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Okay. Okay. Hello, everybody. I'm just trying to get this up and running. Give me just 26 high video pedal. Uh, do you, uh okay, Can you all see this? Yes, that's great. Great, Thank you. Ok, hi. So my name is still Doctor John Bogle. I'm a recently retired consultant in intensive care, medicine and anaesthetics. And so today I want to talk to you about acid based disturbances that we will see or, you know, could see an acute medicine. Well forms, intensive care, accident, emergency, etcetera. Um, the reason I like to talk about this is this is a subject that is used throughout your career, and almost nobody I've ever talked to really understands it. And in fact, I was in the same position. And one day I tried to explain this to somebody in depth, and I realized I don't really understand this. So I took about four or five months with a friend who's a chemist, a doctor in chemistry, and I worked out a way of explaining this simply so this, like here, in fact, is going to be two lectures. It's going to be, um, a lecture on traditional methods of how we are taught acid base, and they're just basically rules of thumb so you can work most things out. But they don't really explain. Uh, what's going on with mechanistic terms. And those are the types of cases where you that are complex, that you do need to understand the mechanisms. So we'll go through the traditional methods in this first lecture and because I did not want to overwhelm you. The second lecture I give next week will explain the more mechanistic technique, which is called the Stewarts model, after Peter Stewart, a biochemist and physiologist that's used, uh, in in, uh, in subjects where the you're likely to deal with complex acid baseball. Okay, so just give you a taste of what I'm talking about. This is a true story, a clinical case that I had one Sunday evening after a very long week on call for the intensive care unit, and this woman arrived unwell in the accident emergency department of our hospital four days prior to have just been discharged from a third center tertiary center with a diagnosis of severe inflammatory bowel disease, and we had a discouraging fistula. Now we had no idea of this woman's history. We had no idea where the fish she was coming from. What kind of fluid was coming from that fistula? Because you can have various, um, uh, concentrations of different electrolytes. Um, And if you're in the intensive care unit and you're dealing with someone with a discharging official, you will take samples of official. You will analyze it and then give the person or treat the person with with the fluid they're missing here. We had no idea. And so, um, the question was, when you look at these gasses and we were having to look so the accident emergency department, the doctors there, the consultants there were a bit lost, they didn't know what to do. And they asked us to come down and look at it, and I I did. So this is what this blood gas shows and how might you treat it? So he obviously had a very, very low pig. She had a base excess of minus 14. So it's a base deficit of 14. I'll explain what that means. In a few minutes, her CO2 was normal, so it wasn't a respiratory acidosis, and her lactate was pretty normal. So it was normal, in fact. So the question is, what's going on? And the doctors who were receiving this woman and didn't know how to handle this didn't know how to start. And so what I will do. And by the end of these two lectures, you will be able to look at this with your understanding of the mechanisms, and you'll be able to figure this out. And we did. It was not that difficult. In fact, if you understood the mechanisms, if you don't, then you just follow rules of thumb. Then you will have a hard time. So today we're going to talk about the traditional methods, the ones that you know most people get taught. But next week we'll go into a great deal more depth using the Stewarts model, which is more mechanistic, which would make this sort of acid based problem a lot easier to understand. Okay, so, um, let me just get rid of this, Okay? So the outline today, part one we're going to talk about why worry about all this part, too? Well, sorry. Still in part one today we're going to go over the traditional methods that you'll have to learn. And they're very useful as rules of thumb for the routine case, that doesn't require a lot of, um, in depth understanding because it's pretty straightforward. Part to next week, we're going to go into Stewart's physical chemical method, Um, which is a method that requires a lot of maths. But I'm going to explain this to you without using maths, and most people find it's understandable. And then I'm gonna give you a clinical examples to to back these up. Okay, so the first part of this lecture today is What's the big deal about acid base? Why are we worried about it? So, first of all, a lot of people have talked endlessly about what we call a hyperchloremia acidosis, and you mustn't give, for example, saline. In most cases, they