DIP Episode 422 - Pulmonary Pathophysiology Series 12

All right, welcome. My name is divine. This is episode 422 of the Divine intervention on podcasts. And so these podcasts will continue the Poinari Path of Physiology series. And this is going to be series 12. So let's just get right into it. I'm going to try to bring in some stuff I talked about last time, but I'm also going to go into discussing long zones. I'm going to go into discussing long, long zones. So again, just for the sake of time, we know that first, ventilation and profusion are greater at the base of the lungs. Remember the lungs has and the lungs have any beds. That's the very top. That's where panko tumors like to hide out. And it has a base, which is at the bottom, closer to the diaphragm. So ventilation and profusion are higher at the base of the lungs. So why is that? Well, the thing is ventilation is greater because your intrapural pressures tend to be higher as you go from the top of the lungs to the bottom. Basically, the bottom of the lungs has higher intrapural pressures. If you want to understand intrapural pressures more, listen to the earlier parts of this Poinari Path of Phys series. I just can go back there because I'll take a lot of time. But intrapural pressures are higher at the long base than at the long apex. They're basically less negative as you go from the long apex to the long base. So they are higher at the long base compared to the long apex.

So if you think about it, since you have higher intrapural pressures at the base of the lungs, that means the alveoli at the bottom of the lungs are more collapsed than the alveoli at the top of the lungs. Maybe a better way to explain it is think of the apex and the base of your lungs as being a series of balloons. The balloons at the apex, that's the top of the lungs, they are less deflated. But the balloons at the base, which is the bottom of your lung, are more deflated. They are more deflated. Think of them as being almost completely deflated. So obviously if you have a balloon that is almost completely deflated, then it would make sense that the alveoli at the base of the lungs are more compliant. It would make sense that the alveoli at the base of the lungs are more compliant. Think about it, when you have a balloon that is almost deflated, it can allow you to blow more air into it so that it can expand. But an alveoli balloon that is almost fully inflated is not as deflated. When you blow air into it, you can only blow so much and for every little air blow, the pressure on the balloon walls rises significantly. So that's the weight of the prets. So since the alveoli at the base of the lungs are more deflated than the alveoli at the apex of the lungs, the alveoli at the base of the lungs are more compliant. Because they are more compliant, they can capture more oxygen in the process of inspiration.

So since they can capture more oxygen, that explains why there is more ventilation at the base of the lungs. Although I'm going to say something that almost seems to contradict this, but it actually doesn't contradict it at all. It will just help you put more things together, basically. Now, so I've explained why the insulation is higher at the base of the lungs. So I also say that perfusion, as your cue, remember ventilation is V, perfusion is your cue. Your cue perfusion is also greater at the base of the lungs. Why is that? Well, remember, blood flow depends on the pressure difference between two points. That's an important principle to know. Now, the thing is pressure differences are much greater when you altitude, when your vertical distance is increased. I'm just going to think of it this way. If you're trying to pull water from a two-foot height into a bucket versus point water from a 10-foot height into a bucket, the water coming from the 10-foot height, right? It's just a bigger pressure gradient between those the 10-foot high versus the two-foot height. So you're going to get greater flow with the 10-foot height. So blood flow depends on pressure differences between two points. So the thing is pressure differences, they're much greater when the again, when the vertical distance is increased. And we know that for blood to get oxygenated, it literally has to flow from the heart to the lungs. It literally has to flow from the heart to the lungs.

So obviously, that's going to depend on the gradients that exist between the two organs, between the heart and between the lungs. So because blood is flowing from heart to lung, you'll make sense that the heart should hopefully be at a higher pressure gradient. At least the right side of the heart should be at a higher pressure gradient than the lungs. So the thing is, if you think about it, the base of the lungs right is located at a lower level relative to the heart. So the pressure gradient is higher. If you look at the apex of the lungs versus the base of the lungs, the base is just located much lower relative to the heart. So because the vertical distance between the base of the lungs and the heart is bigger, then the vertical distance between the apex of the lungs and the heart, then that tells you all you need to know. That's why there's more flow, gravity, more flow at the base of the lungs, right? So the pressure gradient is higher at the base of the lungs. So that's why the base of the lungs receives more profusion. Now, there's this common question that arises, you know, USM Ls or amongst med students that are okay. So the one you're just saying that there's more ventilation at the base of the lungs, there's more profusion at the base of the lungs. Why is it that TB likes to go to the apex of the lungs? Well, let's explain. The thing is, so I just said that again, ventilation profusion greater at the base of the lungs.

