DIP Episode 419 - Pulmonary Pathophysiology Series 10

Okay, welcome. My name is Devine. This is episode 419 of the Divine Intervention Podcasts. And into this podcast, we will be continuing our Pomonari Path of Physiology series. This is series number 10. And again, the goal of this series is to help you really understand Pomonology. Pomonology is a subject that many people just might really struggle with. They don't really understand it. And unfortunately, many resources just don't really explain things and explain them well. So I decided to break this subject open to bite-sized pieces that can just be really accessible to most people. So let's continue. So the last thing that we met, we talked about, I think I left off on this concept of FIO2 that you need to think about. You know, we said that atmospheric pressure is 760 millimeters of mercury. And we said that approximately 21 percent of that is oxygen. That's about 150 millimeters of mercury approximately. And then we said as you go to a higher elevation, the atmospheric pressure goes down. So let's see, it drops from 760 to 700. I just going to think of it this way. You know, pressure is a measure of force exerted over a giving area. I just kind of think of it as you go to a higher elevation. You are supporting less weight of air. So let's say you are at 1,000 feet, you're supporting more of a weight of air, more force than if you are at 10,000 feet. Well, there is that 9,000 feet of air that you don't have to carry.

So atmospheric pressure decreases as you go to higher elevations. So since atmospheric pressure is plummeting, it would then make sense that the 21 percent of that lower numbers should give you less oxygen. Right. So we said that, you know, as you go to higher elevations, there's less oxygen, the atmosphere, but it's still 21 percent of what you're seeing. And then I said that you should be especially careful with ventilators. Right. The ventilator questions really lead people out straight on the exam. Remember, and ventilator, you can adjust that 21 percent. You can make it not, you can pretty much give it, make it any percent you really want for the most part within reason. Right. So just something you want to keep in mind. And obviously, the higher you make that FIO2, the more risk of problems the person has. Right. Because again, oxygen, you know, just as there's such a thin ass high-boxy, there's also such a thin ass hyperoxy. Right. We never have too much oxygen on board because that causes an almost theoretical damage, but that's a different conversation. Okay. And then we also talked about PBG A02 where we say that is the measure of the amount of oxygen the alveoli. So some of you may think that, ooh, okay. This oxygen that is in the air, you know, when you inhale it, oh, you know, it's about 150 millimeters of mercury in terms of partial pressure. Oh wow, that 150 must stay as by the time you get to the alveoli. No, that's not really not true. That doesn't happen.

And by the time you get to the alveoli, the partial pressure of oxygen has decreased about 100. Right. So why is that? Well, if you think about it, I think you get to the alveoli. It's not only the oxygen that is contributing to the overall gas pressure. Right. In the alveoli, you have all the gases like carbon dioxide, especially, that contributes to the overall gas-spatial pressure. So I think of it as the carbon dioxide in the in the lungs, essentially diluting, diluting the oxygen-pastial pressure. Right. So the PBGEO2 kind of works out to about 100 millimeters of mercury. And maybe let me say something, in case you see it on an exam, so it doesn't throw you for a loop. Right. So FIO2 relates to the percent of oxygen in the inspired air. Right. The percent of oxygen. Well, sometimes in Pomonology world, this just term you may hear, known as PIO2. PIO2. PIO2, I means inspired. It just means the partial pressure of oxygen inspired air. So you can see that PIO2 term. Right. So PIO2 is what is about 150 millimeters of mercury. FIO2 is the 21%. Is the percent? FIO2 is a percent measure. PIO2 is like the actual measure. So FIO2 in the inspired air is like 21%. It can change. Right. PBGEO2. Right. PIO2, again, is the actual amount in millimeters of mercury of oxygen inspired air. I said that that's like 150. Right. And then I said PBGEO2 is about 100. I will talk about why it drops from 150 to 100. Right. And then we go to P little EO2. Right.

