Anatomy Exam Review PDF

Right? If you're getting rid of too much hydrogen, then how are we how does that equate c o two equate to hydrogen? Somebody wanna help her out? With carbonic anhydrase and that reaction. Okay. What's that called, Henderson? Oh, Henderson Hasselbeck? Is it that way? The heder yeah. The Henderson Has...

Right? If you're getting rid of too much hydrogen, then how are we how does that equate c o two equate to hydrogen? Somebody wanna help her out? With carbonic anhydrase and that reaction. Okay. What's that called, Henderson? Oh, Henderson Hasselbeck? Is it that way? The heder yeah. The Henderson Hasselbeck equation. So, basically, what we're saying is c o two and water in the presence of carbonic anhydrates is going to give you hydrogen and bicarb. So if you have, if you're getting rid of c o 2, then you're getting rid of one of the components of that Henderson Hasselbeck equation, which is going to get rid of hydrogen. So now you're getting rid of hydrogen. And we're gonna cover that in a lot more detail in, hopefully, in about 10 slides. Okay. So they're saying hydrochloric acid, strong acid. Right? So no surprise, we talked about dissolving human tissue in hydrochloric acid. Weak acids, such as carbonic acid, less likely to dissociate their ions and release hydrogen with less vigor. So it makes sense that in all of the body's buffering system, we're using something that is a little jettler than hydrochloric acid. Could we have designed this human body to use hydrochloric acid in this Henderson Hasselbeck equation instead of carbonic acid? Maybe we could've, but it would've been a lot harder to control because hydrogen is so rapidly dissociated from hydrochloric acid. Does that make sense? K. Are you guys happy to be back in lecture? Me too. Me too. I feel like I'm home. Alright. Strong base, is going to react rapidly or strongly with hydrogen. So if you have hydrogen and you have, o h, then it doesn't take to rocket scientists to say, okay. If I have 2 hydrogen and an oxygen, I'm getting dihydrogen oxide or water. H two o. Right? Alright. Let's see. Wheat base is gonna be, by car because it binds with hydrogen much more weakly, And so that makes sense right, we said. Well, we don't want we want carbonic acid in in physiology, not hydrochloric acid. We want a weak acid and we want a weak base so that we can titrate these things very finely without things getting out of hand going overboard that type of thing because if you have. Hydrogen protein, protonated hydrogens being released at a rate that is higher, let's say it's intracellular, you may start damaging the cell. So you want these things to be slow and and steady, reliable, and not overreacting. Overreacting is actually a good term for that. So if you had hydrochloric acid, then, yeah, that would make sense. Right? It would it would cause, protonation and damage to the cell. Alright. Oh, just hydroxide, by the way. Sorry. Alright. So this is talking about we've already talked about this, how pH per hydrogen is a negative log of your hydrogen ion concentration. K? And it has to be a negative log because, you have 40 net equivalents per liter, point zero zero zero zero zero zero zero zero four. All of that is equaling a pH of 7.4. The titration of hydrogen in just a a liter of fluid has to be so fine that they have to come up with this negative log because the numbers are so infinitesimal, it would be hard to measure any other way. So now you have per hydrogen 7.4 with this very small amount of hydrogen in a liter. In a liter of fluid, you have a very very small amount of hydrogen, and this is why that gives us a pH of 7.4. So you can see that you one failure of one of these mechanisms either the blood buffering system, the respiratory buffering system, or the renal buffering system, and you can get these, deviations in hydrogen ion concentration either acidosis or alkalosis, and that can cause all kinds of problems. We talk in the respiratory section, we're gonna talk about the oxygenoglobin dissociation curve, and we're gonna talk about, how having acidosis in a tissue will cause hydrogen to be or c02 to be preferentially released, and how left shifts and right shifts and all of these things are all serving to either get rid of CO 2 or hold on to oxygen either get rid of oxygen and let it go to the tissue. Or get rid of CO 2 and let it be exhaled out. That's all based on very, very, very, very finite control of just a few hydrogen ions per liter of, fluid or liter of body tissue. Does that make sense? K. Yep. And I think we got that. Normal pH of arterial blood's gonna be 7.4. Venous blood's gonna be 7.35. You have, carbonic acid in venous blood from the c02 and the venous blood, and that's gonna be the difference between 7.47.3 5. K? We all understand that. So we all know that 7.35 to 7.45, that's gonna be your normal pH range. We'll continue to use that. If I give you an example on an exam, that'll be based on your clinical prior knowledge of 7.35, 7.45. Now I've said it in lecture, so now you're responsible for it. Right? So if I give you pH of 7.1, you're gonna know that that's acidotic. If I give you a pH of 7.5, you're gonna know that's alkaline. Can anybody see any acid base questions on the exam? Like, AVG questions on the exam? Oh, yeah. It's coming. Anyway, obviously, what we're talking about here is we're talking about arterial pH. Right? 7.35 to 7.45 inch arterial pH that we're primarily concerned with. Alright. Intra saver pH is gonna be a little less than plasma pH because you're gonna have those cells producing acid, specifically carbonic acid. And depending on the type of cell, this is kinda what I was talking about earlier, pH can be anywhere from 6 to 7.4. So a parietal cell that is creating vesicles of hydrochloric acid in the stomach or a really active, metabolically active cell that's producing a lot of carbonic acid can have a PHS 6, but what you're going to notice especially when you get the respiratory, section typically that acidotic intracellular environment is also going to cause that acid to be able to leave the cell easier than, than any other type of cell. So just by the fact that they produce more carbonic acid, that's also going to allow them to get rid of that acid easier because of the oxyhemoglobin dissociation curve, because of 23 DPG, because of these things that are offloading, either oxygen or offloading hydrogen. Alright. The pH of urine, and we talk about this in more detail later on in this lecture. 4.5 to 8. So typically, 4.5 is gonna be the lowest your your urine pH can be. That probably has something to do with the epithelial cells of the urethra, and the ureters and the bladder not really being able to tolerate, hot lower, excuse me, lower pH is more acid than about 4.5. So what you're what you're doing here is you're going to get rid of so much hydrogen that that's causing your pH to fall, but what your kidneys will start to do is bind that hydrogen to things like ammonia so that it doesn't count against your free hydrogen load in your urine because your your tissue, specifically your tissue of elimination, your urethra, and things like that don't want that highly acidic urine. Does that make sense to everybody? K. Let's see. The hydrogen concentration in the, stomach is 4 10 times greater than the hydrogen concentration in the blood. So this is what we're talking about earlier. You've got, 3 main systems that are controlling this hydrogen concentration. So, you'll notice it does not say we're controlling bicarb concentration. Everything is focused on hydrogen. Everything is all about hydrogen. Do I need hydrogen? Do I need to get rid of hydrogen? The bicarb is going to be a byproduct. It's gonna be buffering, but what we're trying to do here is either get rid of hydrogen or hold on to hydrogen. So you have the chemical acid based bumper system, which we're gonna talk about in the body fluids. That's gonna prevent excessive changes in hydrogen. You're gonna have respiratory center, that's gonna regulate the removal of c02 from the extracellular fluid, and then you're gonna have the kidneys, and that's going to either excrete alkalotic or acidotic urine. Again, the ceiling on how acidotic that urine can be is gonna be what? 4.5. PH of about 4.5. Right? Typically, the most alkalotic it's gonna be is gonna be about 8. The buffer systems are not necessarily eliminating hydrogen from or adding hydrogen to the body, but keeping them tied up until balance can be reestablished. Well, you can look at this as insulin does not decrease your potassium. Insulin allows potassium to go intracellular. Alright? This is not decreasing hydrogen concentration. It's binding hydrogen. Does that make sense? Okay. Respiratory system is gonna act within a few minutes to eliminate c02 and, carbonic acid from the body. C02 and therefore carbonic acid from the body. So you got the first line, buffer system in the tissue and the blood. You got the second line, respiratory, and you got the 3rd line, which is gonna be kidneys. Kidneys, just like pretty much everything else, like we talked about regulation of blood pressure, kidneys was long term control. Right? Same thing here. We're talking about getting rid of hydrogen, kidneys are gonna be kinda long term. It's gonna be a long term play in getting rid of hydrogen. Most powerful of the acid based regulatory systems. What is your fastest, compensatory mechanism? It's gonna be kind of the tissue, but, you know, if you, Scott Hartman, just because I'm looking at you right there. Hey, buddy. If I were to have you right here on this OR table and I had an IV connected to you and I said, you know what? I'm gonna inject carbonic acid into your IV. I don't know. They don't like injecting carbonic acid in your IV. What would you do, Scott? What would be your physiologic response? Probably you breathe a little faster. Yeah. You would do your minute your entire medical issue, high volume and your respiratory rate both would increase significantly very, very quickly. Within within seconds, you would start to your body would notice this increase in hydrogen ion concentration, and you would increase your minute ventilation, very, very quickly. Now what would happen, Scott, if I were to intubate you or I paralyze you and then inject carbonic acid into you and have you on a set minute ventilation on the ventilator? I I couldn't make the compensation. You would either have to do it. It would reflect on a blood gas, or we would have to wait for my kidneys to pick up for it. Yeah. Where would I see just curious if anybody can join in. I'm not picking on Scott yet. Hopefully, you don't see that as me picking on. Where would I see that? Jamie? Jamie's raising her her My real hands? Real hands? In type of c o 2. End tidal c o 2. Okay. So what would happen to the end tidal c o 2? It would increase because you're not breathing off the c02 because you're at a set rate. Where's the c02 coming from? From I'm giving him carbonic acid. Where's the c02 coming from? Is it not from the Henderson though? Yeah. Carbonic anhydrates and hydrates. Harmonic anhydrates is cleaving the hydrogen and the bicarb. And then if you go the opposite direction, you have water and c02. Right? So when I exhale, what do I get? I get water vapor and c o two being released. So the end title what are we saying end title? At the end of exhalation, I'm reading a c o two. At the end of a tidal breath or at the end of a breath, I'm reading a c02 level that is coming from this carbonic acid. My body converted carbonic acid to water and c02, and now I'm getting when I exhale now when I say exhale, I'm on a ventilator. So the ventilator is allowing for passive exhalation. So now all of a sudden I'm seeing my c02 go up. Every every time I breathe, if I just continue to inject and stop some carbonic acid, my c o two is gonna go up with every breath. It's just gonna continue let's say I put him on a carbonic acid drip because I'm evil like that. Right? So what's gonna happen? My c o two is just gonna hit c o c o two. His c o two is gonna continue to go up and up and up at the end of every expiration. Does that make sense to everybody? Okay. Now what would it also happen to his blood pH, his arterial PH he would become acidotic right his c 02 would be elevated just curious what would happen to his Bicar. Is Bicarb would do what? It is Bicarb would be buffering. Yeah. Bicarb would start to he would start to hold on to Bicarb because what's gonna happen? The kidneys now and we're gonna talk about this in a few, slides. His kidneys now are gonna go, we got way too much acid in this. They're screwing around with the vent minute ventilation on this ventilator. The kidneys are like, this is ridiculous. The the lungs are doing jack squat for us right now. Let's get rid of some hydrogen on our own and reabsorb bicarb because the kidneys are gonna have c o 2, and that c o two is gonna go through the tubular cell. Henderson Hasselbeck is gonna happen, and the kidney is going or the the individual, tubular cell is gonna get rid of hydrogen. So you excrete hydrogen, and it's gonna reabsorb bicarb now. So it's like, okay. The the wrongs weren't working because I put him on a ventilator, stopped his compensatory mechanism. Now, Scott or no. Scott, you don't have to necessarily have to answer. Let's say I take you off the ventilator. Right? And I reverse you. I give you 16 milligrams per kilogram of and completely reverse your paralytic. Don't get hung up in that, but you're completely reversed now. What what are you gonna do, Scott? Increase the minute the wet ventilation on my own? Yeah. You're gonna be breathing probably faster than you've ever breathed in your entire life. But see what I did is I took away that respiratory compensation, and now the kidneys are having to do it long term. It's that going to automatically, is that going to do a very good job in the short term of buffering your PH? No. It's gonna do a good a better job in the long term. But what you really needed was that respiratory compensation that I took away. Does that make sense? So what would happen, Scott, you're the kidney now, but give me some numbers. Like, how fast is your respiratory rate? 30. 