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

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I’m having difficulty finding a clear answer to this. An earlier thread posed a similar question but no response: Air embolism with empty lungs

My understanding of an AGE event is caused by the lungs physically unable to expand further when exposed to expanding gas within the lungs. Specifically I am referring to the actual physical expansion of the lungs with the diaphragm moving.

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)?
Or would the lungs not physically inflate and therefore an AGE will occur because even though the lungs have the capacity to physically inflate, they don’t and instead the gas enters the arterial system?

From what I’ve read, I infer that the former is true since there are discussions on lung barotrauma, which would indicate an expanding lung, but then again this goes back to the original question: will my lungs physically inflate (along with diaphragm movement) to accommodate the increased gas volume upon ascent?
 
I’m having difficulty finding a clear answer to this. An earlier thread posed a similar question but no response: Air embolism with empty lungs

My understanding of an AGE event is caused by the lungs physically unable to expand further when exposed to expanding gas within the lungs. Specifically I am referring to the actual physical expansion of the lungs with the diaphragm moving.

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)?
Or would the lungs not physically inflate and therefore an AGE will occur because even though the lungs have the capacity to physically inflate, they don’t and instead the gas enters the arterial system?

From what I’ve read, I infer that the former is true since there are discussions on lung barotrauma, which would indicate an expanding lung, but then again this goes back to the original question: will my lungs physically inflate (along with diaphragm movement) to accommodate the increased gas volume upon ascent?
Couple thoughts:

1. There's more than one way to get gas into the arterial system. However, the way you're thinking of is due to lung overexpansion injury which ---wait for it--- involves overexpansion of the lungs.

2. Don't even think of doing the experiment from 20 m up holding your breath. Perhaps most importantly, you really don't know how empty your lungs are. There's always residual gas in there unless your lungs are collapsed. There's also gas in your bronchi, trachea, esophagus above the epiglottis, mouth, nasal passages, sinuses, etc.. All that is an interconnected system and the gas expanding in one will get pushed to the other spaces.

3. I don't know if your diaphragm would get pushed down, especially if you were "holding your breath" and consciously or subconsciously keeping it in place. Seems like it's a strong muscle and is quite capable of outlasting the more delicate linings of your alveoli. But ask a person doc, not me.

4. Your lungs will expand on your putative ascent.

5. The real issue is panicked divers holding their breaths and bolting.


Googling some numbers from a random site, it seems a "typical male" might still have 2.4 L of air in their lungs after a normal exhalation. (Not after trying to fully exhale all air.) The total lung volume for our typical male is 6 L. I don't think those numbers include the volume of air in "airways" outside the lung. All to say is that if you double the volume of all the air in the system, I think it's the alveoli that are going to be your failure point.....
 
From a very simplistic standpoint, the lungs inflate because the diaphragm moves....the diaphragm doesn't move because the lungs inflate.

-Z
 
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.
 
The answer is that you won't have a lung injury going from 10 to 20 meters. This assumes that you are healthy and have no obstructions in any air passages in your lungs- I'm not sure how you could safely confirm that.

If you use a conceptual model of the lungs as a simple balloon, then you can hold your breath and ascend until the lungs are expanded to capacity (possibly even a little more). But the reality, is that your lungs are not balloons. The anatomy is more complex, the alveoli are tiny delicate, dead end sacs.

Rather than thinking of your lungs as a balloon, it is probably better to think of it more like a giant clump of grapes that have a series of ever smaller branches. If any one of those branches is occluded by mucus, or a tiny physical defect, then a small branch of the lung could be blocked off and allow a localized area of (excess) expansion, even though the lung as a whole, is not yet at its volumetric capacity. If a small area fails, you can get raw air into the circulation, and even outside of the lung - which is not good either.

So yeah, you can exhale at 20 meters and come up to 10, but these are not the types of games to play.
 
Or would the lungs not physically inflate and therefore an AGE will occur because even though the lungs have the capacity to physically inflate, they don’t and instead the gas enters the arterial system?

This is more a basic misunderstanding of lung physiology. The alveoli are for the most part not ever fully empty. Some are, sometimes, but when they fully empty they collapse on themselves. This is called atelectasis and requires increased force to overcome. There is some degree of atelectasis in all lungs here and there. But for the most part the lungs always contain some air. There’s no big hole between the alveoli and the arterial system. In fact there are no real holes at all. The gas diffuses across a thin (single cell layer) of tissue into the capillary bed. This is why I doubt the mechanism of volutrauma giving rise to air embolism.

I’ll add. Ignore the diaphragm for the purposes of understanding the pathophysiology of this condition. It is irrelevant for these purposes. Its position in the thoracic cavity will change with lung volume whether you want it to or not. The amount of physical force you would have to exert to prevent that would be so high that it is not an important component.
 
I’m having difficulty finding a clear answer to this. An earlier thread posed a similar question but no response: Air embolism with empty lungs

My understanding of an AGE event is caused by the lungs physically unable to expand further when exposed to expanding gas within the lungs. Specifically I am referring to the actual physical expansion of the lungs with the diaphragm moving.

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)?
Or would the lungs not physically inflate and therefore an AGE will occur because even though the lungs have the capacity to physically inflate, they don’t and instead the gas enters the arterial system?

From what I’ve read, I infer that the former is true since there are discussions on lung barotrauma, which would indicate an expanding lung, but then again this goes back to the original question: will my lungs physically inflate (along with diaphragm movement) to accommodate the increased gas volume upon ascent?

So yeah, you can exhale at 20 meters and come up to 10, but these are not the types of games to play.
Why would one even think abut doing this? What is the point?
 
Empty lungs -- 1.5l air residual volume (what cannot be physically exhaled).
Ascend from 20m to 10m. (3bar to 2 bar) lungs now have 2.25l air.
You've also added .75kg buoyancy due to lung expansion, so you're now quite positive at 10m.
That next 10m to surface (2 bar to 1 bar), lungs will now have 4.5l air. On a small frame body, that's into the danger zone. If you haven't arrested your ascent, those last 10 m will find you adding 2.25 kg buoyancy, and it will be difficult to prevent corking.

The good book says breathe constantly, and exhale on ascent. Somebody learned this the hard way, the rest of us can be happy taking lessons.
 
This assumes that you are healthy and have no obstructions in any air passages in your lungs- I'm not sure how you could safely confirm that.
A chest CT scan can reveal physical obstructions caused by disease etc. Obviously not a practial solution for a person who seems healthy, but something to consider for a diver with any signs of lung disease. A slight persistant cough or feeling out of breath from moderate physical activity could be warning of underlying lung issue that could cause problems for a diver.

Rather than thinking of your lungs as a balloon, it is probably better to think of it more like a giant clump of grapes that have a series of ever smaller branches. If any one of those branches is occluded by mucus, or a tiny physical defect, then a small branch of the lung could be blocked off and allow a localized area of (excess) expansion, even though the lung as a whole, is not yet at its volumetric capacity. If a small area fails, you can get raw air into the circulation, and even outside of the lung - which is not good either.
This sums up a first hand experience with pulmonary barotramua and AGE. Despite following the rule of constant breathing, air trapping on ascent occured in a very localized area of the lungs. In this case the physical defect was caused by minor bronchiectasis that was not discovered until after the accident.
 
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