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

[BlueTrin]

Where is @Dr Simon Mitchell when you need him?

Or @Duke Dive Medicine

 

[Gelirfella]

Nope, NOT buying it now. Freedivers go down way over 100 or 200 feet and then shoot to the surface and don't get it, but a scuba diver goes to 15 feet for 20 seconds is going to get all these bubbles? Makes zero sense.

That’s a fair point. I’m not sure if the physiology of breath hold diving applies perfectly. are there any cases of air embolism documented from a short duration dive? Also, it is an incredibly rare event though pneumothorax is more common. Why would it not be more common than it is? Perhaps, the circumstances that lead to direct pressurization of gas into the arterial system are just extremely rare. Or perhaps it requires a person with specific microbubble formation characteristics, depth, time, and ascent profiles? Free divers that can achieve those depths may already have been selected to be individuals with decreased susceptibility? I didn’t make this theory up as I’ve said. I just find it to be more plausible than the alternative.

 

[Angelo Farina]

Free divers GET lung overexpansion.
I remember one of the first cases occurred to Enzo Majorca in the seventies.
This is due to the "blood shift".
Let's make an example.
The free diver has a total volume capacity of 6 liters (including lungs and airways).
He starts with lungs full, after some minutes of "lung pumping", that is doing profound ventilation, exhaling through partially occluded mouth, so during this preparatory ventilation the lung pressure is, on average, positive. This slowly "pushes away" blood from lungs, so that they can get some more air. Thanks to this trick, he manages to incamerate slightly more than 6 liters with the last breath, let say it is 6.2 liters.
During the deep dive the ambient pressure is conspicuous, squeezing the lungs to their very minimal volume, or even less. At that point an amount of blood is attracted into the lungs, causing some sort of oedema.
This avoids the cage to be crushed, or the lungs to be ruptured. But then, when ascending, the lung volume is smaller, and cannot accomodate the initial 6.2 liters.
So if the diver is breath-holding up to the surface, the risk of lung over-expansion is real. The risk is avoided exhaling some gas BEFORE reaching the surface, as almost all deep free divers do in the last few meters.

 

[Angelo Farina]

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).

Of course no one could recommend doing this experiment!
However, just for theoretical analysis, let's assume that your total capacity is 6 liters (lungs + airways), and that, when you exhale, you manage to get your lungs "relatively empty": that is, they contain just 2 liters.
So there is space for a 3x expansion before lung over-expansion occurs.
As you are down to 20m (3 bar abs.pressure) you can ascend to surface (1 bar abs.pressure).
You will end up with completely full lungs (6 liters), but yet no over expansion.
This is on the edge, indeed, hence VERY dangerous: just a bit more than 2 liters left in your lungs, and over expansion will occur.
However, if you stop at 10m (2 bars abs. pressure) your 2 liters will expand just by a 3/2 factor, so they will become 3 liters. You will feel your lungs expanding (usually it will be chest expansion more than diaphragm expansion).
But this should not kill you; still I do not recommend doing this!
Breath holding while scuba diving is not so dangerous as many people think, provided that you do not ascend while breath holding.
Actually when I started diving we were using CC rebreathers, not air tanks: with such apparatus the correct way of breathing was very slow exhalation, very slow inhalation and an inspiratory pause of several seconds (5÷10).
But when ascending, even just a couple of meters, the pause had to be removed!

Regarding the question if a lung over expansion always results in embolism or not, I cannot answer, as I am not a medical doctor.
But even without embolism, lung damage due to over-expansion is already quite severe, so better to avoid it!

 

[Dr Simon Mitchell]

Hello,

Gelirfella, while it is true that the exact mechanism by which alveolar gas enters the pulmonary circulation during pulmonary barotrauma is not well defined, there is overwhelming (essentially incontrovertible) evidence that it occurs. Specifically, in arterial gas embolism occurring in many experimental and diving settings, there is no other possible source for the gas.

In several posts you have proposed the alternative explanation of venous microbubbles formed from dissolved inert gas finding their way into the arterial circulation (I presume you mean via a PFO or pulmonary shunt). It is true that this can happen, but these bubbles are very small and have very short lifetimes in the arterial circulation. They can contribute to some forms of decompression sickness, but will not cause the gross focal stroke-like brain lesions that we see in arterial gas embolism (AGE). More importantly, as others have pointed out in this thread, AGE has occurred in many experimental and clinical scenarios where there is little or no inert gas loading that would drive venous bubble formation, so the lungs are the only possible source of gas. Finally, some cases of pulmonary barotrauma and arterial gas embolism involve volumes of gas (e.g., complete airlock of the left heart) that could not possibly have evolved from dissolved gas and even if they did, the air lock would be in the right heart, not the left heart.

In the interests of open disclosure, there is one case in which venous microbubbles introduced as bubble contrast for a PFO test, appear to have coalesced on the venous side before crossing a PFO as a large bubble to produce a stroke-like event. However, this is an unusual scenario where a large concentration of bubbles were introduced into a single very peripheral vein, and thus not really comparable to diving. Moreover, as above, AGE has occurred in many diving scenarios where venous microbubble formation simply could not have occurred e.g., see here and here.

I certainly admire your curiosity, but in this case we just have to accept that something essentially proven to occur, occurs, even though we don't fully understand the mechanism. At a simplistic level, one could say that its not a huge intellectual leap from over-expanded alveoli rupturing their gas content into adjacent blood vessels which also get damaged. A significant proportion of divers (though not all) suffering AGE present with signs like hemoptysis (coughing blood) which support such a mechanism.