Again, is the measure of the amount of oxygen in the blood leaving the lungs. Right. In the pulmonary capillaries. This works out about like 90 to 92 ish millimeters of mercury. Right. So it's not going to be like, how to find? But the PBGEO2, the oxygen in the LVLI was like 100 millimeters of mercury. Like, dude, like what happened to that each to 10 millimeters of mercury that's gone by the time you get into the pulmonary capillaries. Well, think about it. The blood that's in the pulmonary capillaries actually mixes with less oxygenated blood in the lungs because the thing is many people just think the lung is the gas exchange organ. Remember, like, there's like actual stuff in the lungs that, you know, like need to eat, need oxygen for like, coluses and all those things. Right. So I'll viola need to live as well. Right. So because they need to live from the ametablesim, they produce some CO2, right, and things like that. So the blood that's coming from those notchered of your lie has less oxygen than the blood that's coming because it just got oxygenated from the LVLI. So the thing that happens is because you have that blood mixing that oxygen, partial pressure drops a little bit, right. It drops up on 90 to 92 millimeters of mercury. Now, if you understand all these things I've said, then we're going to go into the concept of the Ae gradient, the Ae gradient, right. Literally, what does Ae gradient? And Ae gradient is like big A, little A gradient, right.

So basically, what's the Ae gradient? The Ae gradient is essentially the spread between the oxygen, partial pressure in the LVLI and the oxygen, partial pressure in your pulmonary capillaries. Right. Basically, it's like your PBG02 minus your PLELELE02. Right. Usually, the normal Ae gradient is between 10 to 15. Right. Between 10 to 15, that's the number you want to keep in mind. Right. That's the number you want to keep in mind. Definitely, the number you want to make sure you keep in mind. Right. So just make sure you can calculate Ae gradient, right. Is your PBG02 minus your PLELELE02. And one factoid that's really helpful to know for Ae exams is that your Ae gradient increases with Ae. Right. In fact, there's, believe it or no, there's another formula for Ae gradient. We don't really need to know it, but it can kind of help you explain while while your Ae gradient goes up with Ae, right. It's like literally your Ae plus 10 divided by four is your Ae gradient. That's what your expected Ae gradient should be at your age. So say, for example, you're a 20 year old person. Well, if you think 20 plus 10, that's 30 and divided by four, that's 7.5. So you expected Ae gradient should be 7.5. But if a person is an 80 year old, well, 80 plus 10, that's 90 divided by four. If I'm going to math right, it's 22.5. Right. So your Ae gradient should rise with age. And some of you may be like, the divine, okay, I know you've given us the formula. Can you actually explain why this happens?

Well, think about it. As you get older, right, your body has gone through a lot of inflammation, a lot of fibrosis, right. So you may have like some mild fibrosis, some mild long changes that make it harder for blood to equal for oxygen in your of your life to equilibrate with the oxygen in your pulmonary capillary. Well, I mean, to equilibrate with the oxygen, your pulmonary capillary. Right. So that means that's spread just a little bit bigger, right. So your Ae gradient rises, okay. So it's pretty high to know that your Ae gradient is supposed to rise with with each. Right. Now, the thing is your PB, your P little AO2, you can actually measure it from an EBG, right. So what's an EBG? An EBG is an arterial blood gas. It's something that's done in almost every hospital in the US. You can easily measure it from an EBG, the P little AO2, right. But the PBG AO2 is really hard to measure. It's really hard to measure directly. It's almost impossible to live or not to measure it directly. Let's use some very sensitive instrumentation. But what is one way that you can calculate this, that PBG AO2, you example, or the PBG AO2, you example, you can calculate it by using the formula, it's called the Avio Lagasse equation, right. It's like 150 minus your P little AO2 divided by R, 150 minus your P little AO2 divided by R. So maybe like, huh, divine. What is R? Well, R is like a respiratory quotient, respiratory or coefficient. It's actually usually chosen to be 0.8.

It's literally the formula for that is like your CO2 produced divided by your oxygen consumed. Let me make it make sense because again, as much as possible, again, I know some people may be like, wow, divine. This pathophysiology series is taking a long time. But again, if you truly understand poem, there are many other things in medicine that will be like extremely easy to you. So R is 0.8 and R is calculated as your CO2 produced divided by your oxygen consumed. So you need to be like, huh, divine. Why is it 0.8? It's 0.8 and because usually, ideally, you would want the oxygen that you consume to match up one to one with the CO2 that you're producing, means for every oxygen you're consuming, you're producing one CO2, right. And that will make that ratio of CO2 produced to oxygen consumed one. But we know that the ratio is 0.8 is 8 over 10. So that means it's almost like, oh, for every 10 parts of oxygen your body consumes, you produce a path CO2. So why is that the case? Well, think about it. How many machines do you know are 100% efficient? That's a very simple question. How many machines that you can read with that are exactly 100% efficient? Or guess what? Not many machines. I mean, the body is probably one of the most efficient machines that exists, believe it or not, right. So literally, the efficiencies of converting the oxygen that we consume for the production of CO2 is about 80%. That's where that 0.8 number comes from, right.