30. And what's your tidal volume? Let's say a liter. Let's say a liter. Okay. So his tidal volume is 30 liters a minute. Damn. That's a lot. Right? You're really bringing off a lot of c o two. You're really trying to compensate. So what would happen then, Scott, if I looked at that and didn't realize that, maybe I came in to relieve somebody and didn't realize that you had gotten an infusion of carbonic and carbonic acid. Excuse me. I'll do that a couple of times. I'll say carbonic and hydroxy, so I mean carbonic acid. Carbonic acid and, I didn't realize that you've got that infusion. They had already taken it down and I'm like, oh, his manipulation is 30 liters. That's crazy. What would I maybe wanna give you? What would I see that as a sign of? Christina, I can't hear you. You're you're muted. Well, isn't, hyperthermia? Okay. Maybe I see that as a sign of a leaky hyperthermia for me, but your body temperature is small. And maybe I just think that the CRNA I'm just relieved is a kind of a dummy. Maybe they're too awake? Patients in pain? And Patients in pain. Patients in pain. So, awake, that would be entitled, anesthesia gas concentration or maybe a BIS by spectral index monitor that gives me a quantitative measure of the, level of sedation. But now I'm gonna say that they're in pain. So then I start to give, what what drug do you wanna give? You guys have had your opioid lecture? Ben. Same junk though? Some dental probably. Do you know? Okay. How much dental you wanna give, junk though? I don't know. 50 bikes? 50 bikes. Okay. What are we doing to, their respiratory rate with 50 bikes a pickle? You're gonna knock out my own compensation. It's 30. Let's say we decrease it to 26. Is 26 still too high? Yeah. So we get some more. I wanna get them down to 12 so they have a nice smooth wake up. Now granted, I'm not paying attention to the fact their entitled c o two is 55 or 65. So I'm gonna give some more fentanyl. I'm gonna give a 100 mics more. Now I'm giving a 150 mics, and their respiratory rate is 12. What am I doing to their acid base balance? They're taking out that compensation still Taking away the respiratory compensation. Exactly. Exactly. Taking away the respiratory compensation. Oh, by the way, Joe Phil, this patient is in renal failure. You're gonna hang on to that fence. Yeah. You probably just killed your patient because they have no compensation other than tissue, buffering. Right? Does that make sense? Sometimes you'll get patients, that are acidotic and, they're spontaneously breathing. You intubate them, put them on a ventilator, and what do you do? You do what you always do. You put them on, you know, 600 tidal volume rate of 10, and and you're not really paying attention to the fact that they were were respiratory they were in respiratory compensation, and you just took that away from them. Does that make sense? Right? Alright. Let's see what we have to say. Buffer. Buffer is any substance that can reverse bind hydrogen. So this is, not anything, but you have buffer plus hydrogen, and this is a two way reaction. That's what those arrows mean. Two way reaction, and in this particular case, they are just as easily to dissociate into hydrogen plus the buffer as they are to associate into a combined molecule or combined, chemical. Not molecule. Chemical. So it's without buffering, the daily production and ingestion of acids would cause lethal changes in the body fluid hydrogen concentration. Do we ingest acid? Yes. What how do we ingest acid, Justin? We have citric acids. We have acids on candies, sodas, beers, all kinds of things. Yeah. I mean, you have acid in your diet. Acid is what makes things, taste tart. If you ever have something that's tart, some things that are savory are also, because of the acid hitting your tongue. If you ever drink, Coca Cola, water, hot fructose corn syrup, caffeine. Bosporic acid is the 4th ingredient in most Coca Cola, formulations. Bosporic acid, pretty strong acid. Courtney, what you drinking? I'm just kidding. Don't answer that. Alright. So the bicarbonate buffer system that we're talking about, we'll take a break here in about 2 minutes, is gonna be a weak acid, carbonic acid, and bicarbonate salt, such as sodium bicarbonate. So you get carbonic acid formed by the body by the reaction of c 02 with water. So we said, how do we get hydrogen equaling c02? You've all thought that for your entire ICU careers. You've looked at ABGs, and you looked at their p c o 2, and you also looked at their pH. The pH is for hydrogen. It's talking about hydrogen. You're saying c 02 high c 02 makes them have a lower pH. Because of the negative log relationship, the c 02 makes them acidotic. This is how c 02 is making somebody acidotic. So it's a small reaction unless you have carbonic anhydrase. Carbonic anhydrase, not surprisingly, is going to be, very specific in the type of tissues that it occupies. So you're gonna have carbonic anhydrates in the lung alveoli. Does it not make sense that if I have carbonic acid in the lung alveoli that I can quickly convert that to c02 and water? Oh, by the way, the lungs exhale c02andwater. That makes a lot of sense. You also have it in the epithelial cells of the renal tubules. We're gonna I'm gonna show you the same kind of renal tubule cell pictures that you looked at for multiple weeks now and show you how, this acid, the c o two, is entering from the the urine and, going back into the cell and being converted so that hydrogen can be ex excreted in the urine and bicarb can be reabsorbed or the the opposite of that occurs. Alright. Told you we would take a break in 2 minutes. It's been 2 minutes, so let's take a break. 5 minutes. See you. Testing 1, 2, 3. Testing. Simulance. Simulance. Okay. So we're talking about the bicarbonate buffer system. Somebody on the brink sent me a text and asked, would you also produce then more water? Technically, yes. You're gonna have more water production at the level of the alveoli, that could potentially be exhaled as water vapor. That also depends on the body temperature of, your patient and whether or not the the water has turned to vapor. You would not have so much water that you would have, like, fluid in the lungs and the alveoli, things like that. Remember, we're talking about microscopically not microscopically. No. It's the wrong word. Very, very, very, very, very, very small amounts of hydrogen that we're even converting because we are remember, it's like point 0. Right? We're we're doing such a small amount of hydrogen per liter just to maintain body pH. If you had that much hydrogen, you you would, quickly perish. You would cease to be. But, yes, technically, you would have more water production because you're going through this process. Alright. One thing I want you to notice, it says carbonic acid ionizes weekly to form small amounts of hydrogen and bicarb. You'll notice that the arrow here going from hydrogen, and bicarb to carbonic acid, the arrows are going both directions. But what it's saying here is that, carbonic acid is going to ionize weakly to form, so that's why this arrow is smaller going in this direction than that arrow going from hydrogen and bicarb to form carbonic acid is going in the other direction. Does that make sense to everybody? Yes? Ethan, I can't hear you. I saw your lips moving. I actually just saw your beard moving. Weakly just because it's a weak acid? It's ionizing weekly to form small amounts of hydrogen and bicarb, but in this case, not necessarily that it's, just because it's a weak acid. It is more likely to hydrogen and bicarb is more likely to form carbonic acid than carbonic acid is in the absence of carbonic anhydrase to form hydrogen and bicarb. Now that's what I mean. This is a smaller arrow. This is a longer A much longer arrow. So the showing the relative relationship of how easily these things are occurring. So, bicarbonate salt, and this just means we've added a metal to it, and the one that you all know that's sodium bicarbonate. You give that quantitatively, and this is going to form sodium and bicarb. So when you give sodium bicarbonate, what are you doing? Very quickly, the ionizes to form sodium and bicarb. So when you give that big huge syringe full of 50 m l's or whatever it is of sodium bicarb, are you increasing extracellular sodium? Yes. Because it's going to ionize very quickly and form sodium and bicarb. You want the bicarb, sodium is gonna be a byproduct of that. So this is going to be the entire, I guess, the entire buffering system, c o two and water, carbonic acid, hydrogen, and bicarb. And if you have sodium bicarb, you'd have sodium. But notice that it's going in either direction. If I have c02 and some water, I can make hydrogen and bicarb. If I had have hydrogen in bicarb, I can make c02 and water. It's going in either direction. Okay? Okay. This we've already covered. I'm not gonna I'm not the phosphate buffering system is going to be very, very weak and not not effective, not overly effective. I'm not gonna cover much on the soap of the phosphate buffering system at all. Alright. Proteins are gonna be important intracellular intracellular buffers. Like we talked about. You've got this big huge honking negative protein molecule, negatively charged protein molecule that is going to serve as a buffer. We talked about in blood how you have hemoglobin is gonna be a buffer. Well, proteins intracellularly are going to be a buffer. So let's see here. Most plentiful buffers in the body because they're high concentrations. Slight diffusion of hydrogen and bicarb through the cell membrane. And you remember, I think it was week or week 1, like lecture 2, to show the cell membrane and talk about the things that easily transfuse through the cell membrane right so. You're going to have it's gonna require several hours for you to reach equilibrium with the extracellular fluid from the intracellular. So you have hydrogen being produced and carbonic acid being produced in the cells as a natural product of cellular metabolism. Cells are producing carbonic acid. Carbonic ionohydrates is there. Hydrogen is being produced and that is going to take a little while for the cells to actually get rid of that hydrogen and reach equilibrium with the extracellular fluid is what it's saying. C o 2, though, remember, like we talked about week 1 lecture 2, maybe it's lecture 1, rapidly diffuses through all the cell membranes, and then you can have you can have that change in the extracellular pH. Now that's c o 2. So if it's hydrogen, maybe it has to go through the buffer system. If it's c o 2 that's produced, then c o 2 is rapidly gonna go through the cell membrane, and then it's gonna be, subjected