DIP Episode 418 - Pulmonary Pathophysiology Series 9

Okay, welcome. My name is Divine. This is episode 418 of the Divine Intervention Podcasts. And into this podcast we'll be continuing the Pomonaig Path of Physiology series. This is going to be series number nine. Series number nine. So today we'll be discussing a lot of stuff in relation to ventilation and perfusion. And again I'll make it a goal of mine to go very slowly because this is something that you really need to understand. This is not something that you want to be struggling with. Again, if you understand the stuff, it's going to make so many things make sense to you. So let's just jump right into it for the sake of time. The very first thing you need to understand is all the tissues in your body need oxygen in one way or the other. That is just true. Every single tissue in your body needs oxygen in one way or the other to mediate metabolic demands. And how do these tissues get the oxygen? Well, they get the oxygen by virtue of the blood that flows to these tissues. Right? Blood flows to these tissues. That blood is carrying oxygen inside it. So the oxygen in that blood is what makes those tissues live. Now, let's then talk about the concept of this oxygen delivery. Because again, tissues need oxygen delivery to work right for literally the tissues to live. So oxygen delivery to tissues is really a function of two things. It's literally a function of two things. The first thing is that blood that's carrying the oxygen. How much oxygen is there in that actual blood?

Because if blood does not have much oxygen in it, even if it gets to the tissues, then that blood is not particularly useful to those tissues. So that's the oxygen content. And then the other thing that controls how much oxygen is delivered to a tissue is how when are those organs being perfused? So it doesn't matter. Blood can contain all the oxygen you want. What if that blood is not getting to the tissue that actually needs it? Then it's useless. For example, when a person has a myocardial infarction, the blood that may be proximal to the infarct may contain a lot of oxygen. But the blood that is distal to the infarcts, there's almost no blood flow. There's almost like a hundred percent occlusion of that coronary artery. The person's cardiac muscle is going to die. So the thing is when you're talking about oxygen delivery, there are two things you always have to think about. You need to think about oxygen content, which is the amount of oxygen in the blood. And then blood probably perfusion, like, ooh, is this blood actually getting to the tissues that need it? Now, this thing about perfusion, relates very heavily to cardiac output. Well, cardiac output is more of a cardiology topic. So who knows, maybe in the future, when we have a, I mean, I have a little cardiology podcast right now, but that's not the focus of this. So we're not going to spend too much time on cardiac output.

But the thing I want to focus on since we're talking about pulmonary pathophysiology is the blood oxygen content, right? And the thing is there are three factors that affect the oxygen content of blood, three. Now, what's the first one? Well, we know that hemoglobin is the primary oxygen carrier in blood. And the thing is with more hemoglobin, more oxygen can be carried. That just makes sense. Hemoglobin is literally the bus that moves oxygen around in the blood. If you have more hemoglobin, you can carry more oxygen. If you have less hemoglobin, see for example, you have anemia, then there are few fewer buses available, less oxygen can be carried. That's the thing. Now, the second thing I want you to keep in mind is that hemoglobin has four sets for oxygen molecules. It literally has four seats, right? So, yeah, remember the first factor we said is the amount of hemoglobin, right? But now we're zoning in. We're lasering in on each individual hemoglobin molecule. Hemoglobin has four seats for oxygen molecules. Well, all these seats can be fully occupied or they could be partially occupied. Obviously, if you want to deliver more oxygen to the body, you want all these seats to be fully occupied. You want this hemoglobin bus to be running a full capacity. You don't want this hemoglobin bus to have empty seats, right? So, this is what oxygen saturation involves. Your S little AO2, your S little AO2, right?