That's where that 0.8 number comes from, right. So let's maybe delve a little deeper into this AA gradient of a thin. Before we delve a little deeper into it, again, I'd like to encourage you if you're taking your USMLE exams anytime soon, have a bunch of classes that will help you, have announced these before. I have an NVME Testic and Strategies class. It's for step two, step three, and for those taking shelf exams. And it's going to be taking place this Friday from 5 to 7 30 PM, Pacific Standard Time. This Friday the 21st, over Zoom. And then I have a bio statistics bootcamp that is for step one, two, step three, and complex level one, two, three. It's going to be taking place this Thursday. That's October 20th from noon to 4 PM, Pacific Standard Time. And then if you're taking step two, step three, or complex level two, or three, or you're present that's a 30-year medical student and you're like, I want to get a very good, strong overview of a lot of the mature that'll be tested on my shelf exams and I'll see on the words. The 20-hour review course I offer is going to be perfect for you. That's going to be taking place from Monday to Friday next week by God's grace, from noon to 4 PM, Pacific Standard Time. All of these courses over Zoom. Again, if you see the way explained things in my podcast, that gives you an idea of how I teach. And the classes are going to be based almost exclusively on case scenarios because again, you exam doesn't ask simple questions.

The questions are behind the clinical context. So if you want to be very good at clinical context, boom, that's a class you want to, these classes are things you want to attend. But let's continue. Right? So let's say, like I said, let's delve a little deeper into the EE gradient. So the EE gradient is extremely important. Because the thing is, it's very useful on exams. He's also just very useful clinically to determine or delete the cause of a patient's hypoxia. The cause of a patient's hypoxemia. Because of a patient's hypoxemia. Because the thing is, remember, I say that hypoxia is not the symptoms of hypoxemia. I've made that very strong differentiation in a previous podcast. I'm not going to waste time on that. So let's continue. Right? So whenever we're determining causes of hypoxemia, right? We just divide them into those that are associated with a normal EE gradient. And those that are associated with a high EE gradient, right? So anything higher than 10 to 15. Right? And the thing is, to be honest with you, sometimes it's just very difficult to reason through this stuff. But I'm going to break it down. If you understand what I'm going to teach you right now, then EE gradients are going to be like your bread and butter. They're going to be very easy for you to understand. Right? Now, let me give you a simple. Here's the same portal.

So two part rule, whenever you have a person that is hypoxemic, and the cause of the hypoxemia is a problem in the lungs, a problem within the lungs, your EE gradient is going to be increased. I'll say that again, whenever you have a problem that is needed to the lung, that the lung parankham is involved with, the lungs are not okay. Your EE gradient will be increased. That's rule number one. What is rule number two? Rule number two is whenever a person is hypoxemic, and that hypoxemia is caused by a problem that is outside of the lung. The lung is not involved. The lung is good. Then your EE gradient will be normal. You see many medical students, they take a list of, oh, normal EE gradient, they memorize a bunch of stuff. High EE gradient and memorize a bunch of stuff. You literally never have to do that. If you can just think and understand. Many people these days, they do not want to think. They do not want to think. Which is really unfortunate. Just take some time and think. If you just understand this rule, boy, does he solve a lot of problems for you? It's just going to make your life very easy. So let me maybe try to break down why this rule makes sense in the first place. Well, think about it. The very first thing you need to realize is that a normal EE gradient means that the ovuli and the vessels feeding the lungs are completely okay.

Because if you think about it, if you look at hypoxemia with a normal EE gradient, the one on the line principle is anything that makes your PB-802 low. If your PB-802 is low, you're almost certainly going to get some kind of hypoxemia. That is associated with a normal EE gradient. Your PB-802 is low. That's the underlying principle behind most causes of hypoxemia with a normal EE gradient. So if you think about this, essentially less oxygen is being admitted to your ovuli because your lungs are not okay. Your lungs are okay. Sorry, your lungs are okay. But it's almost like your lung is a machine and the input you're bringing in. So I said a few moments ago, lungs are not okay. That's not right. For a normal EE gradient, your lungs are okay. But your lung is a machine. The input you're giving is not good. Your PB-802 is low. A low PB-802 is the underlying path of physiology. Behind essentially every cause of hypoxemia with a normal EE gradient. You're bringing less oxygen into the ovuli. And remember, I said it a few podcasts ago that your PB-802 is the thing that creates your P-802, which is the thing that creates your S-802. So since your PB-802 is the primary determinant of your P-802, low PB-802 will also manifest as a low P-802. If your PB-802 is low, your P-802 has to be low. So since the low is happening on both fronts, the spread between those two numbers should stay the same. Right? Should stay the same. Should stay the same. Right?