to the buffer system extracellularly. Hemoglobin, important buffer. So 60 to 70% total chemical buffering oh, I'm sorry, Kia. I didn't see you. Did you have your hand up a while? Oh, yeah. I was just trying to let you finish up with that last slide. When I went through it, it was pretty confusing with what was going where, like, which direction to buffer what. Do you would you mind, like, maybe drawing a picture to show what is going on? Interesting. Can't draw. Do your best if you need it. You know I can't draw, but we'll we'll try. That's gonna be a cell today. And you have mitochondria in here that and you have, that are producing energy. Part of that energy production, you're gonna have CO 2 as a as a natural byproduct of that CO 2 and water is gonna produce carbonic acid and that's gonna further dissociate into hydrogen. Now the CO 2 can rapidly go through the cell membrane. That's week 1, lecture 1 or 2. We showed the cell membrane and how c o two can rapidly go through that. The hydrogen is pretty rapidly going to get buffered with bicarb and form carbonic acid. So if that stays intracellularly in here, then it's going to have to be converted to c02 to go into the extracellular space. Then that that will then be acted upon by the buffer system extracellularly. So c o two is gonna rapidly go across here, be extracellular, and allow for the the buffer system. Hydrogen is gonna rapidly, basically go, into with bicarb, form carbonic acid, and then have to be converted to c o two before it can leave and go extra sterile. That's why I'm saying hydrogen, it takes a while for hydrogen to finally buffer with the extracellular space because it's gonna have to go through that that chemical buffering intracellularly to form c o two so that it can rapidly go across the the cell membrane. That make sense? I'm just I don't I'm not understanding how the proteins are actually doing the buffering, the intracellular protein. Yeah. So the the definition of a buffer is the ability to take up a hydrogen. So if we're talk I'm sorry. I I answered the wrong question then if you're asking about proteins. If I can take up a hydrogen, then what have I done to the hydrogen load in your site? If I bind up a hydrogen so that it no longer has any activity. It's not a positive proton all by itself floating out there doing damage to my DNA. It's just a hydrogen, right, or doing damage to cellular walls or mitochondrial walls. It's just a hydrogen that is now bound up to this protein. So you've got this big huge honking protein molecule with a hydrogen stuck to it that, oh, I can't do anything with that hydrogen. I have buffered hydrogen until I can release this, allow it to be mixed with bicarb once the intracellular bicarb level is sufficient enough, form carbonic or excuse me, Form carbonic acid in the presence of carbonic anhydrase, then it's c o two and it goes out the cell. So what have I done intracellularly with this big huge green protein molecule? Is I buffered the hydrogen till I could put it through that chemical pathway to that pathway and get rid of the c02. Does that make sense? Yes. It's just like it's just like you. If you have, let's say you're acidotic, and I got you, Catherine, in just a second. If you're acidotic and I give you Bicar, okay, what am I doing by giving you Bicar? I'm allowing that hydrogen and Bicar to, to to I'm allowing the Bicar to buffer the hydrogen. So now that's together. Right? Until you can do 1 of 2 things with that. You're either going to exhale in the c o two or you're going to your renal tubules are going to get rid of the hydrogen. But me giving you bicarb is lowering excuse me, lowering your acid load, increasing your pH. Let's just say it the way it actually is momentarily until your body's physiology can actually get rid of the hydrant. Same thing here, intracellularly. I've got a big huge protein molecule. It's gonna bind up that hydrogen until my body's physiology can get rid of the c o two. Makes sense? Yes, Catherine. So does the hydrogen bind because of, like, the large negative charge of the protein, or is it a different reason? Primarily, what we're gonna be concerned with is the negative charge of of that, and it's the protein's ability to accept the hydrogen. Typically, that's going to be charge related because it's it's an ionic. It's an ionic, not mixture, ionic bond. It's an ionic bond, and that ionic bond is easily reversible. So if it were a covalent bond, that would be hard to reverse. But what we're trying to do is bind up hydrogen until our body's physiology can process that and get rid of extra hydrogen to be buffered up as well? So what we're talking about specifically here are gonna be intracellular buffers. We're talking about intracellular. Albumin is primarily gonna be an extracellular plasma protein. But are you talking about giving albumin and allowing that that to buffer? I'm sure it does have some buffering capability, extracellular. But specifically, what we're talking about here are the acids that are made intracellular. This is the first step. It's like, okay. You made some acid inside your cell. What's the first step? Do you need to buffer it? I'd say you can get rid of it through the other two mechanisms. But the albumin extracellularly probably does have some buffering capability. It's gonna be a negatively charged molecule, But you're still gonna have to go through steps 2 and 3 to actually get rid of the hydro. That makes sense? And, you have to also have to realize that if you're giving 5% albumin. You're not really changing their albumin level to a significant degree giving 5% primarily what you're doing there is giving volume Right? And you're increasing osmotic pressure, in the in the capillary or in the vessel so that you have this negative pull. You're not necessarily changing giving that much albumin. You're not increasing plasma protein load so much that it's becoming a buffer that is significant. I don't think because if you were trying to treat primary papalalbuminemia, what would be the drug you would give, Jake? 20.25 percent albumin? So yeah. You'd give albumin 25%. What's the volume of that? Much smaller. Much much smaller. Right? 250 of 5 percent albumin versus 50 cc's of 25 percent albumin. So you would have to give a bunch of 25% albumin ampules or whatever you wanna call it in order to increase albumin systemically enough to be a buffer, I I would think. Maybe it has some activity as, as a buffer. It would be better to get by card. Alright. DoorDash make it plan. I'm just kidding. And it's just a joke. Just a joke. Alright. Respiratory regulation of acid based balance. So this could be your second line of defense, and we've already talked a lot about this. But, before we do that, this is gonna be your end tunnel c o two waveform. So right here. Is where your c 02 capnographer or capnogram is going to measure your c02, and let's let's put some numbers here. 20, 30, 40. So our n title c o 2 in this example is gonna be 30. Right? 30. Now so what are we saying here? This is inspiratory phase. This is all inspiration that's occurring. This is exhalation that's occurring. So you get exhalation hold the exhalation at the end of exhalation right before you do an inspiration. This is where your CO two is gonna be measured and then you're gonna get an inspiration Couple of things you should notice here. What is my I to e ratio? In this example, how much longer am I exhaling than I'm inhaling? Is it 1 to 2? Yeah. Or 2 to 1. If it's I to e, it would be 2 times exhalation time. Right? Because this is exhalation. This is 2 times longer than this. I tried to draw it 2 times longer. Right? So Right? So much, shorter exhalation time. What you would typically see is inverse of that or actual physiologic exhalation, which should be about 1 to 2. I just drew it this way just as a as an example of a 2 to 1 instead of a 1 to 2. So right here, I'm gonna measure entitled CO 2. Have you guys already had this in another class? Okay. So we intubate a patient, and, we are giving them a minute ventilation of 700 times 10. 10 is gonna be my respiratory rate. Tidal volume is going to be 700. So I'm ventilating them, oh, at a minute ventilation of 7 liters a minute. Can you guys still hear me? Sorry. I I swear there's something that pushes the thing out as I talk. Pushes this little earbud out. And this is giving me an entitled c02 of 30 right here. K? And I'm ventilating this patient. Now what is something if I keep this 7 liters a minute, and all of a sudden, we've already covered this in another class. What would happen if my end tidal CO 2 now comes up to 40? What has happened? Joe Phil. I would say something metabolically is causing the rise in c o 2. Like, I think you mentioned in like, hypothermia, that'd be one of the first cases you'd see. Right? Yeah. Okay. No. We're just let's let's not say anything is wrong. Nothing's wrong. There's no pathology here. This is just happening. It's normal physiology. You wanna Christina's got her hands up, then Sam, then Jamie, then Justin. Alright, Christina. Is it a drop in blood pressure? Hold on. Our c02 went from 30 to 40. Okay? That's not exactly what I'm looking for. You're on the right track, but Sam? Oxidative, metabolism. So the more you perfuse, the more your CO two is gonna go up. So it's gonna increase your drive to breathe. So now my CO two is 40. So and if a steel 2 is 40, I have more hydrogen being produced because I have more metabolism that's occurring. And if I have more hydrogen being produced, I have more c02 because of that Henderson Hasselbeck equation that is being exhaled into my system. It's the same thing as giving Scott carbonic acid. I'm just doing it through my cells. I'm making more carbonic acid because I am perfusing more tissue. If I have an increase in blood pressure, I have an increase in perfusion. I have an increase in perfusion. I have an increase in hydrogen hydrogen production. I have an increase in hydrogen production. I have an increase in carbonic acid production. I have an increase in carbonic acid production. I have an increase in CO 2 production. Does that make sense? Because remember, the equation went either way. Right? So if I'm producing more hydrogen because of more perfusion, you'll see this all the time. You'll have a patient in an area of static ventilator. What do I mean by static? I'm not jacking with the ventilator. Nothing happened with the ventilator. I'm I'm 7 liters a minute, 30 minutes ago, and I'm still 7 liters a minute. Patient is intubated, and they are paralyzed, and I'm breathing for them. My CO 2 goes from 30 to 40. There's only one thing really that can cause that unless you have pathology in the lungs or something. And that's an increase in perfusion. I made more hydrogen. If I made more hydrogen like, so what's the opposite of this? I have an area of static minute ventilation, and I went from 30 to 20. Now my c02 is 20. What happened? It's the opposite. Somebody turn on your microphone and talk to me. What happened to this patient? Decreased perfusion. Decreased perfusion and what happened as far as vital signs? Decreased heart rate possibly and blood pressure? Decreased blood pressure. Decreased blood pressure. So if I have an area of static manipulation, I've been cruising right along, my patient's CO 2 is 30. All of a sudden, it decreases to 20. Wanna say all of a sudden within, you know, 1 to 2 minutes, all of a sudden, my CO 2 is 20. Most CRNAs are reaching for the phenylephrine while the blood pressure is cycling. They're not even waiting for the blood pressure cuff to finish. Just go ahead and get the phenylephrine because it was a decrease in blood pressure that caused the decrease in hydrogen production, that caused the decrease in carbonic acid production, that caused the decrease in CO 2 production that went back to the lungs and caused a decrease in end tidal CO 2. Does that make sense? Are you on board? Uh-huh. So we're cruising right along, and, we gave some fetal eye print to that patient. And their heart rate decreased, their blood pressure increased, and their CO 2 came up from 20 to 28. What can I also do? Their blood pressure is now normal. Their CO 2 is 20 let's say it didn't come up to 28. Let's I'm gonna change the number. Came up to 26, but their blood pressure is normal. Their blood pressure is 120 over 70. It's a 123 over 50 45. No. I'm just kidding. It's 120 over 70. Right? So it's perfect. What could we also do to increase this patient's in title c02? And my my patient's in title c02 is what? 20 what did I say? 26? It's 26. Are they acidotic or alkaline? Alcoholic. Emmanuel, what do you think? They're alkaline. Right? What am I doing to their ability to push oxygen off to the tissue? I was thinking if you decrease the, reparations, it could go up. Mhmm. Yeah. Yeah. So they're alkalotic. I'm decreasing their ability to actually oxygenate the tissue. It's wanting to stay on the red blood cell. So what do I need to do to to offset this decrease in c02 is decrease the minute ventilation. I could either decrease the tidal volume or I could decrease the rate or I could do both. If I decrease the tidal volume, if I decrease the tidal volume to 8, instead of 7 liters a minute, now I'm 50, what, 50 1456 100 milliliters a minute. Right? If all I do is decrease the rate if I decrease the tidal volume by a 100 and leave the the rate at 10, then I've decreased the, minute ventilation by 700 milliliters. There does that make sense to everybody? Now instead of being 700 milliliters, I've decreased the minute ventilation to 63100 milliliters. So not 700. 