The thing is, as you go towards the lung apex, based on what I've literally just said, your ventilation and your profusion both decrease. They both decrease. Well, the only problem is that they do not decrease at the same rate. They do not decrease at the same rate. Your profusion, as you cue, it decreases a lot more than your ventilation. It decreases a lot faster than your ventilation. So actually, if you compare the VQ ratio at the apex, it's actually a higher ratio than at the base, right? So if you think about it, if you think about it, V over Q, right? That's your VQ ratio. That's your ventilation of your profusion. If, as you went from base of the lungs to apex of the lungs, they both decrease at the same rate, then the ratio at the base of the lungs will be the same as the ratio at the apex of the lungs. But as we all know, that is not the case. That is not the case because again, the Q goes down a lot. The V also goes down, but it doesn't go down as fast as Q. So the denominator is going down much faster than the numerator. So the overall net effect is going to be an increase in the ratio. That's why your VQ ratio goes high as you go from the base of the lungs to the apex of the lungs. So the thing is, your VQ ratio is just higher than the apex. So essentially, there's this extra oxygen that kind of exists at the top of the lungs. That TB really, really likes, right? That TB really likes. I think I want to also try to maybe use an analogy to explain this thing.

Let's say at the base of the lungs, you're being paid 10 an hour for working 10 hours. You're being paid 10 for working 10 hours. You're like, wow, okay, I worked 10 hours, I mean 10. Well, that's great. If you think about you're basically making a dollar an hour. Now, let's say as you then go from the base of the lungs to the apex, you're being paid 10. Let's say you've been paid 5. How's that? You've been paid 5. So wow, the amount from these to apex has gone down in half. But at the apex of the lungs, you only have to work one hour to make that 5. Notice the pay, if you're looking at the pay, the nominal pay at the apex of the lungs is less, you're like, wow, I used to make 10 at the base of the lungs. Now, I'm making 5 at the apex. And then if you'll, but maybe like, wow, the pay has gone down, but nominal pay has gone down by half. Okay, but look at the hours worked. It's literally gone down from 10 hours required to make 10 at the base to one hour required to make 5 at the apex. So your hours, your hours that you need to work have decreased by like 90%. But the nominal pay only decreased by half by 50%. So the hours decreased more faster than the nominal pay. So overall, at the apex of the lungs, since you're only working an hour to make 5. You're making 5 an hour. The nominal pay is less, but the per hour rate is much higher.

Obviously, because you have those extra nine hours where you don't have to work for money, then you can use that time to enjoy yourself. Right. So that's kind of like an analogy as to why TB likes the apex of the lungs. It just has more oxygen relative to the blood flow. All the oxygen that is at the apex of the lungs, not all of it has to go into the blood vessels that are profusing the apex of the lungs. So it has more oxygen to enjoy. So that's why TB loves the long apex. So hopefully that makes sense. Now, it's kind of higher to understand that your vitro ratio is going to get closer to one. It's going to be as close to one as possible when you are orthostatic, when you are lying down, right? Because think about it, when you lay down, then you essentially put in your heart at a similar vertical distance from the apex and the base of the lungs. So that gradient you have of vertical differences in height, it just doesn't really exist anymore. And also when you exercise, right, when you exercise, you hyperventilate, because you're hyperventilating, you're kind of changing the game of many of the intra-avual intra-plural pressures, you're kind of changing that game. So that's just something, you kind of something kind of want to keep at the back of your mind. You want to make sure that you understand, right? You want to make sure that you understand. So one question then I want to ask, given what you've discussed is, why is there more dead space at the apex of the lungs?