Because here your lungs are working fine. Your ovuli is working okay. Your pulmonary vessels are working okay. So since those are working okay, the spread between those values should stay the same. It should stay close to normal. Right? So think about it really. What are some things that can cause you to have a low PB-802? Really any cause of respiratory depression. Right? Let's say for example, you take an opioid, right? Or you overdose on a buried rate or you overdose on a benzodiazepine or you have weak respiratory musculature. Think of these neuromuscular diseases. ALS, Lugeric disease, myestiniaegraphic, Guillain-Barrés syndrome. All these things, if you have weakening of your diaphragm, right? Your PB-802 will be low. But these are, notice all these long list I gave, has nothing to do with the lungs. These are all problems that are extrinsic to the lung. Right? All these things will cause a low PB-802. If you have a low PB-802, you'll have a low P-802. Right? Same thing goes for high altitude. When you go to a high altitude, it's not like your lungs just get destroyed. No. You're just going to a place that has less oxygen. So your PB-802 will drop. If your PB-802 drops, then your P-802 will drop as well. Right? Your drop as well. But the spread between those two will be the same because the lungs are completely fine. They're completely normal. Right?

Again, remember, the reason that your PB-802 drops when you go to high elevation is that the amount of oxygen in the inspired air goes down with high elevations. But remember, your F-I-O2, that's the percent of oxygen in the inspired air, stays the same at 21%. Again, some of you may be like, wow, divine, you're being very repetitive. But I'm telling you, the reason I'm being very repetitive is I've seen many people watch these things on exams. I do not want you to be one of those people. Right? So you just need to, you just need to be careful if you understand the stuff here. You're golden. Anything that lowers your PB-802 will cause hypoxemia with a normal EE gradient. Right? With a normal EE gradient. Just going to keep that in mind. Just going to keep that in mind. Right? So again, if you have a low PB-802, right? If you give more oxygen, then that should increase the PB-802 and that should fix the hypoxemia. I'll say that again. One of the easy ways to know that, hmm, I have hypoxemia with a normal EE gradient is many times that hypoxemia is typically responsible, responsive. Let me put it this way. It's typically responsive to oxygen, right? To give you an oxygen, right? Because again, this is almost like a novel concept that some people are not familiar with, right? You see some people they just think of shunts and this and that and they've memorized whatever. No, no, no, you can also understand it in this context because think about it.

Again, don't just stick with I'm saying as fat, reason through it. If I give you more oxygen, then your PB-802 will go up. Since your lungs are normal, then your PL-802 will respond and go up as well, right? So what are some ways you can give people more oxygen? You can give people more oxygen by giving more oxygen at a higher pressure or giving oxygen at a higher FIO2, right? So let's maybe just kind of delve a little deeper here, right? Think about it. I said that atmospheric pressure is 760, okay? And we said that 21% of that inspired air is oxygen. Well, imagine if by some magic, you could take that up on, you could take the pressure of inspired air from 760 to I don't know, let's say like a thousand. That will obviously give you more oxygen because if you're dating 21% of 760, right? As we did the math last time, we say there's like 159. But then if you think 21% of a thousand, that's 210, that's a big increase, right? So if you give inspired oxygen at higher pressure, then the person will get more oxygen. And guess what? Is there a fancy machine that can make this happen? Hmm, I don't know, like a ventilator. Ventilator can literally make this happen for you. Alternatively, you can give that same 760 millimeters of mercury of inspired air. But you just give it at a higher FIO2. It's almost like you're enriching that air for oxygen. Instead of 21%, you're like, you know what? Let's give it to you at like 30% or 40%, or 50% FIO2. Guess what?