say today, because you may induce a hyperchloremia acidosis and you'll see at the end of the second lecture why that's not a proper term. In fact, it's not the right term, but that's what we use is a term hyperkalemic acidosis, and it's become I find almost an obsession well, in several papers. In fact, almost every paper I've seen they say that despite being a frequent cause of metabolic acidosis, So if you give too much saline, a lot of chloride, they say, um, you'll get a hyperkalemic acidosis, and that will be terrible. In fact, it's not been associated with increased risk of acute kidney injury, AKI nor mortality. Other paper comparing saline, the dreaded saline or lactic lactated ringers or heartburn solution is the same. They say there's no meaningful difference in the risk of hospital mortality or complications, including renal complications. So this is going against kind of, um, a leitmotif, a theme that everyone's talking about. So the evidence now is not that there is an increase in mortality with hyperkalemic acidosis. Why does it matter again? So let's take an example here. This is somebody who has a mild metabolic acidosis with a base deficit of five. And again, I'll come into I'll come on later. What a base deficit means. And you look at the cause of this and the risk of death because it's the risk of death that really matters. Is this going to predict someone doing badly? Were not? If you look at someone who has a mild metabolic acidosis, the severity which leads to a base deficit of five. So that's not too severe. But it's it's significant, and someone who has the same severity of acidosis do, too. Too much chloride, too much saline. For example, Chris, A line has equal amount of sodium and chloride well. The lactate will have a two times risk of death, so your risk of dying is double if you have even a relatively mild lactic acidosis. And if you have hyperchloremia acidosis, the evidence is there's no change in your mortality. So the point of all this is to say that what's important with hydrogen ion excess, or is acidosis, is it is a symptom of an underlying problem. Usually it's not the problem. It's it's not the acidosis itself, you know, within reason. Okay, uh, it's not the acidosis itself. That's the problem. It's the cause of the acidosis, so it's a symptom of an underlying disease. So this is a really interesting old study that really illustrates this beautifully. There is a There's a a drug called dichloroacetic it and that causes your, um, it causes you increase in glycolysis in yourselves, and it's a way of treating electric acidosis that we know is associated with a very strong association with mortality, and what they did was they were going to use D. C a dye chloral acetate to see if it actually can reduce lactic acid. And you can see in this case it does. It reduces lactic acid dramatically compared to placebo, which does nothing to the level of active kassid. What about P h DC? A. Increased your pick from a low level. So if your acid so 7.0 or 7.1 giving DCA will reduce your lactate and it will increase your pick towards normal, placebo doesn't. And what about mortality? In that case, you'd assume that getting rid of lactate, which it does, would be good for you. Therefore, you're more likely to survive. That's what placebo so has no effect. And there's DCA no effect. So what this really illustrates is it's not the lactate per se. That's the problem. It's the fact that the lactate is the symptom of something else that's causing that lactate arise. Could be an abscess. Could be could be a lot of things. And so, um, it's in fact, one of the interesting things I noticed was in intensive care. A lot of the junior doctors I would be with would want to dialyze lactate off of somebody as if that was going to cure their problem. And in fact, there's no evidence at all that dialysis reduces mortality from lactic acidosis. You can get rid of not even that successful. But if you did get rid of the lactate through dialysis, so hemodialysis to an artificial kidney, it doesn't make any difference to the mortality. Unless you treat the cause of that, uh, increase in lactic acid. Uh, why does it matter? This is another example. This time we look at a respiratory acidosis, so if you don't breathe enough, your seo two rises and you get your respiratory acidosis. And I found this amusing because this is a study that was done in 1959 in 1980 for I did a very similar study. I took a year off and did research, and the results were almost exactly the same as this study from 1959 that you could create a severe respiratory acidosis. Not without without an oxus, you're giving some one CO2 to breathe, not making them anoxic, and we will ask it for over 30 minutes and was very well tolerated. In fact, the textbooks will say, If you're CO2 goes above a certain level, I don't know. 10 you'll fall into a coma. That's absolute nonsense. I was one of my own volunteers, and I can promise you the last thing you're going to do is fall into a coma. Your eyes are bulging, your