7 liters. Now that's 63100. Hey, Jamie. So what is the time frame? Because I know you don't wanna do, like, a lot of stuff at once. So you notice a drop in your in total CO 2, and you gave phenylephrine. At what point then do you want to, like, manipulate the 26? So you have made the patient alkalotic, but is the patient in danger? Not necessarily in danger. It's not something you wanna keep. But if you notice the blood pressure is now normal and your CO two is still not what you want it to be, then maybe you make a subtle change to the ventilator. But, the change in perfusion changes c02 precipitously. So, I'll give you an example we talked about in this class. If you have a tourniquet on the lower extremity and they're doing a total knee replacement and it's been 2 hours with that leg completely, with a tourniquet on, you've got lactic acid being produced in all of that ischemic tissue below the tourniquet, and they release tourniquet. What's that gonna do to your blood pressure? It's gonna decrease your blood pressure. Right? What's that gonna do to your c o two? It's gonna decrease your c02 based on blood pressure. You may have a little bit of an offset of that because you've got c o increased c02 produced in that ischemic tissue. But for the most part, you're gonna get a decrease in c o two. If you have a patient and they have a a tourniquet on their leg, when they've let down that tourniquet, most CRNAs are just gonna go ahead and give the phenylephrine. But what you'll notice is you'll give or ephedrine or whatever it is you wanna give. You'll notice that the c o two will drop precipitously when that heart is stunned by that lactic acid, and you'll get a decrease in blood pressure. Or you get a decrease in cardiac output or you get a decrease in blood pressure. So, you'll get a decrease in c02. This is gonna be one of the one of the clinical questions you're gonna be asked the most. C CRNAs are famous for saying, I see something. Do you see something? Something has happened. What do you think happened? Joe Phil, what's happened? And the only thing that changed was their c o two. You're in between blood pressure cuff tanks, but the CRNA is going something's happened. Now my now I have a lower blood pressure than I did have because my minute ventilation is static. I didn't change my minute ventilation. Only one thing can change my c o two, and that's a decrease in blood pressure. Does that make sense to everybody? Okay. So I am done with this case. The surgeon's like, hey. I got 5 minutes. I don't care if they start breathing. They'll never tell you that, by the way. So it's time to wake this patient up. Their c o two is 30. How are we gonna how are we gonna get this patient breathing? Let's not worry about waking the patient up. How are we gonna get this patient breathing? What's our strategy? Joe Phil? You, don't lift their c02. You get them to trigger their own breathing. So So you wanna, like, give them carbonic anhydrase, like infusion? No. You no. Manipulate the vent to, lower your wait. Am I thinking right? Lower your rate of volume? No. I already know. Are are you asking me? Because I already know. I'm just joking. I'm messing with you. Yeah. You wanna decrease your minute ventilation. Right? Yeah. So if you decrease your minute ventilation, what's that gonna do to your c o 2? Everybody use your your fingers. Okay? So your c o 2 is now up here. And we talked about in this class already that you've got a certain c o 2, a certain hydrogen ion concentration in the, ventral respiratory group, the dorsal respiratory group, the pneumotaxis center, that entire part of your ponds and your medulla has a certain concentration of hydrogen ions that is going to cause you to start spontaneously breathing. I told you in the very first day of lecture, very first week of lecture, certainly, we all talked about how c o two is the primary motivator. I even did I put a, a sac probe on one of you and had you hold your breath? It was was it you, Joe Phil? It was you. Right? So if you hold your breath and c o two is the primary motivator to breathe, the c o two is gonna go up as I'm decreasing minute ventilation until I hit this trigger where you're gonna start to want to breathe. Now let's, let's take it the opposite direction. Let's say you're doing crappy anesthesia. Your c02 end tidal c02 is 46 just because you haven't really been paying attention. You're in the middle of the case, and now your entitled c o two waveform kinda looks like this. And the patient's starting to breathe over the vent. What could you do to make the patient stop breathing? Jamie. Paralyze them. Okay. That's one way. If they're not in pain. Let's say they're you're 10 minutes from being done and you don't wanna paralyze them. But you don't need them to breathe just yet. Jake, what do you say? Can you increase the respiratory rate to decrease their c o two levels so they stop rebreathing from their c o two level not being too high? Yeah. Yeah. So you don't have to give them narcotic. You don't have to paralyze them. Just increase their minute ventilation, drive their c o two level below this threshold, and they'll quit breathing. That make sense? And I do this all the time. If not that my patients breathe when I don't want them to. But if I do start to see a that's called a curare cleft, by the way. Where'd it go? Oh, did I erase it? If you have this type of situation and they're starting to breathe right in the middle of that exhalation, there's you're noticing they're starting to breathe. You can increase their minute ventilation, blow off all that c o not all of the c o two, obviously, but blow off a large portion of their c o two. And now you're gonna drive them below this level, and they're gonna stop breathing. Because what did you do? You buffered. You you made their seat go to exactly what you wanted it to be, and it's far below this threshold for them to start breathing. Does that make sense? K. Is that helpful for anybody? And, guys, we are manipulating this every day. Every day, we're manipulating this. So how do you get a patient to start breathing? Somebody tell me again. Decrease the rate, allow their c o two to rise a little bit. Which is doing what? Is it making them acidotic or alkalotic? Did I say this backwards a while ago? Acidotic. It's making them acidotic. Hopefully, I didn't say it backwards. It's making them acidotic. Is acidosis good? Is it good for my patient to be acidotic? It is for breathing. So we're being acidotic within the normal physiologic pH, but we're not being acidotic outside the normal physiologic pH. If you're trying to get your patient breathing and I come in and do an ABG and your pH is 7.2, you're not doing a good job. You're being way too aggressive with that apnea or with that decreased minute ventilation, and you are allowing that patient to retain way too much hydrogen, dropping their pH down too low, making them too acidotic. Does that make sense? K. Now let's say you have decreased your minute ventilation. You've driven your patient's seat go to up. You start to see this, this. I'm sorry. This on the, entitled CO two waveform and you're you take them off the ventilator, they're completely reversed, they have no paralysis left, And you're noticing it'll look like this. It'll start to go up a little bit at a time. And then all of a sudden you've got this. Not this. That was just me being dramatic. If you have this, you've got a problem. But okay. Now you've got this. Now this patient is breathing spontaneously all by themselves. Title volume is adequate. You're getting rid of gas. Their tidal volume's coming up. By the way, sevoflaurin, what's the effect on minute ventilation of sevoflaurin? Sevoflurane is the an inhalational anesthetic, by the way, in case you did not. Just joking. What is the effect on minute ventilation of sevoflurane? It maintains respiratory rate and has a slight decrease in tidal volume. It'll be good for you to know that. It's a nonpungent inhalational anesthetic that maintains respiratory rate and decreases tidal volume. So you're getting you're getting rid of cevoflaurane, and now your patient is pretty much completely, not awake, but they have hardly any gas on board. They're not having any of the deleterious tidal volume effects of seborrhein, and they have a good tidal volume and a good respiratory rate. What is that tidal volume and respiratory rate completely dependent upon? Two things. How fast is the patient gonna come back breathing? And and not how fast is the patient gonna come back breathing. How fast is the patient going to breathe, and what's the tidal volume once they are spontaneously breathing? That's the question. What's gonna determine that patient's respiratory rate and tidal volume when they are spontaneously breathing? If cerebral form pain is not the factor, is this useful for y'all? Can we move on? You good? Okay. C02. What is c02 and there's one other factor. O 2? Opiates. Opiates. So if you have remember, you've given them opiates. What you're doing is increasing that level that is caught excuse me. Sorry. Yeah. If you've given them opiates, yes, you are increasing that level required for them to breathe. If they are in surgical pain, you are decreasing that level required for them to breathe. So what does that look like? Let me draw it somewhere else. This, blue is gonna be your normal respiratory, drive to breathe. This is gonna be opiates, and this is going to be, surgical pain. K? So what's gonna happen? C o two is gonna go let's, which one do you wanna start with? Opiates? K. Patient's got a lot of opiate on board. C o two's gonna build up, build up, build up, build up, build up, build up, build up, all the way up here to the opiate level and then inspiration exhalation. Build up. Build up. Build up. Build up. What does that look like? Slow respiratory rate. K? Go over here. Surgical pain. Build up. Build up. Build up. Build up. Breathe. Build up. Build up. Build up. Build up. Breathe. Build up. Build up. Build up. Breathe. Build up. Build up. Build up. Breathe. What's that look like? Fast respiratory rate. Increased minute ventilation. What does this look like? This is normal physiology. This is you didn't even have surgery. You didn't have any narcotic. What about what is it dependent upon now? Hydrogen ions. Just how much you're metabolizing. And this is why your normal title respiratory rate's like 12 to 16. Surgical pain, 24, maybe. 30. 30. 