Is there a magic machine that can do that absolutely yes? That's what a ventilator does, right? So if you do these things, you can literally fix. Those are ways you can fix hypoxemia, right? Again, hopefully you understand what I've just said. I feel like I've kind of given a lot of heavy stuff today. So I'm going to, I'm going to try to pause here, and I will pick up right from where I left off in the next podcast in the next podcast, because I really want to make sure that this is something that I sure don't know that you can say, you know what? Let me go back and release into this thing and really get it down. So as I do at the end of every podcast, I do for one or one tutoring for all the USML exams. Step one to three, complex one to three. The only thing I don't tutor to is women. And I also don't tutor the pediatric milestones because I've just never found it to make more sense to try to memorize. It's usually like a question or tone on exam. That's not going to make a, well, that can make a break a person's score, but like, it does just never really need sense to memorize to me. So that's something I've decided that you know what, never going to memorize this stuff. And then I do offer review courses for again, the USML exams. If you're interested in any of those or reach out to me through the website. And then I have these podcasts on Apple podcasts on Google podcasts and on Spotify. At least the most recent 150.

So go on those apps, look for the Divine Intervention podcasts and you can find them. If you want everything from episode one to episode 419, go ahead and check out the website Divine Intervention Podcasts.com. If you actually sign up with your Word Press account, I'll subscribe to my podcast with your Word Press account. You get an email notification whenever I make a new podcast. And then I have a You Tube channel, Divine Intervention, USML podcasts and videos. That's a You Tube channel where I make podcasts and post the videos that I make, Divine Intervention, USML podcasts and videos. And then finally, I have this new website called Divine Intervention Life Lessence.com. You know, I occasionally put life lessons at the end of these regular podcasts, but I got a lot of emails from people saying that Divine, I really love these podcasts. Is there a possible way to make more of them or something like that? So I was like, okay, fine. So I started a new website, the Bible Base website, Divine Intervention Life Lessence.com. There's actually an Apple podcast associated with it. Just look for the Divine Intervention Life Lessence Podcasts on Apple podcasts. Then basically every week I post two podcasts, they're about 10 to 20 minutes long. And they address like some problem that's faced by humanity from a biblical perspective. So if you're interested in that, go ahead and check that out again, Divine Intervention Life Lessence.com.

And then the life lesson I just want to leave you with today is think, literally think, think, think, think, think. I feel like we live in a world these days where people just go along with the crowd, they go along with whatever one is doing because they're not thinking. And in fact, I feel like these days one of the biggest problems that the US educational system has is that it trans people to memorize, it trans people to recognize patterns, but it doesn't train people to think. You see people, they're very good with patterns, but boy, they don't think at all. Are you wonder, man, why is the educational system going down? It's going down because people are not being trained to think. Critical thinking is a skill. I'm telling you this, even in medical education, medical education, unfortunately, many settings is being heavily watered down. People are not being trained to think. Honestly, sometimes I ask myself, what kind of exam strategy would really help people think and think better? The exams that just have a lot of like word problems, exams that cost people to really reason. That's one of the reasons why people hate the USMLE's and they're like, wow, this thing doesn't match up with my medical exam because many times medical exams do not train people to think, they train people to just recognize patterns and see those words and boom, right?

To be honest, we feel some of my best undergrad classes, where classes that have essay exams and those essays were based on not like tell me the definition of black glasses. No, no, no, no, no, no, no, you get a problem and then you have to walk through and tinker with that problem. Tinker with a problem is harder on the mind, but it's better for your learning long term. That's just the truth. I remember organic chemistry, you know, one of my one of my professors in college, he wrote these very intense questions and many people did not like his questions. To be honest with you, I was even in that comfortsome point, what man? After a while, I was like, wow, these things really forced me to learn organic chemistry. A lot of my exams were straight up essay exams. They were almost no multiple choice questions. Was it harder for the professor to grade? Absolutely. Was he really trying to help us? Absolutely. And some me say, that organic chemistry knowledge is useless. No, no, no, it's not useless. Even if you may not use the knowledge in your D to D practice, well, the thinking, that critical thinking, let me tell you this, sometimes education is not about the knowledge you're getting, it's about the mood of thinking that you're getting. Just being able to think. I'm telling you, if you can think, you can avoid many problems in life and you can solve many problems that arise on your path.

