It seems people tend to get rather confused by the math. The change in pressure with respect to depth is (basically*) a constant. There's the same pressure difference between zero and six feet as between 100 and 106 feet. When discussing the expansion of gases, however, the volume change is related to the *ratio* of pressures.
Consider a rudimentary mental model of a curly/wavy flexible glass fiber. You can push the ends closer together, and you can stretch them farther apart. You can treat it as a fully elastic system (i.e. you can extend and contract the fiber, and it can return to the original at-rest state). However, if you continue stretching the ends farther apart, you eventually get to a point where there is no more "slack" in the fiber. If you pull the ends any farther apart, the fiber breaks, as without any slack to give, it is brittle with respect to further attempts at stretching.
You puff open the alveoli more and more, but eventually the support matrix on which their structure is assembled reaches its elastic limit. As it has no more "slack" to give, any further expansion causes a break -- a tear -- in the structure, i.e. barotrauma.
Now, as to the question about why embolism instead of pneumothorax, I haven't come up with anything better than my previous conceptual idea (that of it being a function of resistance -- i.e. while unconscious, you're not putting pressure on the lungs from the diaphragm and chest, so the lungs just pop and you get pneumothorax, while when you're conscious, the diaphagm and muscles are preventing overexpansion into the chest cavity, so the air takes the next least difficult route and enters the bloodstream).
*Basically? Well, temperature and salinity both affect the density of water (thermoclines and haloclines being obvious results), and water is not completely incompressible (even though you can assume it is for scuba purposes).
When not fully expanded, this may be the case, however, I do not believe that you can treat fully expanded alveoli as elastic structures when it comes to attempted further expansion. Once you reach full expansion, the alveoli would need to be considered brittle rigid bodies. Expansion beyond this critical point ("full expansion") even a small amount is not possible without breakage.TSandM:
Consider a rudimentary mental model of a curly/wavy flexible glass fiber. You can push the ends closer together, and you can stretch them farther apart. You can treat it as a fully elastic system (i.e. you can extend and contract the fiber, and it can return to the original at-rest state). However, if you continue stretching the ends farther apart, you eventually get to a point where there is no more "slack" in the fiber. If you pull the ends any farther apart, the fiber breaks, as without any slack to give, it is brittle with respect to further attempts at stretching.
You puff open the alveoli more and more, but eventually the support matrix on which their structure is assembled reaches its elastic limit. As it has no more "slack" to give, any further expansion causes a break -- a tear -- in the structure, i.e. barotrauma.
Now, as to the question about why embolism instead of pneumothorax, I haven't come up with anything better than my previous conceptual idea (that of it being a function of resistance -- i.e. while unconscious, you're not putting pressure on the lungs from the diaphragm and chest, so the lungs just pop and you get pneumothorax, while when you're conscious, the diaphagm and muscles are preventing overexpansion into the chest cavity, so the air takes the next least difficult route and enters the bloodstream).
*Basically? Well, temperature and salinity both affect the density of water (thermoclines and haloclines being obvious results), and water is not completely incompressible (even though you can assume it is for scuba purposes).
