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What is transpulmonary pressure?

  1. Nov 24, 2009 #1
    Ok I researched but I don't understand what they are saying.

    Transpulmonary pressure= alveolar pressure-pleural pressure= elastic recoil of the lung.

    How is transpulmonary pressure equal to the elastic recoil of the lung? I don't understand what you get when you substract pleural pressure from alveolar pressure.

    Also while I was reseaching this pneumothorax came up. It seems that elatic recoil of the lung is pushing one way and the chest wall is pushing one way. When equilibrium is reached between these two pleural space is negative. So when you puncture air fills the pleural space and becomes zero. So how does this make the lung collapse?

    Thank you!! Moonbear,Andy or anyone please explain!!
  2. jcsd
  3. Nov 24, 2009 #2

    Andy Resnick

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    The transpulmonary pressure is the pressure jump across the alveolar wall (at least, that's what you wrote). The lung itself does not have the ability to expand or contract via elastic stress- that's driven by the diaphragm- so I'm not sure what 'elastic recoil' refers to. Similary, I would call a 'tension pneumothorax' a 'compressiion pneumothorax' because the effect is to keep the lung compressed

    Pneumothroax, as I understand, occurs when the pressure jump becomes zero- either the lung is punctured, or there is some other injury that allows air into the pleural cavity. Then, even though the diaphragm is still functional, the lung won't expand or contract since there is a low-resistance alternative flow path for air to follow.

    hope this helps...
  4. Nov 24, 2009 #3
    Thanks Andy. I found this video on youtube

    It states that the higher pleural pressure pushes on the lungs making it contract. Is this the right way to understand this? Can you explain a bit further on which air that follows lower resistance. I didn't really understand. Also I though lungs are elastic, is this wrong?
    Last edited by a moderator: Sep 25, 2014
  5. Nov 24, 2009 #4


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    One thing to keep in mind is that in normal conditions, the pleural cavity isn't a space at all, but a potential space. The two layers of pleura, visceral and parietal, are usually sandwiched together with nothing but a little fluid lubricant between them.

    In a situation where an injury has occurred, that potential space between the layers of pleura becomes a real space, filled with either air (pneumothorax), blood (hemothorax), or other fluid (hydrothorax).

    In terms of lung elasticity, your initial terminology is correct to call it elastic recoil, but I'm not sure you've understood the direction of that from the remainder of your explanation. Elastic recoil refers to the ability of the lung to return to it's "normal" shape, which is collapsed. Elastic recoil pressure (or transpulmonary pressure) is the difference in pressure between the inside and outside of the alveoli (Pal and Ppl, respectively) that determines if it will move from that resting state.

    The greater that difference (i.e., the higher the transpulmonary pressure), the bigger the lung is.

    Think of alveoli very much like a latex party balloon in this case. It's resting state when the inside and outside are at the same pressure is to be collapsed. The only way you can stretch it (inflate it) is to increase the pressure inside relative to outside. With a party balloon, we're talking about blowing into it and increasing the pressure inside.

    With the lung, instead of inside and outside both starting at atmospheric pressure, the outside (pleural pressure) is lower than atmospheric pressure. What is potentially confusing is that for some reason, the convention is to refer to Patm as zero rather than 1 atm, and then the Ppl as a negative pressure.

    When you have a condition of pneumothorax, the Ppl rises to atmospheric pressure, so there is no pressure difference between the inside and outside of the alveoli. This means the alveoli return to their resting state (size/shape), which is a very small lung volume -- collapsed, just like your party balloon collapses if you put it in a chamber that increased the air pressure around it to equilibrium with what you blew into it.
  6. Nov 24, 2009 #5
    Thanks a lot Moonbear :smile: Since you are online I like to ask these two questions quickly.

    If pleural space is a potential space and only has lubricant fluid what causes the negative pressure inside it? Is it the lubricant

    I'm constantly rereading your response to understand at the mean time.
    Last edited: Nov 24, 2009
  7. Nov 24, 2009 #6
    Oh wait after rereading your response this is my understanding. Tell me if this is right.

    *You got the lung and pleural space. They are separated normally and lung has atmospheric pressure and pleural space is negative.
    *Since pleural space is negative the air molecules inside the lung push on the lung walls and try to reach equilibrium with pleural space. This expands the lung.
    *When the pressure outside and inside is equal. There is no force pushing out on the lung walls and lung can recoil back to its orginal position.

    Is this what happens?

    Ok I think I got it but I have some questions.

    You have mentioned that at the start alveolar pressure=atm and pleural pressure=negative

    When you are at rest you have a residual volume right. To have a residual volume you must have an expanded lung. So when at rest shouldn't the alveolar pressure=pleural pressure meaning negative. Are you taking at zero because then you can workout the recoil force, but in reality it must be neagtive right?

    What makes pleural space negative to begin with.

    Thank you!!
    Last edited: Nov 24, 2009
  8. Nov 24, 2009 #7


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    The pleural pressure is only "negative" because it is lower pressure than atm pressure. The reference is atm pressure set at 0 (as a convention).

