Role of surfactant and elastic recoil in lung collapse

[Asparagoose]

I slightly confused on a topic regarding breathing mechanics.

First, the role of surfactant. My understanding is that surfactant reduces the surface tension of the walls of the alveoli, so at a very low radius, when the pressure in the alveolus is likely to increase (due to Laplace's law), a reduction in surface tension caused by surfactant will offset the increase in inward pressure caused by shrinking radius of the alveolus. This REDUCED inward pressure will make it less likely for the alveolus to collapse. Cool.

But then there's the concept of equal pressure points. Normally, the alveolar pressure is GREATER than intrapleural pressure, which is keeping the alveolus from collapsing, especially during exhalation when intrapleural pressure becomes positive. This is due to the elastic recoil properties of the lung (which INCREASE pressure in the alveolus). Degeneration of lung tissue will lead to a decrease in this phenomenon, leading to a DECREASED pressure in the alveolus (in relation to intrapleural pressure), and collapse of the alveolus.

So the rationale for the role of surfactant tells me that a INCREASED pressure in the alveolus will lead to collapse. However, the role of lung's elastic recoil tells me that a REDUCED alveolar pressure will lead to collapse.

I feel like I'm missing something big in understanding this concept. I'm trying not to get frustrated, lol. I've always loved physics because it has always been contradiction-free, and the fact that this contradiction occurs in my mind is bugging me. I appreciate any and all input!

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[Ven0m]

Normally, the alveolar pressure is GREATER than intrapleural pressure, which is keeping the alveolus from collapsing, especially during exhalation when intrapleural pressure becomes positive

Bear with me brah.
- At the end of passive expiration (in other words, you just finished exhaling like a normal person): IPP = -5cmH2O
- As you inhale, the IPP gets more negative, so that at the end of a normal inspiration, IPP is at -8cmH2O.
- As you exhale, the IPP goes from that -8cmH2O back to -5cmH2O, at which point you're now at the end of passive expiration.
To sum it up, the act of inhaling decreases IPP (i.e., makes it more negative). The act of exhaling increases IPP (i.e., makes it less negative/more positive) which returns it back to its original negative value (-5cmH2O).
So, IPP does not become positive (>0cmH2O) with expiration, it never does - except during a Valsava maneuver, where you close your mouth and nose and forcefully try to exhale).

About surfactant:
Surfactant is on the inner lining of alveoli. Surfactant's role is to lower surface tension forces that are promoting alveolar collapse.
Like I stated above, IPP is always negative (ranges from -5cmH2O at the end of an expiration, and -8cmH2O at the end of an inspiration). So, IPP is always pulling alveoli open.
However, alveoli with smaller radii have greater surface tension, which means their internal pressures are higher compared to alveoli with larger radii. And since air flows from areas of higher pressure to lower pressure, the small alveoli will want to empty into the larger alveoli, which would collapse the small alveoli - and once they're collapsed, they're difficult to reinflate (like trying to pull two wet glass slides apart). To solve this problem, surfactant lines all alveoli, reducing those evil surface tension forces, so that they won't collapse. But you may think, "surface tension forces increase as the radius gets smaller, which means smaller alveoli have greater surface tension forces", and you would be correct. That's why surfactant is present in greater amounts in smaller alveoli than in larger alveoli.

edit: here's more information that might help
At the end of expiration, alveolar internal pressure = atmospheric pressure (i.e., the pressure of the room you're sitting in). Assume atmospheric pressure = 0cmH2O, and thus internal alveolar pressure = 0cmH2O. Because internal alveolar pressures = atmospheric pressure at this point, there is not net airflow, and thus no expansion/shrinkage of the alveoli.

During inspiration, the increasingly negative IPP pulls the alveoli, making them larger, and you know what that means: their internal pressure will become lower than atmospheric pressure, which makes air get sucked in, until their internal pressure equals atmospheric pressure, at which point you have reached the end of a normal inspiration.

Then your lungs will passive exhale because the elastic recoil. Specifically, the elastic recoil increases the internal pressure of the alveoli so that it's greater than atmospheric pressure, and thus air flows out by itself, until internal alveolar pressure equal atmospheric pressure.
- Think about when you're inhaling. It takes effort because you're using muscle (diaphragm and whatnot) strength to pull the chest walls out against the intrinsic elastic recoil forces (which are acting against you). So when you just let go at the end of inspiration, you automatically exhale without using energy to do so.