36. Something like that. Really fast. Opiates, really, really slow. I told you, 1st week of class, Prince did not euphoria himself to death. In other words, the euphoria is not what killed Prince. What killed Prince was the fact that this number was so freaking high that he went apnea for so long before he was stimulated to breathe, or maybe it would completely went away and he didn't even have a drive to breathe. And it took away completely his hypoxic drive to breathe, so he just quit breathing, went anoxic, cellular death. Right? K. What would I do if I gave too much Fentanyl? If I gave a 100 and let's say I gave 250 mics of Fentanyl to somebody that is, Shelby Shelby size. If I give 250 mikes, Fentanyl to somebody Shelby size with very little little surgical stimulation, Is she gonna breathe, you think? No. She's gonna be basically in the same situation Prince was. He ordered some some, what he thought was like Lore tab or something on from an online farm. Pharmacy, and they ended up sending him Fentanyl. Right? That's what killed Prince. So he ends up taking Fentanyl. And, Shelby, we give 250 max of Fentanyl. She's not gonna wanna breathe. I need Shelby to breathe. I don't want to park Shelby in an ICU on a ventilator, which would be one option, but that's gonna make you look like a horrible CRNA. I gave too much Fentanyl. Sorry. Let me give you a report. So what do you do? What can we do? Jake? And you just give her an ARCAN? So she just had they split her open like a chicken at, the Dixie Stampede. They split her open like a chicken, and I'm a take away all of her opiate. Really, Jake? Are you being are you sadistic? Not all of it. And you you could dilute it like we learned and give her small little doses until her respiratory drive comes back without taking away her pain. Yeah. Exactly right. So, you know, I could take, 4 of Nar Narcan and dilute it into 10 cc's, make it point 04 of Narcan, and give her, point 04 at a time until I start to see what on the entitled c02. Put a bump. Now what's the problem with get doing that, Jake? Marcus, did you I did have a question. I'll just wait till he finish. I'm sorry. I was gonna Jake oh, I'm sorry. Go ahead, Marcus. I thought you said you'd wait. I'm sorry. Yeah. Finish up. I'll wait. Okay. Jake, what's the problem doing that? In giving her small doses of Narcan? Yeah. Let's say, bump her with Narcan. She starts breathing. I'm like, I look like a rock star. I'm not even charting the Narcan. Don't ever do that, by the way. I don't wanna take her to recovery. And I'm like, here she is breathing 12 times a minute. Doesn't she look pretty? Sorry, Shelby. She could still she could develop pain faster because you took away some of her? No. Nope. Nope. Nope. Jamie, what do you say? In 30 minutes, the Narcan could wear off, and she can go back into respiratory, depression. What's that called? Renarcitization. So your Narcan duration of action is shorter than your fentanyl duration of action. So all of a sudden, you renarcatize, and the Narcan, which is an antagonist, pulls away from the receptor sites, and the fentanyl can go back on to the receptor sites. And now all of a sudden, you've got a patient that is, apneic in recovery. Sam? I was gonna say that's because, it's a competitive antagonist, the Narcan is. Yes. That's right. Yeah. It's reversible. So that's how the fentanyl was able to go back and Right. Right. In the same position again. Yep. Exactly. Or even worse, your IC or your PACU nurse is like, I've got orders, and I just I can't be bothered with listening to patients today. So I'm just gonna give some. Everybody's getting on me. Woah. For everybody. Right? And then all of a sudden, your Narcan wears off, and the duration of action of Dilaudid is certainly gonna be longer than fentanyl and and Narcan. Right? That makes sense? So you have to be careful. It's called renarcatization. Now, Jacob oh, I'm sorry. Marcus. There you go. Marcus, you had a question. My question you kinda answered it a little bit, but let me just ask anyway. If you were trying if you were you thought you were in trouble, patient was in trouble, patient wasn't looking good, and you gave a higher dose than a 0.04, and you just kind of, like, did snatch all of those pain receptors. I know that was your consideration if you didn't wanna snatch all of the pain medication you gave back because she's a fresh case. Where would you where would your risk benefit, pragmatism fall? What would be my what? I'm sorry. Risk benefit? Oh, risk benefit for Yeah. Like, when when in that particular scenario, you know how you always say it's everything you do is based on risk and benefit. Where would you on, you know, probably Narcan's absolutely the right call. The wrong call was not charting it and not telling the PACU nurse. Like, take your Narcan syringe and hand it to the PACU nurse and say, what's your respiratory rate? I had to give her some Narcan at the end. And as you know, Narcan at the end. And as you know, great PACU nurse, the duration of action of Narcan is shorter than Fentanyl. So she renarcatizes, give her some more. You know? Or, how about this? This is gonna blow your mind. Give her some Nubain. Agonist, antagonist. Now I'm actually activating receptors and antagonizing the fentanyl. And there are places, you'll work probably clinically where you'll have Nuvane in your box for just such an occasion where you don't wanna take away all of their their, pain, their opiate. And so maybe you give Nuvane or Stadol or Tylen or something like that. 1 of the agonist antagonist. Alright. Let's see. C l two is formed in the body by intracellular metabolic processes, and we have covered that ad nauseam now. The c o two is going to go to the alveoli and the exhaled by pulmonary ventilation. If you don't know this, you're in the right place. B a c o 2 of 40 millimeter of mercury. I think you all know that. In the rate of metabolic formation of CO 2 increasing, the p c o two of the extracellular fluid is likewise increased. A decreased metabolic rate lowers the p c o 2. Nah. Nah. Told you. It's right there. Seriously, this is gonna be, one of those things that you're gonna get asked over and over and over and over again clinically. Anesthesia is really, really good at glancing at a monitor and being able to see the entire picture in half a second, and you'll get that way too. You'll you'll notice that your patient's c o two went from 31 to 29, and you haven't touched the vent. And if your pressure is a little labile, you'll be like, maybe they're maybe they're dropping a little bit. Like, you'll you'll start to notice these things. Just like we talked about with the plus variability. You'll you'll see plus variability, like, in glances. You'll you'll say, oh, that patient's dehydrated. You'll start to see these things very, very quickly. If the metabolic formation and CO two remains constant, The only other factor that affects p c o 2 in an in extracellular fluid is the rate of alveolar ventilation. Very, very, very, very important you understand that. And I've got arrows pointing the same different directions or the you know, pointing opposite directions. So what am I saying there? If the rate of alveolar ventilation remains constant, then metabolism is affecting the CO 2. And it's the only thing affecting the CO 2 if alveolar ventilation remains constant. In other words, if we have them on a set rate on the ventilator and we haven't changed it in 30 minutes, is I'll be able to prevent ventilation constant? Yes. So if we have a change in entitled c o two, it can only be one thing, the level of perfusion affecting the level of metabolism. Now can you have beta agonists like albuterol or isoproteranol or something like that? Joe Phil, I think I owe you an answer on a question about beta agonism. Saw that when I was prepping for lecture. But, if you have an increase in metabolism, sepsis, malignant hyperthermia, is that gonna affect your c02? Yes. Yeah. It will. Just curious. Was this helpful for anybody in understanding how all this works? I felt like lecturing today, so, hopefully, that's what we accomplished. This is just saying this is showing the change in pH associated with changes in alveolar ventilation. And, again, we are manipulating this every day. I work clinically tomorrow, assuming I'm strep negative when I go into the doctor this afternoon. And, I work clinically tomorrow. And what am I gonna do? I'm gonna manipulate my patients, minute ventilation, and change their pH to get them to this trigger area of c02 to stimulate them to breathe. I do it all the time. Who in here, shadowed a CRNA when you were getting ready for okay. Who in here saw, raise of hands? Who in here saw the CRNA decrease the minimum ventilation to get the patient breathing versus, don't raise your hand if this is true, turning the ventilator off? Who saw him decrease the minute ventilation to get the patient to breathe? Hussam turned the ventilator completely off? And who in here that saw him turn the ventilator completely off said, what are you even doing right now? You are dangerous. They're gonna write newspaper articles about you as the CRNA that killed this patient. The only person that that a vent off was an anesthesiologist, not a CRNA that I shadowed. Fair. And so what's the right answer, Jake? Decreasing your mid ventilation. What is the what is the negative risk versus benefit of turning your ventilator completely off? Why not do that? That decreases minute ventilation to 0. What do you build up CO 2 faster? What if you can't turn it back on? Then you need to you need to beg your patient rather than just leaving it on, decreasing your minute ventilation. Yeah. Yeah. I like doing, like, mouth to ET tube. Now I wanna have strep. But no. No. Let's say you can turn your ventilator back on. What's the difference? Decreasing your ventilator versus just making them apneic. Are you doing the same thing? You're making them apneic. Risk? Say again? Oxy to the brain. Are you making them hypoxic? What what determines how long you can go apneic without having hypoxia? C02 threshold. We haven't covered it. No. We haven't covered it, so I'll tell you. Functional residual capacity. So the functional residual capacity is the amount of air. And if it's a 100% oxygen, f I o two, it's the amount of air that remains in the lung after a normal exhalation. So if you are apnecd, you are still transferring oxygen, across your alveolar capillary membrane into your blood based on the amount of air that remains in your lung after a normal exhalation. So that's how you can be apneic and intubate somebody and then not drop their stats. Right? But that's not it. What's the risk versus benefit of turning your ventilator completely off versus decreasing the minute ventilation? Jamie, raise your emoji hand, Jamie. Go ahead. You wouldn't have the benefit of having the, waveform, your entitled waveform is what I thought. Oh, you mean so I wouldn't know what my c o two is? Correct. So you Like, how Ohio is getting? Yes, sir. Like, if Yeah. Like, opiates are on board or something. Yeah. But that's not that's not gonna be the main reason. Let's say I'm doing it, for only 2 or 3 minutes at a time, and then I'm giving them a ventilation. And that ventilation at the end of that ventilation, I'm getting a CO 2. So I'm allowing them to be apnea for 3 minutes at a time. Their option or their, sat is not changing, and I'm checking their CO 2 every 3 minutes to make sure it's not getting too high by bagging them. John? That's what I was gonna say. I feel like it wouldn't make their CO 2 go too high. If you're not not necessarily just their CO 2. Joe Phil, what do you say? Let's see if somebody can get it, and then I'll answer. Well, I feel like if you turn off the vent, you're increasing their acidity a lot faster so you could overshoot. So you're saying c02 too? Well, like, their blood gauge, they could be super acidotic, and you can't monitor it while you, like, see it on the. Let's say every 3 minutes, I'm checking. And you guys don't know this because you haven't done it, but your CO two is not gonna rise that fast. You're not gonna go from 30 to 60 with somebody with a normal blood pressure within 5 minutes. You're not gonna do that. So every 3 minutes, I'm gonna give them a good tidal breath, like a big 700 milliliter breath. I'm gonna check their CO 2 at the end of that breath. It's like, okay. Now I'm up to 42. I'm okay. Nikita, what do you say? I was just gonna say they're not probably breathing off their anesthetic gases either, So they're just gonna stay there, and they're gonna stay asleep for longer. Yep. I like it. I like it. So, this is not the answer. Give me just a second. I'll give you the answer. But, that's not the answer I'm looking for. But that is true. So think about this. You're getting ready to get a patient breathing and wake them up. Getting gas off requires minute ventilation. Right? Getting then breathing requires you decreasing their minute ventilation. This is this is why emergence from anesthesia is difficult because you have to decrease their minute ventilation to get their CO 2 up to a level where they start breathing, but their minute ventilation is the thing that gets the gas off. So they exhale the gas. This is why it's tricky. But that's not the answer I'm