breathing like like mad and your, you know, your your head's pulsating. You're not going to feel like you're going to a coma. It could well be that people that go into a coma breathe less, hence get a rise in C 02. So it's a question of which comes first, the chicken or egg. So this this example of five patient's, you can see the CO2. This is in millimeters of mercury, so just divide by 7.5 if you if you have to. Um, but you can see they're very high, you know. Remember, the CO2 normally would be around 40 and peaches were down to 6.76 point eight, and this lasted for 30 minutes, and the subjects were all fine. And in my in my study, it was almost exactly the same results. So, um, uh, the acidosis caused by, uh, lack of respiration or low respiration hence a high CO2 is not as well tolerated, If that's it's if you're healthy. Um, this was a recent paper that came out, and there's a lot of a lot of, uh, I don't know how to put it. A lot of I don't say myth, but, um, a lot talk about how dangerous in acidosis is and how it's going to impair your Mario cardio contraction. And in fact, if you look carefully at these papers, it's almost always an animal. Models and the animal models are animals that have their cardiovascular system removed from their bodies that are in vitro, and that means that they're not exposed to the sympathetic nervous system, and acidosis will may. And I'm sure it does diminish your contractivity, but it also it stimulates the sympathetic nervous system so they, too, may counteract each other. But in this case, they're asking, you know, what is, uh, what's the problem here? And it says they came to the conclusion that severe acidosis has a deleterious effects on hemodynamics. That's what you're taught, and it's a common belief that there's a positive data that identifies the acidosis itself to be a problem. So they say it in all the textbooks. But there's not a lot of evidence that's true in humans intact humans. And in fact, if you look at Olympic rowers after a race when they're just finishing along, you know hard race. They'll have lactate levels as high as 24 millimeters millimoles per liter with very, very low key acres low lower than 6.8 or even lower without ill effects. So, um, again, it's the cause of the lactic acid or the cause of the acidosis. That's the That's the really worrying thing within bounds of reason, of course. So now let's go over some of the traditional methods. These are the kind of methods that I've used all my career and you'll use in your career, and you'll use them for the average case that you're gonna deal with. It's not particularly complicated before, before we start acid base, I find extremely complicated and maybe unnecessarily complicated because we use different definitions that are different for the same subject where we make things very confusing. So let's start with some definitions, and I would like you to forget the definitions you may have known. And just use these because I'm trying to make life as simple as possible because this is a very complex subject, so I'm trying to make it a little bit simple for you. So what is? Ph. PH is not some magic number all it is. It's a way of quantifying the number of hydrogen ions, and they use that as a negative longer rhythm. Okay, so the higher the number. So if you go from 7.4 to 7.5, that means you have fewer hydrogen ions. It's a negative, longer rhythm. If you go from 7.4 to 7.1, you have, ironically, more hydrogen ions, so it's a negative, longer rhythm. So you might you might ask yourself, Why would you bother making a negative, longer rhythm? You could just use it like sodium millimoles and micromoles and animals. But they do that because it's such a small number. What's an acid? Well, an acid is very, very simple. There a lot of very complex definitions and assets. Very simply, a solution where you have more H plus hydrogen ions than you have O. H. Minus dead easy. So don't make it life. Make life as simple as possible. What's a base? Well, it's the opposite. You have more. Ohh. Then you have a plus in a solution. What's a strong electrolyte? And this will come into play in the next lecture, where you'll see how important this is. A strong electrolyte. Imagine you've got You're going to make spaghetti Yummy. I love spaghetti. Okay, you're going to get a big pan of boiling water, and you have to throw salt in it before you before you cook the spaghetti. So I'm gonna throw in 5 g of salt, a good handful of salt, and you throw it into the symptoms of water and you ask yourself how salt is N a C O. So ask yourself how much sodium chloride salt is in that water. And the answer is, there's none because the entire molecule of N a. C l dissociates totally to n a plus and c l minus. There's no N a. C l. There's only n a plus and C L mice because it's a strong electrolyte. It totally dissociates. So what's a weak electrolyte? Well, it's one where it only partially associates. So let's ahead a molecule. It's a B. I throw it into the water, and now you're gonna have a B and AB, so it's