When you see many people, they don't have the attention on spam to sit down with a problem and groove through that problem. When you groove through a problem, then you are better able to use the experience you acquire to solve more problems in the future. Again, like if you're doing a nice Euro-T-Shift and you have a deep understanding of homonology, then you'll be able to tinker through a ventilator, tinker through why a patient has certain problems. Then imagine if you extend that, wow, that critical thinking, so not just homonology, but to cardiology, to renal and all those things, then you'll be a very good physician. Again, I'm speaking about this very passionately because I'm an educator, I love to teach. When you see many people these days, they just want the boss where they just want the boss phrase. And then you remember medicine is a trust, you're literally handling life and death. You want to be a physician, even fuck just put yourself in the shoes of a patient. A patient obviously wants a person that is competent at what they do. Not a person that has just learned and memorized algorithms. Ask yourself, those algorithms that you learned and memorized, why do they make any sense? Why were they set up in that way? Like for example, in my review courses, one of the things I teach is origin compatibility. You see many people, they just memorize the algorithm. You don't have to memorize the algorithm.

The algorithm actually makes perfect sense if you're just like, wait, okay, if I see this, what makes logical sense as the next step. That's where thinking is involved. When you see people in an organic chemistry, they're like, wow, let me just memorize the mechanism. No, you don't have to memorize the mechanism because all the person has to do is to give you a synthesis problem. That kind of looks a little different or it's novel. And then how do you reason through those things? What if you understand in organic chemistry, that wow, the primary being, the primary foundation of organic chemistry is that the rich give to the poor. The people that are electron rich use a bullet electron poor. You can almost instantaneously recreate a mechanism from memory. You don't have to like memorize anything. You can just literally predict, oh, this is how this mechanism should go. This is how the synthesis problem should play out. Same thing with physics. You see people, they just memorize the equations. No, no, understanding when you understand the physics problem. It doesn't matter how they write the question. You'll be like, oh, of course, this is the thing that makes logical sense to do. Or you see the same thing with bio statistics. You see people would even memorize all the formulas, memorize all the formulas. And then you get a word problem. You see them scratching their heads. And they know the formulas code, but they don't know how to think through those formulas.

And then they completely collapse. So again, I'm just encouraging you. Tray yourself to think. I know it requires more of an attention span. But let me tell you this. A longer attention span is one of the things that I predict was sites for a person that has enduring success. You need to have that good attention span. You see, unfortunately, in the technology world we live in today, people who have to switch from one thing to the other. They call it multitasking. Many times multitasking is just a failure focus. So I encourage you spend time thinking. I'm telling you if you're thinking man, you're thinking woman, you're present that reflects on life. You can get a lot more from life. So thank you for listening to me today. Have a wonderful rest of your day. I'll see you next time. Bye for now. God bless you.

$\text{FiO}_2$ is a percentage measure (e.g., $21\%$) of oxygen in the inspired air, which can be adjusted by ventilators. $\text{PIO}_2$ is the actual partial pressure of oxygen in the inspired air ($\approx 150 \text{ mm Hg}$).

Carbon dioxide ($\text{CO}_2$) contributes to the overall gas partial pressure in the alveoli, effectively diluting the oxygen partial pressure.

$10 \text{ to } 15 \text{ mm Hg}$.

The problem is likely within the lung parenchyma (e.g., V/Q mismatch, fibrosis).

Problems extrinsic to the lungs, such as respiratory depression (opioids, neuromuscular disease) or high altitude.

It should increase with age due to accumulated inflammation and fibrosis in the lung tissue.

The problem is extrinsic to the lungs (e.g., low $\text{P}_{\text{B}}\text{O}_2$ due to respiratory depression or high altitude).

There is a problem within the lung parenchyma (e.g., V/Q mismatch, diffusion impairment).

$\text{P}_{\text{A}}\text{O}_2 = 150 - (\text{PaCO}_2 / R)$.

Due to accumulated inflammation and fibrosis, which impairs the ability of blood to equilibrate oxygen fully in the pulmonary capillaries.

$0.8$.

Respiratory depression (opioids, neuromuscular disease), high altitude, or low inspired oxygen partial pressure ($\text{P}_{\text{B}}\text{O}_2$).

The problem is extrinsic to the lungs (e.g., low $\text{P}_{\text{B}}\text{O}_2$ due to respiratory depression or high altitude).

There is a problem within the lung parenchyma (e.g., V/Q mismatch, diffusion impairment).

$\text{P}_{\text{A}}\text{O}_2 = 150 - (\text{PaCO}_2 / R)$.

Due to accumulated inflammation and fibrosis, which impairs the ability of blood to equilibrate oxygen fully in the pulmonary capillaries.

$0.8$.

Respiratory depression (opioids, neuromuscular disease), high altitude, or low inspired oxygen partial pressure ($\text{P}_{\text{B}}\text{O}_2$).