    In terms of residual volume, you have a partially expanded lung, not a fully expanded one. But, more than just the pleural pressure and alveolar pressure contributes to expansion and contraction of the lungs. Remember you have contributions of the diaphragm relaxing or contracting and the ribs expanding or contracting, changing the volume of the thoracic cavity (not the pleural cavity, which is only between the two layers of pleura).
  9. Nov 24, 2009 #8
    This is a great thread, I have been teaching this stuff (at least on a n introductory basis) and still don't have a clear understanding. My understanding is much lik what Moonbear describes--that between the the inside of the chest wall and the lung itself--you have a balloon. Not really one ballon but two with a small amount of watery material which helps to lubricate maybe, but also provides a strong capillary force which causes the two to move together. So the outer most balloon expands in response to Boyle's relationship (unworthy of a "law" IMO) which never really pulls the two balloons apart--the lungs themselves instantaneously respond. So far so good. One can then imagine breaching one wall or the other. One can easily imagine injecting a fluid into this potentail space--say a transudative process--whereby the lungs are now subject to a new Blowing upcompressive hydrostatic pressure. Blowing up a balloon underwater I think captures the shift in the compliance curve.

    I'm good with that. Where I get confused is with the notion of a tension pneumothorax. The usual explanation is a one way flap valve which allows entry into the pleural space but no escape, so like wrapped within a blood pressure cuff the lung cannot expand. But anatomically how do you pierce one plueral layer and not the other? I may be wrong, but I think that even under surgical conditions this would be difficult, mush less so by a blunt penetrating chest wound. Under these circumstances, I would just assume that the transthoracic pressure is zilch. You have basically short circuited the pressure gradient. So how does this lead to a mediastinal shift?

    Oddly enough, it is the case of the spontaneous pneumo caused by a bleb rupture which leads to a much more intuitive (at least in my modest mind) situation where a one way valve could lad to accumulation of air within the pleural space and cause a "tension" pneumo. The anatomy itself of the alveoli and visceral membrane may be too weak a substrate on which to make a flap valve I realize, but Moonbbear or anyone else who could share up these shaky understandings. I'd be greatly appreciative. Anytime I get into these discussions with the RT's who run the program leads to a lot of handwaving and looking at pictures in a book. I've done that. Not ot highjack but this is a subtle part of A&P which like the West's zone model of the lung, or the misplaced invocation of LaPlace's law may make us believe we know and understand more than we do.
  10. Nov 24, 2009 #9


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    I don't think there is a requirement for a tension pneumothorax to involve piercing of only one layer of the pleura. What would allow pressure to build up inside without being able to escape out the way it got in? One thing I can think of would be blood clotting around the wound that "plugs up" an exit. Another scenario that comes to mind might be something like a puncture from a broken rib that does not involve penetration through the thoracic wall to the outside, so air inside the pleural cavity has no place to escape.

    But, yeah, pretty much I can go into the textbook explanations, but not being a respiratory physiologist or working in a clinical setting where I would see such conditions actually occur, I too can really only handwave a bit about ways I can envision it happening, but not necessarily be able to offer a correct answer.

    Every time I have to think about teaching this stuff, I remember why I disliked respiratory physiology so much as a student. :biggrin:
  11. Nov 30, 2009 #10

    MB, Just catching up this morning. Yes, I hated it as a student, and teaching it can be an abysmal experience at times. Good medical students gag on these concepts. And I'm teaching the commensurate physics in a concurrent class to some whose last science class was in the ninth grade 15 years ago. :cry:

    BTW, thanks for the examples--I'm gonna be pleading to get out into the community with some RT's and pulmonoligists so I have more clinical material to draw from. Otherwise lots of it is just too darn dry to have any adhesion.
  12. Mar 24, 2011 #11
    Hopefully people will still be looking at this thread....

    I've tried every resource I can think of, and still can't figure this out....and would be eternally grateful if someone could help me see the light, so to speak.

    So keeping in mind the last time I did any physics was 5 years ago, I have trouble understanding the idea of elastic recoil pressure. I understand that you have a pressure gradient (transpulmonary pressure) that creates a distending force, and as the lung is distended by that force, it is also developing an elastic recoil force, which as a vector opposes the force vector generated by the transpulmonary gradient.

    What confuses me are the equation used. For example, alveolar pressure = elastic recoil pressure + pleural pressure. What exactly is elastic recoil pressure? We are generating elastic potential energy through the expansion of the lung, but its potential, no? Isn't the pressure within the alveoli dependent only on the volume of gas within the alveoli, and the volume of the alveoli themselves?

    Also, the lung expands until the two force vectors (elastic recoil and transpulmonary pressure force) are equal, no? How then can the elastic recoil pressure be defined as equal to the transpulmonary pressure?

    Thanks in advance!
  13. Mar 25, 2011 #12
    Here is how I think of elastic recoil and transpulmonary pressure being the same thing. Imagine injecting e.g. 500 ml air into a regular deflated plastic grocery bag. You would have an increase in volume but no increase in pressure because there is no elastic recoil in a grocery bag. Now imagine injecting air into a balloon - same 500 ml - and tying it off. Now we have pressure because the elastic recoil of the balloon squeezes the 500ml air inside - the more air the more squeeze - the higher the pressure developed.
    Only with the lung - the pressure generated is in the intrapleural space - and a low pressure is generated because of the recoil of the lung inward - away from that space - the more recoil the lower the intrapleural pressure. Alveolar pressure we always considere to be zero - but as the recoil increases (as the thoracic wall moves outward) and the intrapleural pressure falls the transpulmonary pressure increases.
    Its late - I may not be making as much sense as I think I am!! but I know what I want to say. So essentially it is the force of the elastic recoil that generates the low pressure inside the intrapleural space.
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