only partially associated there's. There are molecules of the parent compound as well as the dissociated products as well. Okay, if you understand that we're well on our way to understanding acid base. So let's look at again. There are two types of traditional approaches. You have the bicarbonate centered approach, and you have the base deficit or excess approach. So let's look at, um, these individuals. Let's look at the bicarbonate centered approach. And this is one where the views pH as a function of bicarbonate and CO2, and this is what we call the Henderson Hassleback formula, and I have to be Austria. This is what I was brought up with, and it's like an old friend and I still use this. Uh, it doesn't really explain things to me, but I just can figure where I out where I am on a map, if you like. So This is what we call the Davenport diagram. And on the X axis you have your P H. 7.4 being normal and the the left. It goes lower, so it's more acidic to the right. It goes higher, so it's more alkaline. On the Y axis, you have bicarbonate, and you can see that normally you have a bicarbonate of 24 a Ph of 7.4. Now you may notice there's a brown line and a blue line, and you'll see where these come into play in a second. But the brown line is the law. This is what happens to your bicarbonate if you have a pure metabolic acidosis or alkalosis, and you'll see this in a second, where this comes into play and the less steep blue line. So it's a lot less steep. Is the change in bicarbonate as you become more acidic or alkaline Knittig due to changes in C 02 again, what? The best way to understand this is looking at examples. Okay, so let's look at somebody who has a metabolic. Pure metabolic acidosis. Imagine you have somebody who's on a ventilator so they can't breathe more or less their their breathing. What, you tell them to breathe. The machine controls their breathing so the CO2 stays exactly the same and imagine they suddenly get, um, a metabolic acidosis, like a keto acidosis that you might get with diabetic ketoacidosis. But they're on a ventilator, so as they get more acid acid and get a metabolic acidosis, the pH goes from 7.4 now to 7.24 in this example, and the bicarbonate drops dramatically along that brown line. If, on the other hand, for some reason we overcorrect or they overcorrect for some way, they get more Alka Logic. They go up the steep brown line and they get a rise in their bicarbonate, and their Ph goes to the alkaline ick side. So 7.56 from 7.4. So you see that steep brown line tells you what's happening on the metabolic side, Um, in terms of bicarbonate and pH. Now let's say somebody has a respiratory acidosis, and it's a pure spirit acidosis. There's no metabolic component yet. If you make that person, um, hypercapnic. So they have a rise in their CO2. You're going to see that the pH drops from 7.4 to 7.24 in this example. But you can see that the that blue line, which is not very steep, is going to cause a slight rise in the bicarbonate. So from a purely respiratory, a pure respiratory acidosis, you're going to get a slight rise in the bicarbonate. On the other hand, if you hyperventilate, you're going to get a slight fall in the bicarbonate, and you're gonna get a respiratory alkalosis. So if someone has, for example, if someone gets excited, I've seen this before where they get what they call some people call spasmophilia. Um, and you get someone who gets Cal stock sign and, um, from hypocapnia hypocapnia causing hypocalcaemia. That's because they're hyperventilating, and you're gonna get a slight drop in bicarbonate, a marked increase in ph. Now, the thing that has you have to remember about these things is they don't usually occur in isolations. You often have, um, an abnormality, whether it's the spirit, your metabolic, and your body tries to correct things. So what happens is that your your pH, which is abnormal after some sort of insult your body will try and compensate by bringing that Ph back towards normal. It doesn't often succeed going totally the normal, but it goes towards normal. So let's look at what happens if you have somebody who has a metabolic acidosis and see how your respiratory system tries and compensate. So the best example I can think of is somebody who has a diabetic ketoacidosis. So initially what would happen is they would have a metabolic component because they're getting all all those ketones being formed. So that's causing a keto acidosis. They're dropping their pH from 7.4 to 7.24. And now, as their body tries to compensate, it's gonna try and drag that gray dot back towards 7.4. Well, quite get there. But it'll try. And what it does is you're going to compensate with your lungs. You're going to blow off CO2. And in fact, it's your breathing pattern is so characteristic they even have a name for it, and we call it cou smells breathing. And so you can see that brown line we call them ice applets that brown line gifts to the right, and so the dot gifts to the right, and they've just increased their Ph towards towards normal. And