DIP Episode 249 - Blood Oxygen Content and the USMLEs

Okay, welcome. My name is Divine. This is episode 249 of the Divine Intervention Podcast. And in this podcast, I'm going to be talking about a topic that I call oxygenation. This will be a physiology podcast, but I strongly suspect that it will help you understand many things that you may see like in cardiology or shock or pulmonary questions on your test. And it should be short and sweet. So let's go right into it. So one thing, I guess what I'll use as the launching point for my conversation today is talking about the formula for oxygen content of blood. Right? So we know that the oxygen content formula, right, is 1.34, right? That's in milliliters multiplied by the person's hemoglobin, right? Usually that's right around 15. And that's multiplied by the S little AO2. So the SAO2 basically is how much of your hemoglobin is saturated with oxygen, right? It can be any percentage from 0% to 100%. And then to that, you then add the P little AO2, right? You add the P little AO2. And again, SAO2 on an MBMI exam, they can refer to it as oxygen saturation. And then that P little AO2, right, is the amount of oxygen that you find dissolved in plasma, right? And then P big AO2, right, is the amount of oxygen you have dissolved in. I mean, you have a, you have a, you're right. So let's kind of talk about some of these things little by little one by one, right? And kind of like, let's see if that would, and I will give you a lot of examples.

I feel like this topic is best elaborated with examples, right? So again, P little AO2, right? Again, for example, the big thing there is the amount of oxygen that you have dissolved in your actual plasma, right? So it actually does not involve the oxygen that is attached to your hemoglobin in any way shape or form, right? That's actually very important to know. Because as you see, there are some things that do not touch P little AO2, but they touch the S little AO2, right? So if remember that that P little AO2, right? Like ultimately comes from the P big AO2, right? The oxygen that you find dissolved in your plasma must have come from oxygen that entered your view line in the first place. So if, for example, right, a person goes to a higher elevation, let's say you go to Colorado or something like that, when you go to a place that has very high elevation, right? There is less oxygen presenting that atmosphere. Remember the FIO2 will still be the same, right? 21% of the oxygen of the area you inspire is oxygen. That 21% is not going to change. You're just going to have 21% of less, right? Because the atmospheric pressure has gone down. So instead of having like 21% of 760, we have like 21% of 730 or something like that. But again, it's very high you to remember that the percent of oxygen in the inspired air is still the same. You just have the same percent of a smaller pipe, right? So again, as you go to higher elevations, right?

You owe to the oxygen tension in the atmosphere goes down, right? And again, when you have that P big AO2, that oxygen would diffuse across the Avila membrane and then ultimately getting to the, getting to the pulmonary capillaries, right? And one thing I will say, so what's the mechanism behind the hypoxemia in a present that has a low P little AO2? Well, the thing is the, so the way oxygen goes is oxygen goes to the Avila first. And then from the Avila, the fusus occurs the capillary membrane into the pulmonary capillaries and then becomes the P little AO2, right? And then that P little AO2, that oxygen does is also in plasma, then diffuses into hemoglobin, right? And mix of saturates that hemoglobin with oxygen. So when a person has a small amount of oxygen, right? Like a decreased P big AO2, they'll have a decreased P little AO2, right? And then that will ultimately lead to a decreased S little AO2, right? So it's almost like a chain reaction. So the thing is, the thing is, so maybe let me put it this way. Whenever you have a low P big AO2, you always have a low P little AO2. If you have a low P little AO2, you always have a low SAO2. The reason you may see me being very particular about these things is the NV Me, right? Like they, they like to give these arrow questions that involve this oxygen content equation. So it's something you want to be prepared for on, on an exam, right? So again, your oxygen saturation, your SEO to go down if your P little AO2 is done, right?

Now, let's talk about the S little AO2, right? This is probably the one that creates the most confusion for medical students. So the thing is, basically again, this is the percent of hemoglobin, right? That is saturated with oxygen, right? And again, is dependent on a couple of factors, right? So we said that it's dependent on your P little AO2. If your P little AO2 is low, right? Then your SEO2 will be low as well. Because again, your SEO2 literally is derived from your P little AO2, right? Another thing that can affect your SEO2 is that, because remember, hem contains iron, right? That iron, the oxidation number of that iron also affects it, right? So if the oxidation number on the iron is plus two, that's fair, sion, if it's plus three, that's very chyr, very chyr, has no ability to bind oxygen, right? Because that very chyr is already maximally oxidized, right? So it cannot be oxidized even further if you're thinking about things in chemistry terms, right? And whenever you have hem that contains iron in the three plus four, that's known as methemoglobin, right? And for the most part, remember that you methemoglobin, you'd actually measure this with a with a pulse-oxymeter, right? You'd actually measure it with a pulse-oxymeter, right? And for the most part, when a person, again, is high-poxymic like this, right? Again, you notice some things, I think I will maybe let me give a few examples. I think that will really portray this point, right?