looking for either. Atelectasis. If you're not ventilating, your alveoli is collapsing. The number one cause of postoperative fever is atelectasis. So your alveoli is starting to collapse now. So it is it better to decrease their manipulation or take them off the vent? Depends on the risk of atelectasis. If you have a morbidly obese patient and they have a lot of mass on top of their chest, then maybe taking them off the vent is not the best thing because they're gonna have a lower functional residual capacity, and they're gonna be at a higher risk for atelectasis, for the alveoli to collapse. There's less air in the alveoli remaining at the end of an exhalation, so they're going to have atelectasis. Right? If that's not an issue for you, maybe taking them off the vent is okay. Is are you gonna form Adelactuses in 2 minutes? And Sam if Sam if we have intubated Sam and we reverse Sam and I take Sam off the vent, is that going to cause Adelictisis to make her apnek for 2 minutes? No. Probably not at all. But if we had somebody really, really big and they had this big central adiposity and they had all of this weight on their chest and I take them off the vent, are those alveoli gonna be crushed by all that weight? Yes. And they're gonna have atelectasis. So the answer to your question, just so we're all clear, is it depends. Do you take them off the vent, or do you decrease their minute ventilation? Well, it depends on what kind of patient you're looking at. Does that make sense? K. The trick is to know what you what you're dealing with and not to do something for somebody, when it's not, their physiology is not, advantageous for you. So you have a patient. Let's just fully make this, 360. You have a patient. You're trying to get the gas off, and you're trying to get them breathing. They come back. They're breathing 24 times a minute. What do you want to do for them? They're breathing 30 times a minute. What do you wanna do for them? They're breathing 36 times a minute. What do you wanna do for them? What do you wanna do? Pain management. You wanna give them pain management. What does that mean? You wanna you wanna do a tap block, or you wanna give them some opiates? Or what do you wanna do? Probably opiates at this point. I guess, depends on the surgery and what you know? Okay. Yeah. Okay. So we're gonna give some opiates. When I when I give opiates, I almost gave away the answer. What am I doing to the respiratory rate? Decreasing. Respiratory rate. What is that doing to my ability to get rid of the gas? Decreasing. What is the opiate doing to my level of consciousness? Decreasing. So what does your patient look like in recovery? I Taking forever to wake up, obtunded. Right? So now they have a decreased level of consciousness, and it's taken forever to get rid of the gas. Is that is that good for you? What would be another way to potentially do it? What could I do? Use their increased respiratory rate to get rid of the gas, and right before they wake up, give them a little bit of narcotic. Now is that ethical to allow somebody to physiologically show signs of pain so that you can use that to get rid of some anesthetic gas. Marcus, what do you say? I wasn't answering if it's ethical or not. I don't think it is. But I was gonna ask another question. Okay. Go ahead. Can you just change what you use? Like, last time we used Fentanyl, can you use something that works a lot quicker? Quicker than Fentanyl? Well, actually, no. Nothing works quicker than Fentanyl. You're right. Yeah. 30 seconds. Yeah. That's it. Alright. Okay. So you'll see this strategy used quite quite frequently. Maybe I don't drop them from, let's say, 30 to 12. Maybe I give them a little bit of Fentanyl, but allow their respiratory rate to be a little higher till some of that gas starts to wear off. And then right before they wake up, give them some more narcotic. Now I've used that increase in respiratory rate to get rid of gas, and so that patient will wake up a little faster. The other thing I can do is we've not we've not really talked about using, like, PSV Pro, like ventilator settings that artificially augment the minute ventilation using the patient's respiratory drive to help help get rid of some of that gas. K? And just so you know, the anesthetic dose of, inhalational anesthetics is 0.5% of MAC. 0.25 to 0.5 percent of MAC. So in other words, if you are trying to get rid of gas, let's say, c before ine's MAC is 2, theoretically, that patient is gonna have an entitled c before ine concentration of 0.5 before they even have a memory. So could you drive them down to about 0.6, 0.5, and then give them some narcotic? Because they're not gonna have any memory of that at all. Marcus, did you still have a question? Yes. Sorry. What I meant to say with the fentanyl thing was something that gets, that wears off a lot quicker. Like Remi fencing. Is that is that something that's like a is that a pluggable thing? So if you if you were to give Remi, Remi can only be given in a drip. It's super, super expensive. And if you've not been running it the entire time, as soon as you bolus it, you're gonna break you're gonna cause significant bradycardia. So Remy is not something you wanna use, Remy, not Remy Martin. Remy Fentanyl. Remy Remy Fentanyl is not something you wanna use short term. It's a drip. And, really, you wanna use it for an entire case. Yeah. So, no. But what you could do is you could ask the surgeon to inject some local so you don't have to give them as much narcotic. You can ask the surgeon, hey. Will you do a tap lock while you're in there? Will you inject some local anesthetic? Maybe you don't give narcotic, and this is kind of more advanced stuff. Maybe you give a bolus of max sulfate and the lidocaine drip. Maybe you do other things that aren't decreasing c 02 respiratory drive other than just opiates. The whole point behind this conversation is there's a lot of tools in our toolbox. Don't buy be myopic with your options. Okay. You guys good? Alright. Let's take 5 minutes. Everybody back? Marcus, did you still have a question? Okay. I'm a take that as a no. The hydrogen ion concentration is going to affect the rate of alveolar ventilation. And so if you think of the symptoms of diabetic ketoacidosis, If you think about any type of acidosis, what are you seeing? It's just like we talked about, with given carbonic acid infusion. What are we seeing? We're seeing tachypnea. We're seeing a rapid respiratory rate from the acids, that are in, that your body is producing. In this case, keto acids that are in that your body is producing. In this case, keto acids. A rise in plasma pH above 7.4 causes a decrease in the ventilation rate. So you all you all know that if you were to, hyperventilate, you, you've you made a 20 on Foster's exam. I knew he was gonna pull the rug out from under me, and you're hyperventilating. You're hyperventilating. You're hyperventilating. As you're hyperventilating, you're blowing off all this c o two. You're blowing off all this acid. And, no, what are you gonna do if you continue to hyperventilate? You're gonna pass out. And when you pass out, what are you gonna do? You're gonna become apneic for a period of time until your CO two level can rise to the level yeah, rise to the level to where you'll start a normal tidal breathing. Okay? Conversely, if you are hyperventilating, what did they use to what do they do in the movies? What do they give you if you're hyperventilating? Oh, you're hyperventilating. They give you a bag. Why? They're giving you a bag so that you will rebreathe your own c o two. Yes. It all makes sense, doctor Foster. We already knew this. Alright. So a respiratory compensation for an increase in pH is not nearly as effective as the response to a reduction in pH. Reduction in pH, acidosis. Right? If you become acidotic, what do you if I give you carbonic acid in your IV, what are you gonna do? You're gonna start having tachypnea. If you get a little bit too much bicarb in, you're not necessarily gonna decrease your respiratory rate. Why is that? Because your body needs oxygen. Oxygen is the other factor here. It doesn't hurt me it doesn't hurt me to have tachypnea because I'm oxygenating even better. But if I have a decrease in respiratory right now, I run the risk of the organism not getting enough oxygen in normal physiology. Does that make sense? So this is a negative feedback mechanism. If I have increased hydrogen ions, I'm going to get an increase in alveolar ventilation, which is going to decrease my p c o 2 and get rid of those hydrogen ions. So it's a negative feedback. So this is saying right here what we said on the previous slide. Aqualosis tends to depress the respiratory centers. The response is less robust than the response to acidosis. K? The other thing is alkalosis and acidosis, if you look at it from an oxyhemoglobin dissociation situation, acidosis is offloading oxygen to the tissue more rapidly than alkalosis. That's another thing you need to understand is that if you have a leftward shift of alkalosis, you're basically your oxygen saturation is gonna be better, but your tissue saturation is gonna be poor. Correct? Yeah. Let's see. How much more we got for the respiratory center? Alright. We'll stop right here, guys. I'm seeing some yawns and blank looks, so that's that's fine. We've actually covered quite a bit that was not on this PowerPoint. You are, gonna be responsible for everything we've talked about, specifically the anesthesia implications. So make sure that you go back and listen to this. I'll post this lecture just as soon as it's available. So, hopefully, tonight hey, Siri. Remind me to post lecture at 8 PM tonight. There you go. So we'll try and post this tonight so you guys can be reviewing that. Look for the concentration of urine and the calcium and phosphorus regulation, lectures to, to drop, within the next day or 2. And I love y'all, and I'll see you on Thursday. Thank you for all your wishes. Bye.Alright. So the respiratory system is buffering, and and we said this is like the 2nd tier of a 3 tier buffer system. You've got the tissue buffer system that you're gonna be your carbonic anhydrase and that Henderson Hasselbeck, and that's occurring, you know, like in the lungs. It's occurring in, in different places. We're going to have this, chemical tissue buffering. We're gonna have respiratory buffering, and this is going to be the effect of hydrogen on increasing or decreasing, depending on which way we're talking about, respiratory rate and effort. The buffering power of the respiratory system, it's gonna be 1 to 2 times as great as the buffering power of all the chemical buffers in the extracellular fluid combined. K? So, we said intracellular, we have proteins that are serving as buffers. Remember that? Then we said extracellular, we have this carbonic anhydrase, and we have the ability with bicarb to buffer hydrogen. And then now we're talking about respiratory and the ability to increase manipulation to, get rid of c 02 or, to, stop getting rid of c02 if we want to decrease our respiratory rate. And recall again that it said that the ability to get rid of hydrogen and c o two specifically is gonna be greater than the ability to, hold on to hydrogen by decreasing respiratory rate. Remember, it said, specifically that the ability to increase respiratory rate gets rid of hydrogen, the ability to decrease the respiratory rate to hold on to some acid, that's going to be diminished. And we've said because you don't wanna decrease minute ventilation too much because then you run the risk of making that organism hypoxic. That make sense? Okay. Alright. Let's see. Impairment of lung function can cause respiratory acidosis, and this shouldn't come as any surprise. If you have an inability to fully exhale like COPD, emphysema. Let's say you have bullae in your alveoli and in your bronchioles, and those bronchioles are not fully, exhaling or, excuse me, fully, getting rid of that, c o two that's in the alveoli, that's gonna cause potentially a respiratory acidosis. It's all it's saying. Other things that could cause a respiratory acidosis would be things like, a decreased respiratory drive. So, like, for example, if we were to give somebody Fentanyl, the first thing they're gonna have is, if you decrease the respiratory rate below a physiologic norm for them, within that physiologic window, they're gonna get that respiratory acidosis because you've