that's very quick because your lungs respond very quickly. So here's a clinical case we're going to try and show you or trying to illustrate how this works in practice. So this is again. This is a very, very typical example. I've seen this so many times. You have an old man who are elderly man whose got a chronic obstructive pulmonary disease, and he's admitted with worsening dis disappear. He's known to have COPD Karnik obstructive pulmonary disease. He's well known the doctor on the A and or the hospital. When the ward calls you as the intensive care doctor because he's worried by the arterial blood. Gest's saturation is 93%. That's okay, but the CO2 is 7.2, and his, uh, normally would be around 5.3 or 5.5. But this is high, and that doctor is getting worried. Are you worried about this value? And if you aren't or if you are, what other blood gas information do you want to have? Because this was a typical case I get. The numbers often were higher than 7.2, there might be 10, and so what would I ask for? Well, the first thing I would ask for is what is the pH? And most importantly, what is the bicarbonate now? Why would I ask that? Because what I'm really wanting to find out Is this something that's acute? Or is this something that's chronic, or is there a cute? Is there an acute component to it? So let's see what might happen. And this is where this will explain this. So let's say you have somebody who's, um, breathing hypoventilating breathing less than they their metabolism requires their CO2 will increase, and you immediately get a respiratory acidosis and you'll get a slight rise in bicarbonate. So if I were to see the person with a pH of 7.24 and a very slight rise and bicarbonate with a CO2, that's high, I might say, Hmm, that's worrying. But if this is something that's chronic and that person is used to over about two or three days, your kidneys will start to compensate. So the compensation from um, from a respiratory acidosis is much slower than the, um, respiratory compensation of a metabolic acidosis that we saw on the previous slide with diabetic ketoacidosis, where you breathe quickly, very, very quickly. So what happens in this case is over a couple of days, you're going to be going back towards normal, and you're going to be going slightly back towards Ph of seven point. Well, 7.5, let's say 7.35. Sorry. 7.357 point 37. And so you're going to get a marked rise in your bicarbonate. Okay, so the acute the acute rise in C 02 because you're on that slightly sloped blue line is going to raise your bicarbonate by about a millimoles per liter for every CEO to above 1.3 above 5.3. So, as you can see on the box there, it is acute you're gonna you're gonna get a slight rise and bicarbonate. As you can see with that blue line, it's not very steep. That's the immediate effect if you stop if you suddenly had a rise in C 02. So that would tell me that person has an acute Um uh acutely HIPAA kapnick. On the other hand, if their kidneys have had a few days to try. And, um Oh, I'm sorry. Let me just go over this again. Yeah. If your kidneys have had a couple of days to compensate, now you're going to see the bicarbonate goes way up. So the question I would have asked that young we're not even so young doctor who's very frightened by a rise in the CO2 And this patient with COPD, I'd say, What's the ph? If it was 7.2, I'd be saying, Oh, that's probably, you know, probably acute. If it's if the bicarbonate say 26 I'd say If the pH was low and the bicarbonate was not too high, I'd say, Yeah, that sounds an acute acute problem because he hasn't had time to compensate. If, on the other hand, he answers all the Ph is 7.36 and the bicarbonate is 35 I would say, Well, that says to me that patient is probably used to this, and so I wouldn't get too excited about it. I'm not saying I wouldn't look at what's going on, but I wouldn't be running around hoping to intubate this man. So This is really a good example of how if you understand this and using this diagram, you can work your you can work yourself out of a few difficult situations. So what's the other approach? And this is called the base deficit or base excess approach. And I have to admit that again we make a relatively complex situation of acid base, which isn't that easy to understand. We make it even more and unnecessarily complex. So what is the difference? So our lab gives us a base success in the results we ask for. And in fact, a base. Excess is a negative based deficit or a negative based deficit, a positive basic cess, and vice versa. So we're making it more confusing than it has to be. Okay, so just for the sake of simplicity, I'm going to use the term based deficit from now on. But bear in mind that some labs will give you basics s and it's just a negative of a based deficit. I don't know why we make it so complicated, but that's the way it is. So what exactly is the base deficit? It's very simple. If you take, um, the plasma of somebody. And you, uh, in vitro. So it's out of the body and you have a pH. You add you titrate alkali