Getting back to the original issue in this thread, in theory, lungs that are partially filled with compressed gas (they are never truly empty) should be able to tolerate some degree of ascent and pressure reduction. However, biology always throws up unexpected twists. For example, and to some extent unproven speculation, in near empty lungs, some of the small airways leading to alveoli may collapse. Thus, during subsequent ascent, if the gas in those alveoli becomes functionally trapped and if the airways don't open quickly enough as that gas expands, the alveoli could get damaged leading to pulmonary barotrauma. As others have said, not something to be experimented with! Best just follow that old advice and breathe normally - never hold your breath when scuba diving.

Simon M

 

[The Chairman]

Edit: I don't want anything I wrote to cloud what the good doctor wrote.

 

[Gelirfella]

AGE has occurred in many experimental and clinical scenarios where there is little or no inert gas loading that would drive venous bubble formation, so the lungs are the only possible source of gas.

This essentially disproves the hypothesis that microbubble load is the source of the gas embolism. Fair enough. You’ve spent a lot more time and energy thinking about this problem than I have. That said, I’m surprised we don’t see this more in hospitalized patients who suffer overexpansion injuries from positive pressure ventilation. I never stated I disbelieve the existence of the phenomenon. I doubted it at first when I read it in my OW materials because the description of alveolar rupture into the arterial system sounded improbable. But I did find case reports so I sought out a mechanism which seems to be simply stated as alveolar rupture into the arterial system which is difficult to conceptualize for me given the nature of the capillary bed and that I would suspect significant bleeding to occur if a larger vessel were injured in just the right way to introduce air into the system withou lt collapsing the vessel and with enough continuous forward flow in the vessel to transmit the air onward and not just generate an air lock right there. It appears to have been definitively shown in circumstances where gas dissolution cannot account for the injury which suggest overexpansion is the cause but I’m still not sure exactly how it’s happening, which I guess is also true of everyone else. So fair enough. It’s a mystery but it happens. Thanks for the response.

 

[Gelirfella]

At a simplistic level, one could say that its not a huge intellectual leap from over-expanded alveoli rupturing their gas content into adjacent blood vessels which also get damaged.

I’m just not sure it’s that easy. I spend a lot of time dealing with bleeding vessels and achieving hemostasis (in fact I was dealing with it just a few hours ago) and given the size of the vessels at the level of the alveoli I find it difficult to imagine. Blood vessels just simply cannot be modeled as rigid tubes (which I know you are well aware of). I accept, however, that it is happening by some mechanism.

 

[ScubaSamScubaStevesFather]

Getting back to the original issue in this thread, in theory, lungs that are partially filled with compressed gas (they are never truly empty) should be able to tolerate some degree of ascent and pressure reduction. However, biology always throws up unexpected twists. For example, and to some extent unproven speculation, in near empty lungs, some of the small airways leading to alveoli may collapse. Thus, during subsequent ascent, if the gas in those alveoli becomes functionally trapped and if the airways don't open quickly enough as that gas expands, the alveoli could get damaged leading to pulmonary barotrauma

Can you elaborate on how the lungs can tolerate some degree of pressure reduction when factoring in the diaphragm? I.e. I expect that lung expansion caused by pressure reduction would either a) be prevented fully or partially due to the diaphragm not contracting, and therefore impeding the lung’s ability to expand or b) be sufficient enough to force the diaphragm to “contract” to allow the lungs to physically expand.

Grateful for your response, especially considering how useless a surprisingly large portion of responses here have been.

 

[Dr Simon Mitchell]

Can you elaborate on how the lungs can tolerate some degree of pressure reduction when factoring in the diaphragm? I.e. I expect that lung expansion caused by pressure reduction would either a) be prevented fully or partially due to the diaphragm not contracting, and therefore impeding the lung’s ability to expand or b) be sufficient enough to force the diaphragm to “contract” to allow the lungs to physically expand.

Grateful for your response, especially considering how useless a surprisingly large portion of responses here have been.

Hello,

Diaphragmatic movement is not the only avenue for lung expansion. Upward and outward movement of the chest wall would also accommodate lung expansion. With that said, all involved structures (chest wall and diaphragm) incorporate skeletal muscle which would have to not be actively opposing expansion in order for it to occur. However, I think under normal circumstances a state of expansion compliance would exist most of the time, allowing the lungs to expand if airway pressures increased. Even if that were not the case (i.e., the lungs were not able to expand during ascent when compressed gas is trapped), pulmonary barotrauma could still occur because the transpulmonary pressure (pressure difference from inside to outside the lung) would be increasing. This has been demonstrated experimentally, though it seems the risk is greatest when transpulmonary pressure is increased AND the lungs are able to expand.

That said, I’m surprised we don’t see this more in hospitalized patients who suffer overexpansion injuries from positive pressure ventilation.

That's because we anesthesiologists are careful to keep the transpulmonary pressures at safe levels during positive pressure ventilation. In general we try to keep airway pressures less than 30 cmH2O and the threshold for a significant risk of pulmonary barotrauma in healthy lungs is probably around twice that (which can be generated with an ascent from about a meter underwater if the lungs are full at the start of the ascent). Pulmonary barotrauma can occur during positive pressure ventilation at lower (more like normal) pressures in diseased lungs (e.g., bullae that trap gas), but this is relatively rare.

Simon M