So say, for example, let's say a person has a couple monoxide poisoning, right? For patients, couple monoxide poisoning, yeah, I think that's one, yeah, let me use, let me use examples. So if a person has couple monoxide poisoning, right? So whether some things that may classically cause this, right? It may be a person that you know is trying to commit suicide, they seem like a car exhaust, right? Or they may say something about a space heater in an NV Me system, right? Or they may say something about like a person being in a recent house fire, right? Or a person that uses some kind of stove at home, especially like those wood stoves, right? Those things can all cause a couple monoxide poisoning, right? And how does this usually present? Typically on NV Me exams, those people have headache. That's actually something very high up to know. The most common presentation of couple monoxide poisoning on NV Me exams is the presence of headache, right? So the person will have headache, right? And the thing is, the blood may have like this cherry red, may have this cherry red color, right? And the thing is, carbon monoxide, the primary side of action is hemoglobin. It actually goes after hemoglobin. It doesn't do much in your blood, right? So people that have couple monoxide poisoning, they have PBG O2 B normal, they have P little O2 B normal, but they are SO2 B decreased because, right?

Couple monoxide has a much higher affinity for the hemoglobin compared with the oxidants like 247-folder increased activity. I mean, increased affinity, right? And remember that, couple monoxide does your double one area. So the first thing is it makes you, it makes your hemoglobin not saturated with oxygen, right? So your SO2 goes down. What I'm not saying that it does is that it would actually make your oxy-hemoglobin dissociation curve left shifted. And if that's left shifted, even the little oxygen you have ready pre-bound to hemoglobin is no longer released, right? So that's a big problem. And for the most part, right? How do we trick carbon monoxide poisoning? I want to remember that you should have like 100% oxygen, right? Like hyperbaric oxygen. And one high-yout, newer association, I want to keep at the back of your mind, for example, is especially if they give you a question about a person that, you know, has had something that may have caused chronic exposure to carbon monoxide for like a long period of their lives. And then they start having like these Parkinson-like things like co-originity and all that stuff. And they ask you like the most likely etiology. You want to think about like, like problems with the global spallidus, right? So if you've probably had like necrosis of the of the global spallidus, that is something that happens to a person that has like long-term exposure to carbon monoxide, right?

Or like big-time acute exposure to carbon monoxide, it can actually cause necrosis of the of the global spallidus. And sometimes you may see this hyperintensity on imaging in the global spallidus. That's actually something that's very high-youtinal, for example. And then I mean, they could give you a question about a person, right? That you know, recently it took some kind of like nitrate, right, for angina, or maybe some sulfur drug, maybe like TMPSMX for PCP-perfiltaxis or TMPSMX for toxoprophylaxis or something, right? And then they tell you that all this person at PSA and audit, right? And this person's blood looks like chocolate-colored, right? If you see stuff like this, right? I hope you think about methemoglobin emia, right? Again, methemoglobin is hemoglobin that contains iron, right? In the 3-plus form, the ferric form, not the ferrous form, right? And that can cause lots and lots and lots of problems, because again, iron in the 3-plus form cannot bind oxygen. It's already maximally oxidized, right? So these people, they are SEO2, will be decreased, right? So again, a person with methemoglobinemia yeah, PBGO2 is fine, Pili LO-AO2 is fine, but SEO2 is decreased, right? That's why they have decreased oxygen in their blood. And again, usually these people will not have helic on an endemic cell, right? And how do we treat this? Right? For the most part, we treat this with methylene blue, right?