Why is there more dead space? The thing is, if you understand these different long zones and their pressures, it's going to really help you understand why there is dead space at the long apex. Again, I've talked about dead space in the earlier podcast in this series, but remember, dead space happens when you have a lot of ventilation, but not enough profusion for it. There's all this oxygen around, but there's not enough blood to take up all that oxygen. That's dead space. That's dead space. Now, let's explain why this phenomenon optates. Well, if you think about if you're going to the base of the lungs, remember I said, the base of the lungs, the vessels there receive more profusion than the apex. So the thing is, the greater amount of blood coming to the base of the lungs increases the hydrostatic pressures exerted on the walls of those vessels that are the base of the lungs. But if you look at the apex of the lungs, the vessels that are there, they have smaller hydrostatic pressures because less blood is flowing to them. Less blood is flowing to them. The hydrostatic pressure in those vessels are much, much, much, much less. Now, the thing is the pressure in the L-view lie is essentially uniform all through the lungs. So, those are not talking about intraplural pressures here. I'm talking about intra-view lie pressures. The pressure in the L-view lie is essentially uniform all through the lungs. Right?

So, since the avial pressure, the avial oxygen tension, the P-B-G-O-2, is essentially uniform as you go from the base to the apex, where the hydrostatic pressures of the vessels that are around those avial lie decreases as you go from the base to the apex. It should make sense that a point will be reached near the long apex, where the pressure in the L-view lie exceeds the pressure in the pulmonary vessels. So, I just said that intra-view lie pressure is roughly similar if you compare base and apex of the lungs. But the pressures, the hydrostatic pressures inside the pulmonary vessels decreases progressively as you go from base to apex because there's just again, like I said, less profusion at the apex than the base. So, we know that many of these pulmonary vessels literally run through the lung parankama, they run throughout the lung parankama. Right? So, the thing is, since there's less hydrostatic pressure in the pulmonary vessels at the apex versus the base, the pulmonary vessels at the apex are more likely to be squished by the higher pressures that exist in the avial lie around them. Those high pressures in the avial lie that exist around those pulmonary vessels are going to squish those pulmonary vessels. Those pulmonary vessels are more squishable if there's a term like that because again, they don't have enough hydrostatic pressure in them.

So, basically, the pressure outside the pulmonary vessel, which is the intra-avial pressure, is greater than the pressure, the hydrostatic pressure inside the pulmonary vessel. I'm just seeing this in many different ways just to really help you understand if you're going to get a little confused. Now, the thing is, this basically will close off the vessels at the lung apex, because of those excess pressures. And that essentially shots of blood flow. Even if ventilation is still going strong in those avial lie, that's basically what dead space is. That's basically what dead space is. So, if you understand what I just explained, you'll see why there's more dead space at the lung apex. Now, our friends at the MV is when they want to give you a very challenging question. They can say, a patient comes in with respiratory failure and this patient having a respiratory failure is placed on the ventilator. And then they can then say, oh, by placing this patient on the ventilator, what is the most likely effect on pulmonary physiology or whatever? And I really hope you're saying, oh, divine, the most likely effect on pulmonary physiology is to create more of something we call zone one lung. So, remember, I talked about lung zones. Maybe this is something I'm going to mention. So, the base of the lungs, we usually call it like zone three. The apex of the lungs usually call it zone one. And then in the middle, between zone one and zone three, we call that zone two.

