardiac output. Hemoglobin, oxygen situation as the three together. Are they adequate? If they're adequate? You're okay, that's all. Okay. Sorry about that. That was a wonderful lecture. And I'm sure everyone on the lecture benefited greatly from it. We're getting lots of thank use. Uh, I'll stay on the lecture for a little bit longer in case there's any issues. You've got the certificate. If you haven't done the feedback for me. Can I just heard you very strongly to do the feedback for me. Really? Really. Are dependent on that to continue this initiative because we need to demonstrate some of the feedback. So I hope you can do that. Um, I see that there are some outstanding questions. Um, but I don't want to hold people up, and I don't want to hold up to focal up and go over our time limit. Um, and maybe you can answer just briefly while stay on for another couple of minutes. Does medical sleep affect blood rate saturation and circulatory system? I don't know if Doctor Google can hear me. Yeah, I can hear you. I'm just for some reason, I lost my screen. Uh, this has been a weird second. Usually goes very nicely, but, uh, not to meeting. That's okay. It happens sometimes. Yeah. Okay. Uh, what's going on? Mhm. Okay. Anyway, um well mm. Do you want to respond to that question or you can hear? My problem is, I can't see anything I just lost my screen for, You know, it's fine because we've ended. Now we've ended. Now, it's just a question about does medical sleep affect blood rates, saturation and circulatory system. I'm sorry. I can't. I couldn't hear that. Does medical sleep affect blood rate saturation and circulatory system? Because I'm sorry. Does what? She's someone written in medical sleep. I'll text it to you. I'm really sorry. I can't. I can't. It's probably It's probably me. It's breaking up. I've texted it to you. What's that to you? The kids. Too much. Um, gosh, I don't know what's going on here, Okay? Not to worry. I'm going to let people people are leaving, so I'm going to let them continue leaving. And if there's anything you need to add, I can send it out on event right? As a response. Okay. I don't know what happened. Suddenly, your voice is much clearer now. It was very it was breaking up. Um, yeah. This is a very weird thing. Uh, it is written sedation, In other words. Yeah, I really apologize. I just you know, I'm just suddenly have lost my zoom screen, and it says upgrade offer. I don't know why it's an upgrade offer on it. And it wasn't It wouldn't let me see anything. Just okay. I'm going to. Okay, I'm going to close the meeting. Don't worry. And we can get that response from you for that question that I've got zapped. You will send it out to people via event. Right? So thank you. So, so much. We've had really positive feedback, and we appreciate this lecture greatly. Thank you to everyone. Okay. Thank you. And stay safe. I'm going to I'm going to end the meeting now. Yeah.