until you get the pH back to 7.4. So the quantity of alkali you'd have to add to take an acidic plasma and make it back to 7.4 will tell you how severe your acidosis is and vice versa. So if it's, uh, if you're salute, if you're plasmas alkala knittig, you'd have to add acid. So whatever quantity of either acid or alcohol you have to add to return the pH to normal 7.4 is the base deficit or base success. But what's key in that is it's when the CO2 don't forget this is in vitro. This isn't a lab. This is not in the body is normalized. What that means is that the respiratory component is removed, so you're only talking about the metabolic component. So if someone has a base deficit of, say, five, which is what you saw earlier note bearing in mind that normal is plus or minus two. So based deficit of five says to me that they've had to add you know five of of alkali to return the PHP normal, so that would be a metabolic acidosis. The problem with the base deficit is it's an average of opposing influences, and people often miss misinterpret or misunderstand this. You, um you can have in the same sample al colonizing effects and Acidifying effects, and they can oppose each other. And if you want to think of a silly analogy and I'm pretty, I'm pretty good at my silly analogies. Imagine I have one, my left foot in boiling water to the point where my skin is almost coming off and I put my right foot in a bucket of absolutely freezing water. I'm getting frostbite and you ask me, What's the temperature on average, you say, Oh, it's 37. So everything's fine, right? Obviously, it's not. Well, you can have the same thing with acid base problems. You can have a very strong alkaline izing effect in a very strong Acidifying effect, and the average will be expressed as the base deficit. You know, I'll show you what I mean by that in a second. So let's look at this is a This is a kind of typical case multiple trauma who develop ARDS and sepsis. And here are the values. The P 02 is pretty normal. The pH is slightly low, the CO2 is normal, the bicarbonate is low and the base deficit is for not too dramatic. So if you ask me, what is this? I would say you do have an acidosis because the pH is not 7.47 point three to your CO2 is normal. So it's not a respiratory acidosis, and most importantly, your based deficit is raised. So that means you have to add alkali to return the pH to normal. So it's a metabolic acidosis mild. Okay, so I just answer the question for you. So let's look at this again. But this time with a bit more information. And again, the extra information I'm giving you now will be, um explained and will become very clear, I hope in the next lecture. But this is just to illustrate what I'm talking about. Having opposing influences and to determine those opposing influences. You need a more sophisticated way of looking at acid base, and that's what we're going to talk about next time. So let's draw this this line here, which is a line of unity. So, um, anything above this line is an alkalinity like influence, and anything below this line is an Acidifying influence. So again, a hot foot in hot water or foot in cold water. So there's something called the sodium chloride effect. And again, I will explain this to you next time. But this is having, in this example, a alkaline izing effect you're having a low album in. So that's also going to have an alkaline izing effect. So the two together are quite strong alkaline izing effects. You've got a very strong, uh, you have a very large acid lactic acidosis in this example, Um and so that's a very strong Acidifying effect. You have some ions that you haven't really accounted for. Could be lots of things. Could be phosphate sulfates, formic acid. I don't know, but it could be something we haven't measured. So that has a slight, uh, Acidifying effect. And there's your base deficit. So you're based deficit of four, as we said earlier, is not very dramatic. It's a sort of mild, uh, metabolic acidosis. If you just look at the blood gas quickly, you'd say that's just a mild metabolic acidosis. But if you break it down into its component parts, which is what we will do next time you'll see that there's some strong alkaline izing elements that are counterbalancing the Acidifying elements, which are very severe. And so your average is four. That's okay, So your foot's and hot water and foot's and cold water and on a whole it's not too bad. Well, you can see that's not true. The severity is greatly underestimated. So what are the problems with traditional approaches? First of all, these approaches the rules of thumb. They're basically what we call heuristics, just sort of like I don't know if, uh, empirical, you see something happening? You don't understand why, but you know when it happens, this is what problems, and they don't teach you understanding. In fact, I can guarantee you will have a very hard time finding many doctors who can explain acid base to you in any sort of mechanistic or detailed way. They don't really teach you understanding these