Methhylene blue, there's this enzyme known as methemoglobin reductase that converts, I mean, a reductase, right? It converts Fe3 plus Fe2 plus, you can use that. And then another thing you can also do is you can give a vitamin C, right? Vitamin C, also again, activates that system to reduce the Fe3 plus Fe2 plus. And then that will go ahead and cut down on that person's cyanosis, right? So that's how you treat methemoglobinemia. And then one thing I think I should throw in here so that you don't mix this up on an exam, right? Is that if a person has, um, um, if a person has, what I want to mention, so for a person has, um, cyanide poisoning, right? Sanite poisoning, I think the thing I should mention is because sometimes many people confuse methemoglobinemia and cyanide poisoning, the thing is, inducing methemoglobinemia is actually one of the ways you treat cyanide poisoning, right? So what do I mean by that? The thing is cyanide is very dangerous, right? It can cause lots and lots and lots of problems, cause lots of problems, right? I mean, like some of the things that cyanide causes, right? Like you can, uh, cyanide inhibits your electron-transport chain, it inhibits complex four, right? If you really think about it, if you inhibiting complex four, um, that's, that's going to prevent your electron-transport chain from being functional. So you then begin to depend more on like anaerobic metabolism, right?

And that will ultimately give rise to, um, an increase in the presence like Dicacet, right? So the way you can get rid of cyanide from the body is you can induce a methemoglobinemia, right? You'll give those people, and how do you do it? We just said that all reduction takes away methemoglobinemia. So to what, if you want to induce methemoglobinemia, you need to bring in powerful oxidizing agents, right? The classic one you mentioned in NBM exam is something like immunitrate. Immunitrate, right? You'll give that to the patient, right? That will convert your FE2 plus FE3 plus, right? And then you give those people, um, thiosophite, and then that will convert that whole thing to a complex iron known as a thiosyanite, and then you can piece, slash, pull out the, basically you'll excrete the, the cyanide safely. Another thing you could also potentially do, right, is to give that person a, um, hydroxyl cobalamine, right? Remember if you give hydroxyl cobalamine, hydroxyl cobalamine, right? It can combine with cyanide to form cyanocobalamine. That sounds an awful lot like B12, right? It's like a B12-like compound, right? Then again, that will then be safely excreted from the body. So again, don't mix up methemoglobinemia with cyanide poisoning or with, um, carbon monoxide poisoning. So try not to mix those things up again. Those things are all high-ovenstional. They show up a lot on, on NVM exams. Okay. Now, what if they give you a question about a person that is anemic, right?

So if a person is anemic, a dehypoxemic, I need the hypoxemic, why is that, right? So, if you really think about this, right? So, um, when a person has anemia, right? There's nothing wrong with their lungs. Their PBG-02 is fine, right? There's nothing wrong with their blood vessels. Their PBG-02 is fine. The hemoglobin that is our own is also working fine as well. So, the SO2 should be normal in those people, right? The only problem is that hemoglobin, there's a decreased amount of it. There are just fewer buses for, um, they're just fewer buses for, for that, uh, for that oxygen on the NVM exam, right? So that's why those people are hypoxemic, right? The reason they have a decreased oxygen content in their blood is because they have decreased amounts of actual hemoglobin. But every other thing, PBG-02, PBG-02, an SO2, those things are all completely normal, right? So, that's why a person will have a decreased oxygen content in the blood when they have an anemia, right? And again, remember, when the oxygen content in your blood decreases, one way that the heart tries to respond is the heart is like, okay, there are fewer buses. So, let's, let's try to make more passes of blood through the body so that we can maintain oxygenation, right? So, ultimately, right? So, because, let me give you an example, let's say, oh, you own a company that operates buses that run from in Europe to California every day, right? Well, maybe every three days, right? 50 buses, right?

But because of COVID, you know, you have to follow a bunch of drivers, so now you only have two buses. If you want to keep up with the demand, then those buses have to make more runs, right? Every single day to try to, let's say, like, oh, before you only have to make one run every three days, well, if you want to keep up with the demand, then you need to make like maybe like two runs every three days or something like that, right? So, the heart has to keep making more and more runs, more and more runs, more and more runs. But if that happens, over time, the person's heart will then ultimately crap out, right? Because remember, the heart is a muscle, right? It cannot work at an elevated rate forever. You know, if you're exercising your heart can, you know, put in a little extra work and be fine, right? But the thing is, if the person's heart keeps working hard, hard, hard, hard, hard, right? Because it's always providing increased cardiac output, now, ultimately, lead to something called high output heart failure, right? And I have high output heart failure, right? Or ultimately, again, if it's not true, it obviously, vision is going to die right? So, this is why it's no good to have severe anemia for a prolonged period of time. And if you really think about it, the high output heart failure, right? From having like really bad anemia is ultimately the mechanism behind the hydrochitalis that we find in a person that has like a average incompatibility, right?