And the thing is, there are pathological conditions where there is poor oxygen delivery. Even if your hemoglobin is normal, because those seats are either not full or those seats are full with the wrong things, right? The hemoglobin bus is supposed to be carrying four oxygens. Whatever the hemoglobin bus is carrying a bunch of stuff like carbon monoxide that is not supposed to carry, that's not a good situation. And then the third item that relates to blood oxygen content is the oxygen that is actually dissolved in the bloodstream. That is what is known as the P little AO2, the oxygen that is dissolved in the bloodstream. The thing is, this third component plays a much smaller role than the other two items. Hemoglobin is the major thing that determines how much oxygen is being carrying your bloodstream. So, to kind of put all these ideas together, you know that people that are pulmonologists, right? You love to take all the ideas, you know, and then put it into an equation. When you see many people, they try to learn the equation first before they learn the ideas. Again, that's not the smart way to go. Because many questions you're going to see on your USMLA exams, many clinical problems you'll see do not depend on if you know the equation. No, it depends on if you actually understand what factors into those equations, right? So, let's then summarize all these ideas in the equation for blood oxygen content, right?

And you know, blood oxygen content sometimes we call that C little AO2, right? C little AO2. So, blood oxygen content is literally two things. The amount of oxygen that is bound to hemoglobin plus the amount of oxygen dissolved in your plasma. I'll say that again. Your blood oxygen content equation is made up of two parts. The amount of oxygen bound to hemoglobin, the amount of oxygen dissolved in the plasma. Again, as I've said, the stuff that's bound to hemoglobin is the most important. The stuff that's dissolved in the plasma is a little bit important, but really all the intents and purposes is not really a big deal. So, let's put that through in the first two days. Well, so you'll see little AO2. The first part, which is the amount of oxygen bound to hemoglobin, is 1.34, that's a million liters, 1.34 multiplied by your hemoglobin, multiplied by your S AO2, right? Again, remember, we said S little AO2 is the amount of oxygen that is on those, basically the level of saturation of those four seats on that carry oxygen on, on hemoglobin, right? So, 1.34 million liters times hemoglobin times S02. That's the first part. And then the amount of oxygen that is dissolved in the plasma is 0.003 multiplied by P little AO2. So, again, by seeing that 0.003 multiplier, that essentially expresses that idea that I said that, hmm, the oxygen dissolved in your plasma is actually not a big contributor to how much oxygen is actually in your blood. Okay.

So, now that you can understand that equation, let's then talk about hypoxia, right? So, hypoxia again is when there's decreased oxygen delivery to tissues. I'll say that again. Hypoxia occurs when there's decreased oxygen delivery to tissues. And to be honest with you, there are many, many, many causes of hypoxia. But one major cause that I'm going to be focusing on in this podcast, one major cause of hypoxia is hypoxemia. The thing is, many people love to conflict hypoxia with hypoxemia. Many people love to conflict hypoxia with hypoxemia. Hypoxia is the general concept of decreased oxygen delivery to tissues. Hypoxemia is just one cause, one important, one major cause of hypoxia. And just look at it in the name hypoxemia. Whenever you see that word, emia, it means, let me think about it like anemia. Anemia means you have low hemoglobin, right? Hypoxemia means that, ooh, there's low oxygen in blood, right? It means that there's a low oxygen content in blood, right? So, please remember hypoxia, hypoxemia, they are not the same thing. It's very important. Hypoxia and hypoxemia are not the same thing. Now, one other thing I also want to make sure that you understand is something that I like to call oxygen flow. It's just a concept that I'm making up, but it will help you really understand things. The thing is, oxygen has to get to your viola first, okay? That oxygen in your viola, like the oxygen tension in your viola is called P big A02.

After the oxygen gets to your viola, it then has to diffuse across the viola membrane and your pulmonary capillary membrane into the lumen, into that blood that is in the lumen of your pulmonary capillaries. When the oxygen gets to that lumen, that blood in your pulmonary capillaries, and it comes your P little A02, okay? So, your P big A02 becomes your P little A02. But then that blood in pulmonary capillaries, right? You know, has to, you know, flow around in the bloodstream blah, blah, blah, blah, blah, blah, blah, blah, blah, blah, blah, blah, blah, blah, blah, blah, blah, blah, blah, blah, blah, blah, blah, right? So, remember what I said, the oxygen gets from the lvioline to your plasma first, right? So, it starts off in your body in the lungs in the lumen of your viola as P big A02. It gets into the pulmonary capillaries, into your bloodstream, into the plasma as P little A02. But then that oxygen has to go from your plasma to your hemoglobin. When it gets to your hemoglobin, that's where we call that S little A02. When something gets into your bloodstream, we use the term little A02, right? Like a smaller A, a lower case A. But when something is your viola, that's where we use the big upper case A, just something to keep in mind. So, your P big A02 is the source of your P little A02, which then becomes the source of your S little A02. Oxygen has to get to your viola first.