decreased the respirations. If you have a metabolic acidosis, this means either you're getting rid of too much bicarb or you have some type of metabolic, end product, lactic acid, something like that that is, ketone acids, that are building up in the body that you are not getting rid of. Now we're gonna talk, about renal control of this acid base balance. We can excrete, like we talked about on Tuesday, an acidic urine up to about 4.5, a pH of about 4.5. Remember we said that the urethra and and all of the urinary epithelium is not really made, to excrete urine much more, acidic than that. So what we typically are going to do, we're gonna talk about this as we go through this lecture, is we're gonna bind hydrogen to other substances like ammonia. And, you'll excrete that ammonia without it having an effect, or or excuse me, excrete that hydrogen without it having a major effect on pH of the urine. K. So it kinda neutralizes that that hydrogen. One thing to and we talked about this in other lectures is that as you are excreting hydrogen, you are absorbing bicarb. So if you are excreting acidic urine or excreting hydrogen, you're it's almost like the 2 for 1. It's like, I'm going to get rid of hydrogen and reabsorb a buffer. It's almost like the body is like, I really don't wanna be acidic. Really don't wanna be acidic. So I'm gonna get rid of a hydrogen. Oh, and by the way, I'm gonna keep a, a bicarb. So each day, the body is producing about 80 milli equivalents of nonvolatile acids. What do we mean by nonvolatile? We say a volatile anesthetic. It means it can be vaporized and got rid of by exhalation. What do we mean here? Nonvolatile acids. These this is not c02. This is not something that can go into the lungs, be converted into c02, and exhale. It's not volatile. It's not going to be exhale. It's saying nonvolatile because they are not carbonic acid and therefore cannot be excreted by the lungs. Primary, mechanism of removal of this acid is gonna be through the kidneys. Okay. So you're going to, filter about 4,320 milliequivalents of bicarb, and almost all of it is going to be reabsorbed from the tubules. And that's going to be that bicarb that is present in step 1 of this buffering system. The extracellular buffering mechanism that we said was the first thing, way we buffer. So you're getting rid of that bicarb in glomerular filtration. You're reabsorbing almost all of it back in to your blood supply. Hey, Catherine. Hi. Can you give an example of a nonvolatile acid? Is that, like, lactic acid? Mhmm. Oh. That'd be a really good one. That was the first one that came to mind. Okay. Yeah. Ketone acids, you do, have some volatility with ketone acids. That's why your breath smells like acetone. But lactic acid, you more than likely can't perceive, lactic acid in somebody's breath, other other than them, like, exhaling a lot of c02 because they're also trying to get rid of CO 2 to offset the lactic acid. But, yeah, lactic acid would be one such example. Let's see. So if you have alkalosis, kidneys are secreting less hydrogen and failing to reabsorb all the filtered bicarb, thereby increasing the accretion of bicarb. So let's just say it this way. You if this works either way, if you're acidotic, you're gonna get rid of hydrogen. K. And you're also going to reabsorb bicarb. If you're the reverse, if you're alkalotic, you're going to get rid you're gonna fail to reabsorb bicarb, and you're gonna hold on to hydrogen. K? So it works both ways. So this is going to be in the nephron where, reabsorption of bicarb is occurring in different segments. Of this renal tubule. You'll notice complete filtration and in the proximal convoluted tubule, almost 85% reabsorption. Okay? And, again, this it's like this nephron is going, get rid of all of it. Give me some back. Give me some back. Give me some back. Let's fine tune this. Okay. Give me a little bit more back as it's going through. Give me a little bit more back. Okay. Now it's perfect. 80 to 90% is gonna be in that proximal convoluted tubule. So it's saying 80 to 90. This graph is saying 85. If I ask you a question on this, as long as you're between 80 90, you're golden. Don't worry about that too much. Don't get caught up in that. You'll notice 10% is going to be in the thick ascending limb of the loop of Henle. This is gonna be your metabolically active part of your loop, that thick ascending limb. We talked about sodium reabsorption is happening there. We, you know, we talked about that thick ascending limb is helping to, in the juxtromedullary nephron, establish that, concentrate med intramedullary, osmolarity through the thick ascending limb. Thick ascending limb is going to be very, active, physiologically active, and the proximal convoluted tubule in the case of bicarb is gonna be very active. So how is this working? As you have So you have sodium and bicarb. Let's just so we're doing some sodium and bicarb. This is in the tubular lumen. So this is going to be our, oh, this is gonna be our filtrate. This is gonna be urine, pre urine, pre PP, whatever you wanna call it. And we got some bicarb that's happening here, and we got sodium that's coming in here. So let's say we gave a patient some sodium bicarb that went in their bloodstream, went to their glomerulus. They filtered out all of that pre PP. Now it's going to be sodium and bicarb. K? That sodium is gonna be used for this counter transport mechanism to absorb a sodium and get rid of a hydrogen. Where this hydrogen comes from, we'll get to that in a minute. But let's just say a hydrogen is coming in here. Now we have carbonic acid. Okay? That carbonic acid is gonna further dissociate in the c o two and water. We talked about this on Tuesday. That c o two is going to be reabsorbed into this, epithelium. Okay? That c02 is gonna bind with some water that's inside the cell, again, to form carbonic acid. Carbonic acid carbonic acid. So it's like a little split, become this. This is easily transferred across the cell membrane. It's gonna bind with water, which is readily available inside the cell. It's gonna form carbonic acid in the presence of carbonic anhydrase. It's gonna split into bicarbon hydrogen. Now this hydrogen is gonna be affected by that sodium hydrogen counter transport. So it's like sodium and bicarb come here. Hydrogen gets kicked out, becomes carbonic acid, c02 and water. That c02 comes across, goes up this, forms a new hydrogen, hydrogen comes out, and it's a cycle. Does that make sense? K? You guys already know all this. Right? The sodium we're using notice there's no ATP here. There's no ATP here. There's a sodium potassium ATPase pump here. I'm pumping sodium out, decreasing the sodium concentration inside the cell. Y'all good, Sam? You good? You good? Okay. I was just making sure, you're decreasing sodium inside the cell, which is making a concentration gradient allowing for sodium to come in the cell. This counter transport is then allowing the hydrogen to be pushed out. Jake. If this is hap this is happening in the ascending thick limb as well, I'm assuming? Or just It's saying all the active areas for this to occur. So if you go back to this, it's saying it's happening here, 85%. Here, 10%. So being that there's no water reabsorption in the ascending thick limb, how's that cell being replenished with water and not causing, like, cellular dehydration? Yeah. Great question. Water is a natural byproduct of, metabolism. So you're getting that as part of the Krebs cycle, producing ATP. Thank you. Yep. Okay. And I'm not saying that water from this is not coming across here. Probably not. Water is probably coming on down here, but you're talking specifically about the thick ascending. So I see your point, but you're also getting water inside the cell from the Krebs cycle. K? Alright. Let's see. Oh, so this sodium potassium ATP s pump, this is ATP. Remember, we're creation creating secondary active transport and counter transport from the getting rid of sodium constantly by the sodium potassium ATPase pump. Does that make sense? K. And that's what that's saying. That's what that arrow means. Alright. And, again, it's saying, urine pH is low as about of about 4 4.5 is what this can create, this mechanism. The secretory process begins with c 02 either diffuses into, Jake, into the tubular cells or is formed by metabolism in the tubular epithelial cells. That's also where you're getting the water. K. So, that's your effect of carbonic anhydrase. This is just saying all the things that we just said. Counter transport right here. Sodium's moving in. Hydrogen's moving out. I covered quite a bit just in that little, it's not it's like I don't even need to read this word for word. Yeah, Ethan. So do carbonic anhydrase inhibitors decrease bicarbryabsorption? Mhmm. Yep. And what is the side effect of carbonic anhydrase inhibitors? Diamox, metabolic acidosis. Justin. Doctor Foster, the, just below the ATP, sodium potassium pump, is that a co transport pump, or is that just bicarb and sodium leakage out of the cell? Below? Hang on just a second. Sorry. I had to grab something. Just below the ATP pump. It's cotransport. Sodium bicarb cotransport. Is that what that is? Yeah. Yeah. That's cotransport. Hang on just a second. Let me look at Diamox and just to make sure I'm telling you right. I don't give a lot of Diamox, and, I don't have a photographic memory. It I have a photogenic memory. Acetasolamide, adverse reactions. Let's see if you can see this. First one, metabolic acidosis. Does that make sense? I've seen a nephrologist, doctor Foster, give that for, alkalosis. What? I'm sorry. What now? I've seen a nephrologist give that for, alkalosis in the past that I had asked about it. I didn't know what it was. That's weird. Okay. I'm not sure. I'm not sure. Let me look at the adult indications. Glaucoma, glaucoma, altitude sickness prevention, edema, heart failure, seizure disorder, pseudo serum pseudotumor, cerebri. No. Urine alco alkanization. It alkanalizes your urine. K. So I wonder I wonder I wonder I wonder if that's the reason he gave it was to get rid of bicarb in that way. That makes sense. You're in alphanalization. Okay. Alright. Oh, I'm sorry. Joe Phil, you're saying you had a nephrologist give it because the patient was alkalotic? Yes. Oh, that makes sense. Okay. I'm sorry. I reversed that in my head and thought it was acidotic. Sorry. Just reversed it in my head. Okay. Bicarb is not readily permeating these membranes, and they have to be broken down into their component parts, c o two and water. I think we've covered all of this. Mhmm. Cover that. Let's see. There is a little bit of differentiation here that they're talking about. You have, a little bit different chloride and c02 exchange in the late segments of the proximal tubule, thick ascending loop of Henley and collecting tubules and ducts. And I don't see where they're showing that in figure 3 15, so just be good to be aware that you have chloride c o two, bicarb exchange. I don't see that they're showing it. So each time hydrogen is formed, an angel gets its wings. No. I'm sorry. Each time hydrogen is formed, bicarb is also gonna be formed, and you're gonna reabsorb that back. So would it not be cool if we're developing an organism that we get 2 for 1 every time we get rid of a hydrogen, we get bicarb reabsorbed back? What we're also gonna see is even with the nonvolatile acids and when we, make hydrogen attached to, like, ammonia, that is also going to give us a bicarb. So that's, really, really a really, really neat way of doing that. Let's see. So this is giving you the differentiation. Rate of tubular secretion is gonna be 44 100 milliequivalents per day in the rate of filtration. Bi bicarb is 4320, and the difference between that is gonna be, the, volatile acids, I think, is what they're saying. Sorry. Excuse me. Non volatile acids. Most of the hydrogen is not excreted as free hydrogen, but is in combination with other urinary buffers like phosphate and ammonia. That's what we talked about. Give me 5 minutes. Let's take a 5 minute break real quick, guys. Alright. Everybody back? Come on. Come on. Come on. Come on. Come on back. Got about 20 minute 20 seconds. Alright. Prime so primary active secretion of hydrogen in the intercalated cells. We've talked about the intercalated cells in the late distal and collecting tubules. We've talked about those before, and that's going to, secrete hydrogen by primary active transport. Again, this