Because again, that baby develops like profound anemia, right? And if the baby develops a profound anemia, right? You would see that the heart will then again try to keep up whenever your oxygen content of your blood goes down. You can just establish this as a relationship in your mind. Cardiac output is going to go up to try to keep up, to try to keep up with everything that is going on. So, again, the kid will develop high output heart failure. And then if the heart stops working properly, right? Then the kid will become a dimiter all over the body, right? The kid will become a dimiter all over the body. Same thing, if a person has a Pavobin 19, right? Congenital Pavobin 19, the Pavobin 19 will go and torch the person's red blood cell precursors. If you torch the red blood cell precursors, right? Then that's going to be a huge, huge, huge, huge problem, right? That's going to be a huge problem because you're basically not going to be able to produce a red blood cell, right? And if you don't produce red blood cells, right? The person will ultimately develop an asthy anemia and again, they will get high output heart failure. And this is one of those reasons why, because if your heart is working at an elevated rate, if your cardiac output is high, the speed of the blood in your vessels will be elevated, right? So, that's why one of the ways, like if you notice that, oh, woman has a rich antibody that she has made, and you know, a baby is at risk.

One thing that is typically done is you would measure the velocity of blood in the middle cerebral artery. You can do that via ultrasound. If you see that increase velocity, that's a surrogate for anemia, right? Again, the reason there is that increase velocity is again, the blood is not as viscous because there is less hemoglobin in it, right? So, again, those are all things you want to keep at the back of your mind on exams. And then one of the things I want to mention from this oxygenation perspective is I want to visit some of these concepts that are related to pulmonary physiology, right? And how those things all again affect the person's oxygenation, right? So, if, for example, you look at a person that has an ephysima, right? The person that has an ephysima, right? Or maybe let me put it this way, I think, to set this up as an equation will help, right? Especially people that think in numbers, right? So, the thing is the feasibility of a gas, right? Is directly related to the area available for diffusion divided by the thickness of the membrane, over which that, you know, thing needs to traverse, right? And then there's also a direct relationship with the spread in pressures from, like, 0.8 to 0.0, right? But I think the big thing we should mention here is the feasibility of a gas is directly proportional to the area available for gas diffusion, and then inversely proportional to the thickness available for diffusion, right?

So, for a person has an ephysima, a person with an ephysima, right? They have all these produces. These produces are literally true the way those people are, are viola, um, surface area, like they're true the way the long parenthesis is. If you're true with the long parenthesis, then you're not going to have surface area available. And surface area goes down, if the surface area available for gas diffusion goes down, then you're going to have reduced the feasibility of the gas, right? That's the mechanism behind the hypoxemia. And if you notice, you know, oxygen can come into those people's lungs, but that oxygen cannot necessarily translate to their bloodstream, right? So, those people have hypoxemia, right? With an increased e-gradient, the P big AO2 will not be able to match the P little AO2, because there is no viola membrane to ensure the passage of oxygen, right? So, it's increased area that ultimately leads to the, I mean, sorry, decreased available area for diffusion. It's what ultimately leads to the hypoxemia in those people, right? If you're conscious, that would have a person that has a pulmonary fibrosis, right? You know, unless they have like a pneumoconyl, says or something along those lines, right? Those people, right? Because of all the fibrosis in their lungs, there is an increased thickness, right? There's an increased thickness of the viola membrane. When you have increased thickness of the viola membrane, right?

Then is, because there's an inverse relationship, there'll be less the feasibility of the gas, right? So, again, normally, your P big AO2 should equilibrate with the P little AO2. But in that case, that does not happen, right? Because again, the distance that the oxygen needs to travel is just a little too great for it, right? So, the mechanism behind hypoxemia in a person that has a pulmonary fibrosis or has some kind of intestinal long disease, right? It's because they have an increased thickness of the fusion, right? So, that makes things a little more challenging. And then, if you think about a person, right? Again, let's say, for example, that has like a systemic scleroderma, right? Like the systemic scleroderma. Remember, those people did tend to develop pulmonary hypertension, right? And the thing that causes their pulmonary hypertension for the systemic kind of scleroderma, right? It's because those people have intestinal long disease, right? So, they get developed pulmonary fibrosis and that will ultimately lead to again an increased thickness, right? I mean, what are some other things that can cause that pulmonary fibrosis, right? You can see a lot of the drugs, right? Nitroferent towing, can cause pulmonary fibrosis, methotrexitis, right? So, they can talk about a person that has been on chemotherapy or a person that has been treated for rheumatoid arthritis for a while. And then the person develops a chronic hypoxia, right?