After it gets to your viola, it then diffuses across the capillary membrane, into your pulmonary capillaries. That's where it becomes P little A02. Then after that, that oxygen that dissolves in your plasma then has to go to your hemoglobin. Hemoglobin literally gets its oxygen from your plasma. So, blood oxygen has to get to your plasma first before it can then be shuffled into hemoglobin. Okay, so now that you understand this oxygen flow business, let's talk about the oxygen content changes with different pathologies. Right? So, let's start with maybe carbon monoxide poisoning. Right? So, again, in carbon monoxide poisoning, your hemoglobin concentration, again, and the thing is, you see how the people try to memorize these charts. You don't have to memorize any of these charts. If you just understand all of them, same with blood oxygen content. Right? Like in carbon monoxide poisoning, carbon monoxide doesn't affect how much hemoglobin you have. The amount of hemoglobin you have is going to be completely normal. Right? Now, what does it do to your S little A02? Well, carbon monoxide poisoning will decrease your S little A02. I literally just said that they have four seats on hemoglobin for oxygen. If all four seats are occupied by oxygen, that's a good thing. But if those seats are either unoccupied or occupied by something else that is not oxygen, that's a bad thing. Carbon monoxide loves to hold onto those seats much harder.

In fact, like, it holds onto those seats like 250 times harder than oxygen itself. Right? So, your S A02 is going to go down. Your S little A02 is going to go down when you have carbon monoxide poisoning. And carbon monoxide deals mostly with hemoglobin. It doesn't really deal much with your plasma. For the most part, that's a reasonable approximation to make. Right? So, what happens to your epilidol A02? Nothing happens to your epilidol A02. Right? So, if you look at that oxygen delivery equation, that, ooh, 1.34 multiplied by your hemoglobin, multiplied by your S A02, that's one part, plus 0.003 multiplied by your epilidol A02. Well, you see that, hmm, that S A02 is down. So, if that S little A02 is down, that tells you that your blood oxygen content has to be down. Right? Or if you look at this from a methemoglobinemia perspective, when a person has methemoglobinemia, the hemoglobin concentration is completely normal. Like, literally, they have normal amounts of hemoglobin. But remember that the thin hemoglobin that actually really binds to that oxygen, in a sense, right, is iron. And that iron has to be in the 2 plus form. Right? Remember, iron can have different oxidation states. It can be in the 2 plus form, that's the fierce iron. It can be the 3 plus form, that's the ferric iron. So, in methemoglobinemia, iron is in the 3 plus form. That 3 plus form can literally not carry oxygen. But the 2 plus form can absolutely carry oxygen.

So, when iron is in the 3 plus form, it literally has no ability to bind oxygen. So, literally, it's almost like the boss is closed. You can't even put any oxygen on that bus. So, obviously, your S little A02 is going to be down in methemoglobinemia. But the amount of oxygen that is dissolved in your bloodstream, your epilidol A02, is going to be completely normal. Right? So, again, if your S little A02 is down, then your total blood oxygen content is going to be down. Now, think about it. How about a person that has anemia? If you have anemia, well, literally, it means you don't have an epilidol B02. You just don't have enough buses to carry oxygen. Each bus is carrying oxygen just fine. You just have fewer buses. It's not having like a thousand buses. You have 200. Obviously, you're not going to deliver as much capacity. So, your hemoglobin concentration is down. But your S little A02 is completely normal. All that hemoglobin is perfectly saturated. The oxygen dissolved in your plasma, your epilidol A02, is completely normal as well. So, obviously, if you have less in the world for hemoglobin concentration, then the total amount of oxygen in your blood is going to be up. And then, polycythemia. If a person is polycythemic, let's say they have a japtum mutation, in polycythemia there, well, remember in polycythemia, your hemoglobin concentration is going to be high. When you have those japtum mutations, your eyeplylosses are going to be very crazy.

