Here is a response I did to another question about emphysema and radial traction, think it might help here too and integrate some concepts.
Part of it is the concept of radial traction. I like to think of this as springs in the interstitium attaching to the airways keeping them open. Fibrosis increases the amount of "springs" and emphysema decreases them. So if you have less springs trying to keep the airway open then it can close easier. Incidentally as you breath in and expand the alveoli/airways radial traction increases and they stay open more easily, thus the increase FRC is actually semi helpful. Now the loss of radial traction means that the airways collapse at a higher pressure (more easily) so that is why they purse their lips to give back pressure and prevent airway collapse.
Tricky question, I'll attempt to address it. So I think you have radial traction (I imagine it as springs connecting the alveoli and airways to the parenchyma). So as you said a deep breath (increased lung volume) you get increased radial traction (the fibers are getting stretched). Now the other principle I'll bring up is that of FRC. So remember there is an equilibrium of the chest wall pulling out and a collapsing force (from the elasticity of the lungs) pulling inward. The equilibrium point is the FRC. There is also the changes in transmural pressures that occur in the respiratory cycle (more on that later).
Ok now on to emphysema. So in emphysema you of course have a loss of the elastic tissue this increasing the compliance of the lungs. So this is going to decrease the collapsing force of the lungs and it is going to decrease the radial traction (less springs if you will between the parenchyma and the lung lung tissue).
The results of this: increases lung compliance means there is less force pulling the lungs in against the chest wall. So the chest wall "wins" a little bit more and the FRC moves to the right. So in order to balance the lungs sit at an increase volume. Thus the barrel shaped chest and them breathing at a higher lung volume. Also this maximizes the traction for that decreased radial traction state (since increased volume increases the radial traction the decrease in radial traction seen in the disease state can be somewhat offset by the increased volume).
Now the other side of emphysema. So remember that as you breath out you increase the alveolar pressure and the intrapleural pressure thus driving the air out. Now with forced expiration you use the muscles to increase the effect, so much so that you cause the alveolar pressures AND the intrapleural pressures to become positive. So now taking that a step further if you know have all this force pushing in what keeps the airways from collapsing? The transmural pressure stays positive! (Transmural pressure is defined as alveolar pressure - intrapleural pressure). So as long as this equation never goes negative in the airways up until the airways with cartilage (that don't collapse) you don't collapse the airways. Now in emphysema you have decreased elastic recoil (compliance) so it is like a grocery bag, inflated easy but there isn't as much pressure wanting to push air out as say a balloon. So alveolar pressure at a max breath in someone with emphysema is lower than in normal. So now when they go to expire forcefully (for say a FEV1 measurement). The intrapleural pressure will increase just the same but the starting alveolar pressure will be lower than normal. The alveolar or lumen pressure is highest at the alveoli so they won't necessarily collapse but once you get out in the small airways and the pressure inside is less then the transmural pressure can go negative and collapse creating resistance which leads to the difficulty with FEV1 and resulting decrease in the FEV1. This is why pts purse their lips when breathing out, this resistance increases the alveolar pressure and can help shift this equation to not let the transmural pressure go negative and collapse the airway.
Just for fun I'll do a little example with numbers since I think it is easier to visualize the transmural pressure and such that way. So transmural pressure= pressure (alveolus)-pressure (intrapleural). So in a normal person in forceful expiration say the alveolar pressure is 35 and the intrapleural pressure is 25. So the transmural pressure is 10. As you go up the airways his number will drop as the "alveolar" pressure decreases but it will stay positive until you hit larger airways with cartilage. Now in emphysema you have decreased alveolar pressure for the volume. So say the alveolar pressure is 28 and the intrapleural pressure created is 25 again. So now it is still positive at the alveoli but then we get to the terminal bronchioles say and all of a sudden the pressure is 23 and the intrapleural is still 25. Now we have a transmural pressure of -2 and now you get collapse and increased pressure= decrease FEV1.
So now with emphysema that decreased radial traction, becomes big as the lung gets small and you would normally have less traction and now because of emphysema you have even less and so you add to the resistance issue.
So long story short: I think the increase AP diameter and increase lung volume at rest is due to the shifting of the FRC due to decreased elastic force from the lungs. This atom action helps actually offset the decrease in radial traction because radial traction is increased at higher volumes. So they counteract one another. Personally, and I'm not sure if this is exactly true but I think of the lung compliance issues in emphysema is the big driver of pathology and the radial traction modifies it at certain points (reality is it is more intertwined but I find it simpler to think about it that way).
Sorry for the novel of a post, hopefully it is of help!
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