Two questions for diving science nerds only

[ClayJar]

I can't argue with your logic, but you have made one error --- the rate of exhalation is not linear --- exhaled air = 0.7 lu/sec (suggesting that it takes less than 1.5 sec to dump all air from the lungs), but an exponential decline

Actually, I do not believe that was an error. I assumed that the reason there is an exponential decline is because there is less air remaining in the lungs. If the air in the lungs is expanding to match the rate of exhalation, there will be no net change in lung volume. The volumetric rate of exhalation, meanwhile, will be set by the delta in pressure from the lungs to the outside world, which is, of course, created by the muscles used to exhale.

Assuming the volume of the air is increasing at a sufficient rate to maintain constant lung volume while exhaling at the maximum rate, and ignoring breathing muscles' fatigue (which is outside the scope of this thread, if it's even been studied at all in this context), one could maintain a constant volumetric rate of exhalation without the exponential decline.

The key is that the volume of the lungs and the pressure gradient between them and the outside can both be held as constants assuming the rate of expansion is matched to the rate of exhalation, which it would be in the limiting case I was using to describe the upper bound. (The total volume of air exhaled may easily be *significantly* more than 1 Lu.)

 

[dumpsterDiver]

I understand that dive training used to involve a swimming ascent with the regulator held outside of the mouth from a depth of 60 feet (a free ascent). I remember learning (I don't know where) that there were a number of cases of AGI, even though the instructor supposedly confirmed that exhalation had occured on the bottom or was occuring on ascent. This is no longer commonly practiced.

My understanding is that the problems arose when people completely exhaled at depth and just swam/floated up fast. Since the residual volume after a full exhale could not theoretically exceed the lung capacity (from 60 ft), this was supposed to be ok. But apparently for some divers doing a complete exhalation at depth causes portions of the lungs or airways to be shut down and isolated from the foreceful exhalation, thus on ascent, even though the total lung volume never reached capacity, the portions of the lung which were "isolated" did not have the capacity to expand. I was taught to exhale relatively slowly and constantly on ascent.

It would be very easy to determine the maximum ascent rate of a scuba diver: Put on or hold 1-2 weight belts (60-80 lbs) that will cause you to be negatively bouyant by 25 lbs-even with the BC inflated. Do not breath from the regulator, swim/sink down to a reasonable depth of say 50 feet, fully inflate the BC with the LP inflator, then drop the lead.. swim like hell for the surface and time the ascent. The entire trip should take less than 45 seconds. A simple experiment and should be easy for a decent freediver...

 

[ClayJar]

Fascinating thread -- one of the things that has puzzled me from the time it was first brought up in OW class was WHY divers who get pulmonary barotrauma get arterial gas embolism.

In my prior practice, we had patients on ventilators requiring VERY high inspiratory pressures, and they blew pneumothoraces routinely -- I have seen a patient with six chest tubes in as a result. Never, ever did we have an arterial gas embolism.

Okay, time to play House (MD)... I have no medical background from which to formulate an answer, so I'll have to settle for what seems plausible to me:

Could it be that the fact the divers are (at the time of the injury) consciously breathing (holding their breath) be the important factor?

If a person is not breathing on their own, there is little *actively* resisting lung inflation, so overpressuring the lungs just blows them out, giving pneumothorax. However, if a person is *consciously* holding their breath, they are likely tensing up, as if to exhale, while holding their throat closed as well. This tensing (via pressure or some associated factor) takes what would have "merely" been pneumothorax and forces air into the bloodstream, yielding AGE.

Might that seem like a plausible answer?

 

[shakeybrainsurgeon]

I understand that dive training used to involve a swimming ascent with the regulator held outside of the mouth from a depth of 60 feet (a free ascent). I remember learning (I don't know where) that there were a number of cases of AGI, even though the instructor supposedly confirmed that exhalation had occured on the bottom or was occuring on ascent. This is no longer commonly practiced.

My understanding is that the problems arose when people completely exhaled at depth and just swam/floated up fast. Since the residual volume after a full exhale could not theoretically exceed the lung capacity (from 60 ft), this was supposed to be ok. But apparently for some divers doing a complete exhalation at depth causes portions of the lungs or airways to be shut down and isolated from the foreceful exhalation, thus on ascent, even though the total lung volume never reached capacity, the portions of the lung which were "isolated" did not have the capacity to expand. I was taught to exhale relatively slowly and constantly on ascent.

It would be very easy to determine the maximum ascent rate of a scuba diver: Put on or hold 1-2 weight belts (60-80 lbs) that will cause you to be negatively bouyant by 25 lbs-even with the BC inflated. Do not breath from the regulator, swim/sink down to a reasonable depth of say 50 feet, fully inflate the BC with the LP inflator, then drop the lead.. swim like hell for the surface and time the ascent. The entire trip should take less than 45 seconds. A simple experiment and should be easy for a decent freediver...

This was a point I tried, perhaps badly, to make earlier --- the lungs aren't simple balloons but rather millions of alveoli and broncioles converging into the main bronchi and trachea. Calculations like Clayjar's presume that air is flowing out of all lung compartments equally, which may not be the case. It is possible that local lung regions might become relatively air-trapped, leading to focal pulmonary injury.

 

[ClayJar]

I was actually taught somewhere along the line that forcibly exhaling to start an ascent can lead to trapping air and the resultant barotrauma, which was another reason to always breathe normally (meaning exhale normally on ascent). Also, the reason they gave for not diving with a chest cold was basically the same idea. If you block off part of your lungs (by chest-cold materials which shall remain nameless this close to supper), you can seriously injure yourself even if behaving properly.

(The physics-of-exhalation discussion is about a limiting case for a diver with balloon lungs, but it's an interesting conceptual discussion about what rate you would have to ascend to suffer barotrauma even in a best-case scenario.)

 

[TSandM]

There may certainly be some differences in the physics of barotrauma from ventilation, and barotrauma from gas expansion, although I would expect the force necessary to rupture alveoli would be similar in both cases. But another factor is also interesting -- rupture occurs in the alveoli, which are the smallest air sacs, and the vessels perfusing those alveoli are capillaries, the smallest blood vessels. So how does one blow enough air into a capillary to end up with an embolism?

 

[ClayJar]

Well, if you're polarising from 33fsw, you would only need to blow half enough air to end up with an embolism, but as for how you'd get that much in, um... er... aquagnomes, perhaps?