So, your hemoglobin concentration is going to be high. And each of those hemoglobin are normal. So, the percent oxygen saturation of hemoglobin is going to be normal. It's going to be normal. And then, the oxygen dissolved in your plasma is also going to be normal. Your epilidol A02 is going to be normal. So, since all these things are going up, it would make sense that your total blood oxygen content should be increased. It should be increased. Again, just something to kind of keep in mind. Something to kind of keep in mind there on the exams. So, I know some people may be like, oh, divine. So, does that mean that everyone that has polycythemia has increased blood oxygen content? No, no, it doesn't. It literally doesn't. That's why, again, you need to understand. Like a person that's a COPD person, let's say you have like really bad infosima. If you have really bad infosima, you're like a big time pseudo-retainer. If you're a big time pseudo-retainer, then not much oxygen can fit into your lungs. So, your PB-G-A02 is going to be down. And if you think about it, PB-G-A02, I said, is literally the source of every thinner. Remember that thing I said with oxygen flow? Your PB-G-A02 is down. So, if your PB-G-A02 is down, well, your P-Lidol A02 is going to be down. If your P-Lidol A02 is down, then guess what? Your S-Lidol A02 is also going to be down as well. If the master is messed up, then the servants below him are also going to be messed up as well. That is just a truth.

That's why your body then responds and says, you know what? Let's make more Ipo. If we make more Ipo, we can create more, we can create more, um, um, um, hemoglobin, right, as our response. So, again, just kind of keep these things free because the thing is, instead of just memorizing the scenarios of giving you, if you just understand it, then it doesn't matter what the scenario is, you're still going to get those questions right on your test, right? And again, if you like the way I've explained things here, you may be interested in the USMLE courses that I have coming up this month. I have a biostatistics bootcamp. It's going to be taking place next week, Thursday, on the 20th of October, from noon to 4 p.m. Pacific Standard Time. I'm not going to just comment just dows you with biostatistics formulas. No, that's not the goal. Most of the USMLE step one to step three questions these days on biostats. They're not equation based. They are reasoning based. That course will really teach you how to reason through biostatistics. And then I have the MBME test taking strategies classes taking place next week Friday. That's for step 23 and for shelf exams. It's going to be taking place on the 21st from 5 to 7 30 p.m. Pacific Standard Time. I will teach you how to rationally and logically walk through MBME questions so that if you combine that with your knowledge piece, you can pick the right answers.

And then I have a 20 hour review course going to be taking place from the 24th to the 20th of October. That's going to be from Monday to Friday. It's going to be from noon to 4 p.m. Pacific Standard Time on all five of those days. We're view more than a thousand concepts from internal medicine, P surgery, OB-GYN, psych, neuro, biostats. We'll do some light biostats, but really if you really want to get a biostats basis, you want to attend a biostats bootcamp. We'll talk about ethics, communications, healthcare systems, multi-systems, processes, and disorders. And again, I'm not going to be giving lectures. I'm going to be using scenarios. Because again, I want to build not just your ability to learn, but also want to build your ability to solve problems. So by seeing things as clinical scenarios, that's just better prep for your exam because you're not just learning concepts, but you're learning those concepts in context. And again, I'm not just going to be giving you facts, giving you facts, giving you facts. I'm going to slow down and explain those facts so you truly understand what's going on. So if you really want to sign up for any of these courses, shoot me an email through the website, and I'll give you some more information. Now, the last thing I want to talk about here today, I want to define a few terms. And I want to define why those terms are the way they are. So the thing is sometimes on the US Emily exams, you'll see something referred to as a PIO2, right?