So think of it that way. The always-negative IPP keeps alveoli open. They want to close because of surface tension, but surfactant lowers (offsets) that surface tension, so surface tension forces are basically eliminated, so you can just think of the negative IPP keeping alveoli open.

 

[Asparagoose]

Bear with me brah.
- At the end of passive expiration (in other words, you just finished exhaling like a normal person): IPP = -5cmH2O
- As you inhale, the IPP gets more negative, so that at the end of a normal inspiration, IPP is at -8cmH2O.
- As you exhale, the IPP goes from that -8cmH2O back to -5cmH2O, at which point you're now at the end of passive expiration.
To sum it up, the act of inhaling decreases IPP (i.e., makes it more negative). The act of exhaling increases IPP (i.e., makes it less negative/more positive) which returns it back to its original negative value (-5cmH2O).
So, IPP does not become positive (>0cmH2O) with expiration, it never does - except during a Valsava maneuver, where you close your mouth and nose and forcefully try to exhale).

About surfactant:
Surfactant is on the inner lining of alveoli. Surfactant's role is to lower surface tension forces that are promoting alveolar collapse.
Like I stated above, IPP is always negative (ranges from -5cmH2O at the end of an expiration, and -8cmH2O at the end of an inspiration). So, IPP is always pulling alveoli open.
However, alveoli with smaller radii have greater surface tension, which means their internal pressures are higher compared to alveoli with larger radii. And since air flows from areas of higher pressure to lower pressure, the small alveoli will want to empty into the larger alveoli, which would collapse the small alveoli - and once they're collapsed, they're difficult to reinflate (like trying to pull two wet glass slides apart). To solve this problem, surfactant lines all alveoli, reducing those evil surface tension forces, so that they won't collapse. But you may think, "surface tension forces increase as the radius gets smaller, which means smaller alveoli have greater surface tension forces", and you would be correct. That's why surfactant is present in greater amounts in smaller alveoli than in larger alveoli.

edit: here's more information that might help
At the end of expiration, alveolar internal pressure = atmospheric pressure (i.e., the pressure of the room you're sitting in). Assume atmospheric pressure = 0cmH2O, and thus internal alveolar pressure = 0cmH2O. Because internal alveolar pressures = atmospheric pressure at this point, there is not net airflow, and thus no expansion/shrinkage of the alveoli.

During inspiration, the increasingly negative IPP pulls the alveoli, making them larger, and you know what that means: their internal pressure will become lower than atmospheric pressure, which makes air get sucked in, until their internal pressure equals atmospheric pressure, at which point you have reached the end of a normal inspiration.

Then your lungs will passive exhale because the elastic recoil. Specifically, the elastic recoil increases the internal pressure of the alveoli so that it's greater than atmospheric pressure, and thus air flows out by itself, until internal alveolar pressure equal atmospheric pressure.
- Think about when you're inhaling. It takes effort because you're using muscle (diaphragm and whatnot) strength to pull the chest walls out against the intrinsic elastic recoil forces (which are acting against you). So when you just let go at the end of inspiration, you automatically exhale without using energy to do so.

So think of it that way. The always-negative IPP keeps alveoli open. They want to close because of surface tension, but surfactant lowers (offsets) that surface tension, so surface tension forces are basically eliminated, so you can just think of the negative IPP keeping alveoli open..

Thanks a lot brah. It makes sense when you look at it that way. I think my confusion still stems from the idea that a high alveolar pressure in relation to intrapleural pressure (or as you said, an "always-negative IPP") keeps the alveoli open, but then surfactant decreases intra-alveolar pressure in efforts to also keep the alveoli open.

Edit: I think my confusion is cleared up. The "pressure" in laplace's law is transmural pressure, which is he inward, not outward, pressure exerted on the alveolus. So yeah, decreasing this pressure would be helpful in keeping the alveolus open. I was confusing transmural pressure with pressure exerted by lung elastic recoil (in the discussion of equal pressure point), which is an outward pressure keeping the alveolus open. Thanks again for your help!