So, obviously, zone one of these lung apex, right? As long as the lung apex, that's the place that has more dead space and explain the mechanism behind that dead space. Well, the thing is, when you get on the ventilator, you're going to have more of your lung is going to be zone one lung. So, maybe like, hard to find. Why does that make any sense? Well, let me explain. The thing is, when you place a patient on the ventilator, you're essentially bubbling, forced oxygen into their lungs. What do you think that's going to do to the intravenous pressures? I don't know. It's going to make it bigger, right? Because you're literally pumping, pumping, pumping, pumping more oxygen into those aviola species. Since you're in intraaviola pressures are going up, then they're going to have more capacity to squish the pulmonary vessels that surround them. If you keep squishing those pulmonary vessels, you're going to tie off blood fluids to those vessels. That's essentially going to create more dead space. That's why. So, what's the thing on the ventilator that can really, you know, want to lay there? So, that's your peep. So, the peep is good when you give peep, positive and respiratory pressure. Yeah, you're going to up your ventilation, because you're keeping those aviola a little bit distended, blah, blah, blah, blah. Well, you just got to be careful because you can peep so hard, one, you can pop the lungs, which is not good. You know, baratrum, that's not good.

But another thing that can happen is you also create more zone one lung, right? You also create more zone one lung because those high intraaviola pressures are going to be squishing the pulmonary vessels around them. You're creating more dead space. So, you need to kind of balance it out, okay? You need to balance things out. These are all the tough decisions a pulmonologist has to take in a nice seal. Yeah, pulmon is just not for the faint of heart. I'll tell you that. Okay. So, now let's talk about a VQ mismatch and let's let's talk about VQ mismatch. Let's talk about VQ mismatch. Just some more. I just kind of want to bring in some more context to what I discussed in the last podcast. So, maybe just present more like extreme examples to really help you understand. So, the thing is whenever a person has like consolidation in the lungs, let's say they have pneumonia or whatever, it leads to a VQ mismatch, right? And for the most part, your VQ ratio is going to be less than one, right? So, why is that? Well, if you think about it, when you have consolidation, so you have pneumonia, you have fluid in the lungs, you know, pulmonary demon, all these badness, it basically takes up stress in the avioli that could have been occupied by oxygen, right? So, the blood that's coming to these regions because they encountering bugs of avioli, right? That contains stuff like consolidation, like fluid and stuff. They won't be able to oxygenate properly, right?

Because there's no oxygen in those avioli. The oxygen has been displaced by something else. So, even if blood is still flowing to those avioli, they're not getting enough, there's not enough oxygen in them. So, the blood flowing to them are not going to get properly oxygenated. Although, parts of the lungs that are not affected will have good ventilation, good profusion, right? But if you notice, as the blood is leaving the pulmonary couplers and going to the pulmonary veins, you have some blood that has been properly oxygenated, you know, coming from parts of the av of the lung that have decent avioli, but you also have blood that has not been properly oxygenated. Because it's coming from parts of the avioli, the blood is coming from, you know, parts of the lung that have a avioli that contains stuff that's not oxygen. So, that mixed blood will have a lower O2 sat than, or lower P little O2, let's not say O2 sat, oxygen partial pressure, lower P little O2 than if you had blood coming from lungs that had no consolidation, had no fluid in them. So, because of that mixing, overall, it would make sense, it would make sense that the P little O2 should go down. If the P little O2 is going down, in that should make sense that your AA gradient is going to be increased, right? So, whenever you have consolidation in the lungs, whenever you have fluid in the lungs and stuff, your AA gradient goes up. Again, I've literally just explained why.

And again, I give this central principle at the top of the hour, where I basically said, oh, at the beginning of this podcast, oh, no, let me just say I've begun this podcast. I think I said in the last podcast, or two podcasts ago, whenever you have a problem that is native to the lung, you have a problem that is intrinsic to the lungs. That's going to cause your AA gradient to go up, right? But in this case, if you notice, this is not a full, this is not a, you know, you have part of your life that are good and are good and are bad, right? So, the things you have good of your life, if you give more oxygen in this case, it's going to help with this VQ mismatch. It's going to help because there are available areas of the lung that are still well ventilated, right? So, giving more oxygen to these areas, you'll ensure that the blood that is coming through these areas is maximally ventilated, right? So, the hypoxemia will go down a bit, right? But again, contrast this with a pure shot. Remember, we said in a shot, the blood is not even making it to the lungs to receive the benefits of oxygen coming to the non-consolely-deferred regions, the regions that don't even have consolidation, right? So, if you really want to think of a shot, think of a shot as just like a very extreme VQ mismatch, right? It's basically a VQ ratio of zero, right? You essentially have no ventilation for all the available blood, right? So, this, why giving more oxygen does not fix a pure shot?