A PIO2, a PIO2. Basically, PIO2 is just a measure of the amount of oxygen that is in your inspired air, right? The amount of oxygen that is in your inspired air. This works out to about 150 millimeters of mercury. I mean, if you really want to be super semantic, it's probably like more like 160. But let me explain how we came about those numbers because it's just been raising that number. Like how did we get there? Well, we get there because the amount of oxygen in the inspired air is 21%. Okay, the amount of oxygen in inspired air is 21%. Right? And we know that atmospheric pressure is 7 at sea level, is 760 millimeters of mercury. So if you literally take 21% of 760, you should get a number that is about 150. 150 is the number you should come into memory for your exams. But if you truly took 21% of 760, it is not 150, right? I mean, literally 20% of 760 alone is 152. And then there are many 1% is like 7.6, right? So it's more like 159.6. But again, we're not going to go there. Just think remember 150, right? So the thing is the key critical thing you need to remember with this PIO2. Again, I'm not going to rush through these is to remember that your PIO2 changes depending on your elevation. I'll say that again, your PIO2 changes depending on your elevation. But the percent of oxygen is still 21%.

So if you're if you're in a very flat place like Florida that is right around sea level, and my heart goes out to the people that I'm going through hurricane, and in a pretty destructive hurricane, it's my prayer that you know things go away with you and you're able to kind of build your life back back up together. But in a flat place like Florida, that's like essentially at sea level. The atmospheric pressure there is roughly 760 millimeters of mercury. But if you go from Florida, all the way to a place like Colorado, that's many, many more feet above sea level. The atmospheric pressure is no longer 760. So it could be like 760, again, these are all approximations obviously. It could literally be 760 millimeters of mercury in Florida. And then if you go to a place like Colorado, it could be less than that. It could be 750, it could be 740. It could be some lower number. But even if that actual number is changing, the percent of oxygen in that number is the same, right? So it's still 21%. That's very important to understand. 21% of air is oxygen, right? And I'm going to explain to you how the USML could try to mess you up here. 21% of air is oxygen. So don't screw it up, right? So that's why people can become hypoxic when they suddenly go from a lower elevation to a higher elevation. If you've ever experienced this, if you've ever climbed a mountain or anything like that, you notice that as you're getting closer and closer to the top, you become more and more out of breath.

Well, why do you think that happens? Well, that happens because you're now taking 21% of a smaller number, right? When you were at sea level, you were taking 21% of 760. Well, let's say who are the top of the mountain atmospheric pressure is like 700 millimeters of mercury. While you're not taking, you're going from 159.6 at the bottom to 21% of 700, which is like 140, right? You're going to 140 for the most part, right? You're going to get very, very hypoxic in those circumstances. That's why people that are having my mountain climbers, they have to take up oxygen times with them. If not, they're going to die before they even get to the peak, right? And obviously, that's not a good thing, right? So the thing is, again, atmospheric pressure is 760, you dig 21% of it, right? So you definitely want to make sure you keep that in mind, right? So how can the USML Es kind of put you in trouble here? And I think after this, I'm going to stop here because there's a few more deep things I want to say, but I just think you'll be a little too much for this podcast. So be careful with ventilators, right? That's why you need to have some basic cursory understanding. Not need that, like in-depth, ICU attended on the standing events, we need to have some basic understanding, right? Because the thing is that 21%, we can modulate it with a ventilator, right? Like literally in a ventilator, we can give you what we want for your FIO2, right? We can give you a different FIO2.

FIO2 does not have to be 21%. Your FIO2, you can make it 100% in a ICU, put your event, give you 100% oxygen. Obviously, that's not something I want to do long-term because oxygen, free radicals, kind of torch the person's lungs, but that's a different conversation, right? So be very careful with ventilators. If they give you a ventilator question, look at the FIO2 that they're giving to you, right? Because you see some medicine and say, like, oh, 21%, 21%, no, it's not always going to be 21%. Sometimes that FIO2 can be 70%, it can be 80%, it can be 100%. And I can totally see our friends at the MBA meetings making these kinds of changes when you're doing a question about like a child that has something like new neural respiratory distress syndrome. Because those kids that have NRDS, they have very high oxygen requirements, or you can give your COVID-19 question on NRDS question or respiratory failure question, right? And then they modulate that FIO2. So that's just something I want to make sure you keep in mind with ventilators, P attiation to that FIO2, because that can change the gain in terms of measurement. So as I do at the end of every podcast, I go for one or one tutoring for all the USMEL exams, step one, just step three, pre-clean, cool medical exams, 30-ish-off exams, a complex level one to three exams. And I also help with applications. So one thing I'm doing a lot of now, I'm mocking interviews.