is not new information to you. You've had this in previous lectures. So this is primary active secretion. What are we seeing here? We're The ATP actively transport hydrogen out as a type a intercalated epithelial cell. Again, you've had this before. So that's, by doing that primary active transport of hydrogen. Hydrogen ion secretion is accomplished in 2 steps. You're getting the dissolved c o two in the cells, combines with water to form carbonic acid, and then the carbonic acid is dissociating into bicarb, which is reabsorbed in the blood plus hydrogen, which is secreted by this active transport ATP pump hydrogen pump. So this is gonna be a differentiation. If you see on the exam a picture of an arrow pointing at a part of a nephron, you need to tell me the means by which hydrogen is excreted from that epithelial cell. It likely will not be labeled. It will just be a picture of a nephron with an arrow asking you how hydrogen or bicarb, is secreted. I don't know that I'm gonna ask that, but makes sense that I would. Once again, 4.5 is gonna be the lower limit of your pH. The late distal tubule and collecting tubules, that's 5% of the total hydrogen secreted, but it's still gonna be important for maximally acidic urine. So what we're saying here is those collecting tubules, late, late distal collecting excuse me. Late distal, tubules and the, collecting tubules are maximally concentrating urine or maximally acidifying urine. This is your where you're fine tuning your urine to get it exactly where you want it to be. Let's see. So to excrete the 80 ml equivalents of nonvolatile acids formed by metabolism, it would require 2,666 2,667 liters of urine if you were doing this according to the old hydrogen in, hydrogen and bicarb and, you know, carbonic acid and then c02 and water, and c02 goes over and goes back through the Henderson Hasselback equation, and then hydrogen get excreted out. Like, that would require 2,667 liters if you were trying to get rid of nonvolatile acids that way. So what you're doing now is you're using things like the phosphate buffers and ammonia buffers so that hydrogen can bind with that. Those, hydrogen from those nonvolatile acids can bind with that and just go, excuse me, go, out of the urine in the urine. So if we were creating an organism that naturally produced ammonia as a part of its metabolic processes, wouldn't it make sense to use that ammonia as something that would bind with hydrogen from nonvolatile acids? So that's pretty beautiful how that works. And this is saying when there is excess hydrogen in the extracellular fluid, kidneys are not only reabsorbing on that filtered hide, bicarb, excuse me, but they're generating new bicarb and replenishing bicarb loss from the extra cellular flu. Excuse me. So under normal conditions, kidney tubules are secreting at least enough hydrogen to reabsorb almost all the bicarb that is filtered. Does that make sense? So you're filtering bicarb in glomerular filtration, and you're, secreting hydrogen so that you can reabsorb all of that bicarb. So these two processes, I gotta push one out to reabsorb the other. Push one out to reabsorb the other. That's the way you need to look at it. And then this is, this 4th point here is talking about in alkalosis, what we've already talked about. Hydratable acid and ammonia are not excreted in alkalosis, in systemic alkalosis, because there is no excess hydrogen available to combine with the nonbicarbonate buffer. So if you're looking at ABGs, and, yes, ABGs are coming. ABG analysis is coming in this class. You're looking at ABGs and you have a patient that is has metabolic alkalosis. You know? What are you looking at there? What do you what do you what are we talking about? Are you what's your bicarb level look like in metabolic alkalosis? Yeah. Your your serum bicarb is really high. Right? What would your respiratory, your c o two look like in metabolic alkalosis? C o two would would look what? I'm seeing some people pointing down and some people pointing up. So if I have 7.5, that's a 7, believe it or not. 7.5 Acidotic or alkalotic? Alcoholic. And and my HCO 3 serum HCO 3 is 32. What's my p c o 2? Oops. C o 2. Somebody give me a number. If I have respiratory compensation, what am I trying to do? What's that, Justin? I said 25. 25. Okay. Am I getting rid of acid by resp by tachypnea? No. No. Not in this case. Well I mean, like If I'm alkalotic Yeah. But I'm alkalotic. So it'd be what? Somebody tell me. 55. You want it to be happy? Yeah. 55. So my PCO so now I'm not tikitnik. I'm actually Brady Kinnick, if that's a word. It is a word. I've just said it wrong. Alright. Aldosterone. Aldosterone is gonna stimulate secretion of hydrogen by these type a intercalated cells by collecting tubules by the collecting tubules and ducts. This is going to add to all the wonderful, amazing things that aldosterone does in the human body. Hint, hint, exam question. If you have excess secretion of aldosterone like Conn's syndrome, you're gonna get increased secretion of hydrogen into the tubular fluid and increase the amount of bicarb added back into the blood, and that's gonna cause alkalosis. Conn's syndrome, primary aldosteronism, right here. Results in alkalosis. This is why. Also, you have inability of the kidneys to concentrate urine. That's because of the aldosterone. And then, obviously, hypokalemia and all that. So we're having a table here that's showing the major factors that influence hydrogen secretion and bicarb reabsorption. I do want you to understand this table. I want you to be able to recount for me facts from this table. So here, we'll make it official. Extracellular fluid volume depletion is stimulating sodium reabsorption by the renal tubules, And that's going to increase hydrogen secretion and bicarb reabsorption. That's gonna be through increased angiotensin 2 levels and increased aldosterone levels. Extracellular fluid volume depletion tends to cause alkalosis due to excess hydrogen secretion and bicarb reabsorption. When we talk about ABGs, we're gonna talk about the role of base excess in this ABG conversation that we have. That's coming. Changes in potassium concentration can also influence hydrogen secretion. High, a hypokalemia is gonna stimulate, and hyperkalemia is going to inhibit hydrogen secretion in the proximal tubule. Did I say that right? Anyway, like I said, want you to know this oops. Know this. Oops. Sorry. I want you to know this chart. Henderson Hasselbeck equation, acidosis is going to occur when the ratio of bicarb to c 02 in the extracellular fluid decreases. So they're specifically talking about bicarb and c02. They are not necessarily talking in this particular equation about hydrogen. The assumption is that hydrogen and bicarb are gonna mix, and you're gonna end up with c02 and water. But this is a different, pH formula. It's 61 plus the log of bicarb to, and the denominator is gonna be 0.03 times the p c o 2. Oh, in acidosis, the kidneys are reabsorbing all the filtered bicarb and contribute new bicarb through formation of ammonia and titratable acids. In metabolic acidosis, you're getting an excess of that hydrogen over bicarb. That's just the definition of acidosis. Again, some of this I'm I'm skipping over because we've talked about it numerous times, and you understand now that c 02 is equaling hydrogen, for our purposes. This is saying if you read through this, it's saying the same thing over and over again. If you have acidosis, you're going to basically try and get rid of hydrogen and reabsorb bicarb. Oh, and by the way, if you have acidosis, you're gonna get rid of hydrogen and reabsorb bicarb. And if you have acid dose, it's saying the same thing over and over again. This is gonna be, a precursor to our conversation about ABGs. This is what your pH should look like in each, one of these types of, events, acid respiratory acidosis, respiratory alkalosis, metabolic acidosis, metabolic alkalosis, you should know this formula is I mean, not this formula, but this chart as well. You should know what is the hydrogen concentration doing. It should be able to tell me what the p c o two is doing, what the bicarb is doing. So in respiratory acidosis, it's acidosis. So my per hydrogen negative log should be decreased. We should have a pH of 7.2, 7.1, something like that. Hydrogen ions is gonna be elevated. If pH is low, hydrogen is gonna be high. These are always always going to be an inverse relationship of each other. They're they're made that part of the chart easy to remember. P c o two should be really high because if it's respiratory, it's coming from the c o two. No problem. Right? Metabolic alkalosis. Bicarb, really high. You guys got it. You know this stuff. I am gonna give you actual ABGs on the exam, and you're gonna need to tell me you're gonna need to describe that ABG, in probably more detail than they're used to. So if you have metabolic acidosis, the primary compensation is going to be an increased ventilation rate. And I showed you Tuesday, you have somebody in diabetic ketoacidosis. What does the respiratory pattern look like? They're breathing 35 to 40 times a minute, and they are angry. Anybody ever taken care of a DKA patient? Aren't they all ill tempered? It's that glucose not getting into their brain cells. Right? The glucose can't get in because there's no insulin, and they're just angry people. Here's another formula for pH. I'm sorry. This is the that, previous formula for pH with bicarb and p c o 2. So, again, if you have alkalosis, you're gonna have a disruption in the bicarb versus hydrogen in the renal tubular fluid. Anybody have any questions over what we've covered today? I've skipped over quite a bit because it's repeating itself, and it's all about reabsorbing bicarb and getting rid of hydrogen or the reverse. And it depends on whether or not you have an alkalosis or an acidosis. I feel like to go over this, each word word for word and have it repeat itself would be too boring for you and for me. I'm just making sure we've covered everything. By the way, this value of p c o 2, if I ask you the value of p c o 2, here it is. But if you say 35 to 45 because that's what you learned in your Laura Gasparis portfolio CCRN review course, then that's fine. 22 to 28 bicarb saying, I don't care. I thought about doing a CCRN review course and, like, taking over the the the reins from Laura Gasparis from Prolia. Time for some new blood. Don't y'all think? Alright. Let's see. Saying the same thing over and over. Okay. Does anybody have any questions about what we've covered? Specifically, oh, a couple. Okay. Megan. As far as the ABGs are going, are we gonna go over some in class to know what Yeah. Yeah. Yeah. Yeah. No. Now that we've covered this, we're gonna look at actual clinical. That's what what we're gonna be on doing on Tuesday. We're gonna cover actual clinical ABGs and talk about what's going on in respiratory and in the kidney and, like, make all of this actually make sense in pathology. Is that what you're looking for? Yes. Thank you. Okay. Uh-huh. Jill Phil? Yeah. Kinda answer my question. I I guess, like, we'll probably go into, like, compensated, noncompensated, stuff like that. Right? Mhmm. And the base access point. Yep. Yep. We're just gonna make sure that you guys know ABGs backwards and forwards. K? Any other is anybody in here know ABGs backwards and forwards? Some people's egos are wanting to raise their hand, and some people don't wanna be called on in class. I'm rusty now since I haven't worked in a while. Okay. Yeah. We're gonna we're gonna cover ABGs and hopefully build upon the knowledge that you that you currently have or re reaffirm the knowledge that you currently have, kinda like we did with the EKGs. Like, let's let's really break it down and talk about Eindhoven's Triangle and lead 1, lead 2, lead 3, all of that kind of stuff. This is kinda one of those areas where I like to slow down and talk about the clinical implications because I want you guys going into clinical looking like rock stars. Will you do ABGs on patients intraop? Yes. You absolutely will. And are you also managing ventilators? Yes. You absolutely are. So you need to know this stuff. And are you given Bicar? And are you giving other drugs to alkalize or acidify or whatever? You know, are you dealing with septic patients that are producing lactic acid? Yes. You are. You know, you need to understand that you don't put a renal failure pat