Confused on AGE; holding breath OK if lungs are near-empty?

[The Chairman]

Always keep your glottis open. You don't have to breathe out. You use your glottis to clear your throat and burp. Just don't close it and you will be fine.

Instructors can't see your glottis. Ergo, the only way they know it's open is to see bubbles coming out. You're out of class now and there are no Scuba police checking for them anymore. Keep your glottis open. You can pause your breathing without worry if you control it with your chest muscles and diaphragm and just keep that glottis open.

 

[Eric Sedletzky]

What’s the very first rule of scuba diving they teach you?

 

[Kendall Raine]

What’s the very first rule of scuba diving they teach you?

Pay?

 

[Eric Sedletzky]

Pay?

Lol
Besides that.

 

[dmaziuk]

If I have relatively empty lungs at 20meters, hold my breath, then ascend to 10meters, would my lungs physically expand (and therefore I would feel my diaphragm move)?

 

[John C. Ratliff]

I’ve dug into the literature on air embolism from scuba a bit and I think the issue is that we don’t really understand the mechanism fully. Most people operate with the idea that air embolism is potentially an extension of over expansion injuries like pneumothorax. I’m not convinced. The probability of a rupture causing air to escape into the arterial system seems small to me. This theory likely arises because there have been cases of air embolism with concomitant pneumothorax. However, air embolism occurs in cases of rapid pressure change so the presence of pneumothorax at the time an embolism does not equate to cause, it’s only correlative. I read one theory that this is more likely just overloading of the capillary bed with microbubble burden to the point that a large number of bubbles pass through into the arterial system. This seems the more likely mechanism to me. None of this is hard science. I guess you could take some rats and punish them for science and design an experiment that would get a large enough volume of air embolisms to help you determine if lung over expansion is causally related, but I doubt anyone is doing that study.

All of that to say, I do not think the degree of expansion of the lungs (ie from very low volume to high or moderate volume, or even over pressurized) is likely to be causal. Which is to say you are not protected from air embolism by having low lung volume at the beginning of a rapid ascent. You are protected to some extent from pneumothorax, but remember that air volume doubles from 10m to the surface.

Now, if I remember my medic training correctly, a pneumothorax is air between the lungs and the chest wall, usually from trauma (like a knife wound). The treatment is to use a needle to puncture through the chest between the ribs and release the air that is trapped between the lungs and the chest wall. This has nothing to do whatsoever with lung overexpansion, although that may be one mechanism for getting a pneumothorax. But the overexpansion injury occurs at the air sac level (alveoli level) where there is a rupture of the air sac which allows air directly into the arterial circulation, which can easily be transported to the brain. One of the older treatments was to place the victim in the Trendellenburg Position, on his or her left side, head down and legs elevated. Oxygen treatment may help too.

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SeaRat

 

[The Chairman]

Now,

Please, we don't need him to think this is easy to remedy. Just keep the airways open so we don't need to remember how to treat this.

 

[John C. Ratliff]

Please, we don't need him to think this is easy to remedy. Just keep the airways open so we don't need to remember how to treat this.

I was trying to illustrate the different physiological mechanisms between the two, embolism verses pneumothorax. Agreed…prevention is the best. Treatment is to prevent brain injury from the emboli. That is something no one ever wants.

SeaRat

 

[Gelirfella]

Now, if I remember my medic training correctly, a pneumothorax is air between the lungs and the chest wall, usually from trauma (like a knife wound). The treatment is to use a needle to puncture through the chest between the ribs and release the air that is trapped between the lungs and the chest wall.

All overexpansion injury occurs at the alveolar level. The bronchi and bronchioles don’t rupture from overexpansion it’s the alveoli. This is the weakest point in the system. This sort of simplistic model of alveolar rupture into the arterial system does not make physiologic sense to me. It’s not a different model than a pneumothorax the claim is just that the air “ruptures” the arterial wall I guess? But the alveoli are only in close contact with a network of thin capillaries. If they rupture the capillaries I’m not sure the gas would travel down the arterial system. I suspect it would escape into the pleural space which has negative pressure. Rapid diffusion would make more sense. But still. Not saying it can’t be true just that I doubt it. I’ve cut into a fair number of lungs but I’m no pulmonary physiologist. I’m just not sure why the gas would escape into the arterial system to release the pressure rather than through the wall into the pleural cavity.

The microbubble theory makes sense to me though as overloading the capillary bed with a large number of micro bubbles could much more foreseeably lead to gas in the arterial system in my mind. There’s not really a way to prove this. Either way that I can imagine off the top of my head. You could probably design an experiment that might lead you in the right direction. But it just doesn’t make sense to me the way the mechanism is described. I also think we would see them way more often if overpressurization of the lungs was the cause of air embolism because we see a reasonable amount of these from errors that can occur with intubated patients. Not in high numbers but in the aggregate for sure we should have noticed it.


I’ll add the microbubble theory explains air embolism that occurs without obvious lung injury and also suggest that a rapid ascent is always dangerous regardless of how you manage your exhalation.

 

[pauldw]

This sort of simplistic model of alveolar rupture into the arterial system does not make physiologic sense to me.

Yeah, it's a confusion. When I took OW in the mid-eighties, there wasn't even such a thing as arterial gas embolisms. Just exploding lungs and fizzing blood, depending on your mistake.