So if you're a person that needs help with mock interviews, again, I have a lot of experience with interviewing people. I have a lot of experience with going through people's applications. If you need any help with the ERS process, just reach out to me and I can meet you one on one and we can work on these things. And then another thing I also do is I do this thing called Logi Gin Note tutoring, where I work with you all through your pre-cleaned QI years. And usually if I work with you in that way, you're going to be super well prepared for step one. And I can also work with you all through your shelf exams. And then when it comes time for a step, you feel very well prepared. So that's something I also do. And I have these podcasts on many different portals. I have them on Apple podcasts, on Google podcasts on Spotify, at least the most recent 150. I also have a You Tube channel called Divine Intervention, USMELY Podcasts and Videos, Divine Intervention, USMELY Podcasts and Videos. That's where I post the videos that I make. And then finally, many people have told me that, oh, Divine, I love the life lessons you put at the end of some of your podcasts. So I decided to start a new website completely. It's called Divine Intervention Lifelessens.com. Again, Divine Intervention Lifelessens.com. And finally, there's an Apple podcast attached to it. It's called the Divine Intervention Life Lessons Podcast, the Divine Intervention Life Lessons Podcast.

And many of you that listen to this podcast, you know, I'm a Christian. And I have these 10 to 20 minute podcasts I post like two every week that just addresses some common problem that's faced by a lot of people in the world from a biblical perspective. Right now, we're, I think, more than 120 or almost 120 episodes. So there's a lot of really good stuff on there if you want to listen to that. So thank you for listening to me today. God will now continue the next podcast. I guess that'll be a episode 419. Very shortly. We'll keep, keep, digging into medical topics that can really help you excel on your USMELY exams. So thank you for listening to me today. Have a wonderful rest of your day. God bless you. Bye for now. Thank you.

Hypoxia is a general state of decreased oxygen delivery to tissues; hypoxemia specifically refers to low oxygen content in the blood ($P_{a}O_2$).

Oxygen bound to hemoglobin (calculated as $1.34 \times [Hb] \times S_{a}O_2$).

The oxygen saturation of hemoglobin ($S_{a}O_2$), because CO binds strongly to the heme sites.

$P_{I}O_2$ decreases because atmospheric pressure drops, even though the percentage of $\text{O}_2$ remains 21%.

Inspired air ($P_{I}O_2$) $\rightarrow$ Alveoli ($P_{a}O_2$) $\rightarrow$ Plasma/Hemoglobin ($S_{a}O_2$).

Both $S_{a}O_2$ and $P_{a}O_2$ are normal because the saturation of existing hemoglobin and dissolved plasma $\text{O}_2$ are unaffected.

$C_{a}O_2 = (1.34 \times [Hb] \times S_{a}O_2) + (0.003 \times P_{a}O_2)$.

Because iron is in the ferric ($\text{Fe}^{3+}$) state, which cannot bind oxygen, causing a drop in $S_{a}O_2$.

It decreases because atmospheric pressure drops (though the percentage remains 21%).

Increased, due to an elevated hemoglobin concentration ($[Hb]$).

Carbon monoxide binds to the heme sites with extremely high affinity, displacing and reducing the available oxygen saturation.

$C_{a}O_2 = (1.34 \times [Hb] \times S_{a}O_2) + (0.003 \times P_{a}O_2)$.

Because iron is in the ferric ($\text{Fe}^{3+}$) state, which cannot bind oxygen, causing a drop in $S_{a}O_2$.

It decreases because atmospheric pressure drops (though the percentage remains 21%).

Increased, due to an elevated hemoglobin concentration ($[Hb]$).

Carbon monoxide binds to the heme sites with extremely high affinity, displacing and reducing the available oxygen saturation.