Wait, are you saying that the parietal pleura comes free from the chest wall and remains in contact with the now-smaller lung/visceral pleura?
I'm not really sure what you're talking about, but I know the pleural space is not filled with air, nor does it fill with air in atelectasis.
That's...kinda my point.
And what will fill the empty space between collapsed lung tissue and chest wall? Is it empty space (i.e. no air)? Thank you!)
I think op is referring to contraction atelectasis. OP , rationally thinking this could lead to both hyperesonence in the lateral most portions of the thoracic cavity if there is no plueral effusion, however it is still likely to lead to dullness to percussion centrally .
Even in that circumstance, which is what I was getting at above, the pleural space does not fill with air, and thus would not lead to hyperresonance. What more realistically happens is a very small net volume change, resulting in decreased pressure in that space, with any further decrease in lung volume resulting in increased inflation elsewhere in the lung and/or elevation of the diaphragm due to the pressure changes.
There is no air there, i am assuming that the increased negative pressue is likely to draw fluid at some point , still leading to effusion still as dullness as the end result on physical exam. However is there a possibility of a space opening up leading to hyperresonance? i would think it is possible.
I mean, sure if they develop a pneumo, but otherwise even if a large 'empty' space opened up in the chest, without air inside it it would not be resonant. At that point, you're essentially talking about a vacuum (which is why it's not likely to develop on more than the micro scale, as those require a lot of force to maintain).
i suppose I understand that contents will shift to compensate for the loss in volume. I am just thinking outloud that the shift in it self would theoretically change the resonance of the lungs, and not necessarily to lead to dullness, is it also possible to have an edge case where the compensatory shift is maxed out or is that just incompatible with life.
I think if we include all of the postop atelectasis, etc., under the resorptive category, that's where it starts to get more common.
Yep. It's what I was trying to get at, too, when I said..
When I see your avatar on my phone, I always think it's a B/W photo of a guy with a mustache and a monocle.
This doesn't make sense to me. Sure, I understand the concept that for the most part, the volume change is smaller scale than most people are picturing (in fact, I pointed that out in my first post), but I disagree that you could collapse an entire lobe's worth and not appreciate a difference. This is why you see shifts with large scale atelectasis - because it's an appreciable size change in the lung, but it takes only an unappreciable size change of the pleural space to create a powerful pressure differential (which, in turn, pulls the diaphragm up and/or the mediastinum over, or induces hyperinflation elsewhere in the lung).
Yes, it causes a shift that you can detect on imaging, but to OP's question, no it doesn't create a giant pocket of air between the lung and the chest wall such that theres any confusion as to why you get dullness to percussion.
I understand that, and in fact posted as such multiple times already in this thread. I still object to the phrasing in your last post, which I think was imprecise to the point of inaccuracy. But glad to see we don't disagree on the actual physiology at play, just wording!