Please, you need to make sure you understand the stuff. It's like extremely high over all the USMLA exams, all the complex, complex exams, right? When you give more oxygen, it doesn't help, it doesn't help with a shot. A shot is basically an extreme form of a VQ mismatch, right? And then again, remember, I give the example of a PE, right? So, another example of a VQ mismatch, essentially, that's one extreme end of the spectrum. It's almost like a VQ ratio of infinity. Let's assume you have like a really terrible PE. There's no blood flowing the lungs. Well, there is a non-ventilation of insulation. The insulation is still happening, but there's not enough profusion. There's zero profusion, right? Again, that's just an extreme form of dead space. PE's create more dead space. Could PE's put you in more in that zone-long, kind of situation? So, again, I'll encourage you, if you have the time, go back and release into this podcast. Many of these things is just understanding. When you understand it, you just be like, well, the findings are very repetitive. I'm just very repetitive and trying to release slow down so people can really get this stuff. So, as I wrap up my podcast, I do have one or one tiering for all the USMLA exams, step one to three, complex one to three. The only thing I don't do is to use OMM. I do also do the pre-clinical medical exams, 30-ish-off exams.

I offer a 20-hour step, two and three, complex two and three review course, I offer an MBA, me testing and strategy scores, and then I also offer a biostatistics review. It's a bootcamp. It's four hours long. Many people have taken these courses and they've done extremely well on the exams. I also help with ERA's applications and mock interviews and things of that nature. In fact, doing that with a lot of people right now. So, that's something I'm interested in just ship me an email through the website. I have the podcast and all the major podcast apps, Apple, Google, Apple Podcast, Google Podcast, Spotify. Then have a You Tube channel, Divine Intervention, USMLA Podcasts and videos. That's where I post the videos that I make. And then finally, I also have another website called Divine Intervention Lifelessens.com. In fact, it has an Apple podcast, associated with it. It's called the Divine Intervention Life Lessons Podcast. People say, oh, Divine, I love your life lessons. You put at the end of your podcast. So, I'd say to make a separate website that from a biblical perspective addresses common problems faced by people. So, I upload to every week. So, hopefully something that will listen to me blessed. But thank you for listening to me today. I'll see you in the next podcast. Have a wonderful rest of your day and bye for now. God bless you.

At the base of the lungs.

Because the base is located lower relative to the heart, resulting in a greater vertical pressure gradient.

The base alveoli are more deflated (closer to collapse) due to higher intrapulmonary pressures.

Because pulmonary blood flow ($\dot{Q}$) decreases much faster than alveolar ventilation ($\dot{V}$).

The high intra-alveolar pressure exceeds the low hydrostatic pressure within the pulmonary vessels, causing vessel collapse.

$\text{V}/\text{Q} < 1$, because blood flows through alveoli lacking oxygen ($\dot{V}_{\text{effective}}$ decreases).

The vertical distance (pressure difference) between the heart and the lung region.

Alveolar gas tension ($\text{P}_{\text{a}}\text{O}_2$) is relatively constant throughout the lungs, but pulmonary vessel hydrostatic pressure drops significantly from base to apex.

A complete lack of blood flow (e.g., massive PE).

The vessels collapse, leading to increased dead space.

Increased alveolar-arterial oxygen gradient ($\text{A-a}$ gap).

The vertical distance (pressure difference) between the heart and the lung region.

Alveolar gas tension ($\text{P}_{\text{a}}\text{O}_2$) is relatively constant throughout the lungs, but pulmonary vessel hydrostatic pressure drops significantly from base to apex.

A complete lack of blood flow (e.g., massive PE).

The vessels collapse, leading to increased dead space.

Increased alveolar-arterial oxygen gradient ($\text{A-a}$ gap).