You want to think about methotrexitis, induce pulmonary fibrosis. And then don't forget the other anti-cancer agent, right? Beomycin, you're so fine, right? And also, amuter, right? So, they can tell you about a person on chronic rhythm control for e-fib, right? Remember, amuter, and can cause pulmonary fibrosis, so you can cause those kinds of problems, right? So, I just think, I just really wanted this podcast to just kind of talk about my thoughts on like these different like oxygenation scenarios, right? On NBM exams that, again, people tend to, people tend to fall for, right? Again, these things are fairly easy if you just know how to reason through them. So, I'm going to go ahead and pause here and hopefully you find this podcast to be helpful. As I do at the end of every podcast, please subscribe to the You Tube channel, the You Tube channel, the, it's called Divine Intervention, US Emily Podcasts and Videos. And then I also have a podcast website, right? Divine Intervention Podcasts.com. Please subscribe to that as well. And then you can also find these podcasts on Apple podcasts, on Google Play and on Spotify. So, please subscribe. And if there are any podcasts you really want me to make, shoot me an email, I can, as long as I have the time, and I feel like it's a reasonable topic, I'll be more than happy to discuss that. And then my next step to CK course is on the 8th of August, 2020, right? Obviously, next, next month.

If you're interested, just shoot me an email, Divine Intervention Podcasts with an SADN at Gmail.com, or you can email me through the website and then we'll take things from there. So, thank you for listening. Probably my next podcast I'll talk about a life lesson. God bless you.

Oxygen Content = $1.34 \times \text{Hb} \times \text{SaO}_2 + \text{PaO}_2$.

$\text{P}_{\text{a}}\text{O}_2$ (Partial pressure of oxygen in arterial blood).

CO has a much higher affinity for hemoglobin than $\text{O}_2$, displacing it and lowering saturation.

Ferric ($\text{Fe}^{3+}$) form (the oxidized state).

Increased cardiac output (high-output heart failure) to maintain systemic oxygen delivery.

Increased thickness of the alveolar membrane ($\uparrow$ Thickness), which inversely reduces the rate of diffusion.

Hemoglobin concentration ($\text{Hb}$), Oxygen saturation ($\text{SaO}_2$), and Dissolved plasma oxygen ($\text{PaO}_2$).

The atmospheric pressure drops, leading to a lower partial pressure of oxygen in the inspired air, thus lowering $\text{PaO}_2$ and subsequently $\text{SaO}_2$.

Normal $\text{PaO}_2$ and $\text{P}_{\text{a}}\text{O}_2$, but decreased $\text{SaO}_2$.

Methylene blue or Vitamin C. It acts as a reducing agent to convert $\text{Fe}^{3+}$ back to the functional ferrous ($\text{Fe}^{2+}$) state.

Systemic scleroderma (due to ILD), chronic exposure to certain drugs (e.g., methotrexate, amiodarone).

Emphysema reduces the available surface area for gas diffusion ($\downarrow$ Area), impairing the transfer of oxygen from alveoli to blood.

Hemoglobin concentration ($\text{Hb}$), Oxygen saturation ($\text{SaO}_2$), and Dissolved plasma oxygen ($\text{PaO}_2$).

The atmospheric pressure drops, leading to a lower partial pressure of oxygen in the inspired air, thus lowering $\text{PaO}_2$ and subsequently $\text{SaO}_2$.

Normal $\text{PaO}_2$ and $\text{P}_{\text{a}}\text{O}_2$, but decreased $\text{SaO}_2$.

Methylene blue or Vitamin C. It acts as a reducing agent to convert $\text{Fe}^{3+}$ back to the functional ferrous ($\text{Fe}^{2+}$) state.

Systemic scleroderma (due to ILD), chronic exposure to certain drugs (e.g., methotrexate, amiodarone).

Emphysema reduces the available surface area for gas diffusion ($\downarrow$ Area), impairing the transfer of oxygen from alveoli to blood.