traditional methods. They work for the average guy and the average patient, and I use them all the time for the average patient. But when something gets a bit more complicated, like the very first case you saw with the fistula, then you can't use these rules with them. You need something a bit more sophisticated. The other problem with them is there's very little quantitative data on the patient's acid base. Status just gives you an average protein and electrolytes, as you saw a second ago, which we'll explain the next lecture or not even looked at. There's no diagnostic information. And most importantly, as I just saw showed you, you can have really major disturbances that will offset each other and hide in what looks like a relatively normal or not too severely disturbed blood gas. Uh, are terrible, I guess so. That's one of the problems of these traditional projects. So to recap acid base, what matters is what's the cause of it. Okay, so the cause of the acid base is what's going to be the big, uh, influencer on your prognosis. The definitions. There are lots of different definitions. Be very, very complicated. Keep it really simple. Just the ones we talked about today. One of the traditional approaches uses bicarbonate Ph. And you have this Davenport diagram, which, as I told you, I was brought up with and I still look at as an old friend, and I still use frequently for simple cases. Or you can go down the base deficit or base excess approach, where you titrate your your sample your plasma, UH, to return the pH to normal. And so whatever you add, whether it's alkaline or acid is a quantity of the of the metabolic disturbance, not the CO2 metabolic disturbance. But the problem is it's an average so you can have a Posey influences hotfoot and cold foot, as we just said that there are there can have some severe disturbances that are hidden in what looks like a generally not too severe problem because you're just getting an average when they could have different elements pulling on both sides of the alkaline epic and Acidifying side. And as I said earlier, the problem is it doesn't really explain what's going on there, just based on rules of thumb. And they don't even consider some of the most important elements, like proteins and electrolytes. And they can have major as you just saw again, major disturbances offsetting each other and hiding what? Into what looks like a relatively normal or slightly abnormal acid arterial blood gas. Okay, so that's a relatively quick lecture today. Um, I didn't want to overwhelm you. And so next time we're going to talk about Stewart's explanation of acid base, which is a much more sophisticated technique, Um, and is I'm going to attempt to explain it without the maths, which most people find quite daunting and that will help you work out more complex as today's problems. So any questions, I'll be more than happy to try and answer. There's nothing currently in the chant. But if anyone wants to write something now, run mute themselves to ask a question. Oh, there's a question. Now, um, would you like me to read out for you? Uh, please. Uh, when we see a B G, which one, uh, do we need to see for CO2 or by calm? Um, well, it depends which, which traditional technique you're using. Uh, what I would probably do is look at the pH. Is it abnormal? High or low? Secondly, I'd probably look at the CO2. Is it high or low or is it normal. Look at the base deficit or basics s depending on the lab you're using and to see what the metabolic component is. Um and then you can use bicarbonate or not, but I think those are the elements for the traditional approach. Now, be careful, because if you have a complicated case like the very first one I showed you with a fistula, you're gonna need a lot more than just that. And that's where I'm going to try and explain how to work this out next week because I thought there'd be too much for you in one week to just cram it all together. One last thing that if you want me saying it's this, like here and even the one on hyponatremia I gave last week. These are fairly, um, complicated subjects, but it's really worth taking the effort to go over it several times. Because once you finally get that light bulb moment where you understand this instead of just memorizing it, But you understand it, then for the rest of your career you can use it without having to go back and back and back to the books. And that's what that's why It may seem quite daunting the first time you see it, but if you've got it the first time, if you understood step by step by step, then you'll be able to understand it. You've proven that, and then you just have to go over it several times. It's it would be impossible. I think it'd be very, very hard for you to see it once and go Wow, I understand everything now, but once you take that effort, go over again and again a couple of times and you finally understand it, then it's with you for the rest of your career, and these are very common problems you'll be dealing with. So it's not like something very esoteric, very