How expiring through pursed lips assists expiration in COPD patients etc? Watch

MedStudentt
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So the explanation, I have is that this pursed lips action adds resistance to proximal airways, this added resistance maintains the patency of these airways?

Can anyone explain this?
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Beska
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(Original post by MedStudentt)
So the explanation, I have is that this pursed lips action adds resistance to proximal airways, this added resistance maintains the patency of these airways?

Can anyone explain this?
The problem with COPD is a combination of emphysema and bronchitis. The emphysema aspect leads to the distal alveoli becoming floppy and losing their structure, which means they very easily collapse on expiration to form a closed sac. In healthy lungs, the alveoli do not close to the same degree - i.e. there is some air left in. Opening of a closed alveoli takes a magnitude of energy more than simply inhaling into a partially closed sac - think of surface tension. By pursed-mouth breathing patients are increasing their peak end-expiratory pressure and splinting open their alveoli, so it's easier for them to inspire afterwards.
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nexttime
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(Original post by Beska)
The problem with COPD is a combination of emphysema and bronchitis. The emphysema aspect leads to the distal alveoli becoming floppy and losing their structure, which means they very easily collapse on expiration to form a closed sac. In healthy lungs, the alveoli do not close to the same degree - i.e. there is some air left in. Opening of a closed alveoli takes a magnitude of energy more than simply inhaling into a partially closed sac - think of surface tension. By pursed-mouth breathing patients are increasing their peak end-expiratory pressure and splinting open their alveoli, so it's easier for them to inspire afterwards.
That's interesting. I was taught a different theory - that its largely because the airways are just narrow and blocked so you need to keep them open, but also that when the lungs are shrinking on exhalation the relatively scarred, stiff alveoli can start exerting pressure on the larger airways making them collapse (so the small airways are collapsing, not the alveoli) and this leads to trapping of air. Pursing lips increases the pressure in the system, meaning upper airways can stay open, trapped air can escape etc.

I've not done any research at all but I'm tempted to say my version has more merits. Yours would lead to inhalation being the problem in COPD, which it isn't. You get pursed lips breathing in young asthmatics who shouldn't have alveolar damage - just thin mucus-filled airways. You can cause yourself to wheeze by doing forced expiration through an open mouth (I see so many resp patients do this when examined on the wards), which doesn't happen in forced expiration through pursed lips... but who knows, often the truth in medicine is weird! If you've read an article with your version I'd be interested to read it.
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Beska
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(Original post by nexttime)
That's interesting. I was taught a different theory - that its largely because the airways are just narrow and blocked so you need to keep them open, but also that when the lungs are shrinking on exhalation the relatively scarred, stiff alveoli can start exerting pressure on the larger airways making them collapse (so the small airways are collapsing, not the alveoli) and this leads to trapping of air. Pursing lips increases the pressure in the system, meaning upper airways can stay open, trapped air can escape etc.

I've not done any research at all but I'm tempted to say my version has more merits. Yours would lead to inhalation being the problem in COPD, which it isn't. You get pursed lips breathing in young asthmatics who shouldn't have alveolar damage - just thin mucus-filled airways. You can cause yourself to wheeze by doing forced expiration through an open mouth (I see so many resp patients do this when examined on the wards), which doesn't happen in forced expiration through pursed lips... but who knows, often the truth in medicine is weird! If you've read an article with your version I'd be interested to read it.
Yeh I was taught that theory I posted - not heard yours! In that case not really sure what the correct pathophysiology is - not done any research either.
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Etomidate
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Increases PEEP which keeps alveoli open. Also the force required to inflate alveoli in the initial collapsed stages is much greater than if partially inflated.
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(Original post by Beska)
Yeh I was taught that theory I posted - not heard yours! In that case not really sure what the correct pathophysiology is - not done any research either.

(Original post by Etomidate)
Increases PEEP which keeps alveoli open. Also the force required to inflate alveoli in the initial collapsed stages is much greater than if partially inflated.
Did a quick google and read the 3 most promising sites - they all seem to agree that COPD is a disease of the airways, not alveoli, and that the problems are on exhalation, not inhalation. None mention alveolar collapse or surface tension, with a fair amount of talk about how the alveoli are less compressible and so reduce lung elasticity.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2707802/
http://www.livestrong.com/article/11...lip-breathing/
http://www.thinkcopdifferently.com/A...of%20COPD.aspx
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