rare, which people love. But it's it's, uh it's the common things you'll be dealing with on day by day basis. So it's really important to finally finally take the effort and understand these. And that's why I'm trying to explain these. And it's often not in the textbooks. By the way. I still do not understand. It is You can't read that. Do you wanna You wanna Would you like to read that out to me? Please? I think he's just saying that he doesn't understand the topic, but it's too difficult, but mhm. Okay, Uh, well, I don't know what to say. If you can just have to look at this again and next and follow next week as well, that will help you. You should be able to Once we've upload everything to model, you should be able to rewatch this lecture. So if you've had difficulty understanding things, you can just re watch it. Don't forget. One thing I was trying to say to you in this lecture is these are rules of thumb. They don't really explain. So in some ways, if you say you don't understand it, that that that's encouraging because it's I wasn't trying to explain it to you. I was. This is most of the textbooks. Don't explain anything they just say. Here, here's the map. Don't understand how you get there, but this is where the map, this is what the map looks like come to differentiate respiratory. And, uh, sorry. I couldn't see what he said. Um, how to differentiate between respiratory and metabolic in a B G? Well, I just explained to you that if you have a pH. That's abnormal, and you have a CO2 that's normal, and you have a based deficit that's abnormal. And this based deficit is an indicator of a metabolic problem. And you could say you have a metabolic acidosis or alkalosis. If you have a CO2 that's raised or low, high or low, and your base deficit is normal and your pH is abnormal, then you could say you have a respiratory acidosis or alkalosis. So if I hyperventilate, I may have a respiratory alkalosis, and sometimes you can have a mixed picture. And the best way to under to determine a mixed picture is to look at those Davenport diagrams, and I think you have to sit down and just look at them. They're not that complicated but just gives you an idea of where you are, um, in the combined respiratory or metabolic component. But have a look at the dive Davenport diagrams. I think those help understand doesn't help you understand the mechanisms, but it just gives you an idea of what the you know, whether it's a pure respiratory pure. Is it abnormal? Is it purely metabolic puree? Respiratory? Or is it mixed. If anyone has any further questions or comments you'd like to post in the chat. Um, And while we still have time, if you could please do the feedback form someone has asked How can Sorry. Yeah, go ahead. I can't read it so I can see the first couple of words. And then it just, uh how can we know if it has mixed picture or both Respiratory and metabolic. Well, as I just explained to you, if you look at the Davenport diagram, so first of all, if you're CO2 is normal and the based deficit is abnormal, then you've got purely a metabolic problem. If you're based, deficit is normal, and your spirit and your CO2 is high or low abnormal. And your pH is of course, in both these cases, your pH is abnormal. Then you have a pure respiratory problem. If they're mixed, I think the best way then to do is look at the Davenport diagram. And as I said, if you have a, um, for example, some of the COPD with a high CO2 and uh, you want to know what the Ph is if the ph is fairly not too abnormal, and the bicarbonate is very high. That means that they're start they've been had. They've had several days to compensate for the rise in the CO2 by by retaining bicarbonate. So I have a high bicarbonate. And again, just look at the Davenport diagram. It really shows it very nicely. So that's why the very good clinical example that I just gave you was that somebody comes in. They have a relatively normal pH instead of 7.4. So it was 7.35 or 36. But they're bicarbonates very high. That says to me that they've had this for a long time, so I'm not too excited about the rise in the CO2 because it's something that's chronic and they're probably used to. But look at the Davenport diagram. If you look at it and think about it, you know that's the whole point of this lecture. It's not going to spoon feed you. It's just giving you an idea. So you can actually, um, you know, work this out yourself. You have to understand this cheap. If anyone else has any questions, um, now is your chance. Otherwise, I guess. Thank you very much, Doctor. As always, Um, people are saying thank you in the chat. Also, um, thank you very much. And, um, we have another few minutes before the next lecture, so if you could please do the feedback form again, it's very important for us. If you have any additional feedback, you'd like to write in the chat. Um, anything you'd like to see in future lectures, Um, or anything of the sort. Um and hopefully you can join for next week's lecture. Okay, Thank you very much. And everybody stay safe. Thank you.