Dear Readers:
PFOs and Arterialization
I just noticed an old thread under General Tec Discussions reference by Spectre. I did not originally see that as I was away at that time without my laptop. The subject of arterialization came up on the thread and the need for the PFO. In actuality, clinicians who measure arterialization (to determine the cause of a stroke in an individual) do find instances where the arterialization of the saline contrast gas bubbles occurs and a PFO is absent. In this case, it is postulated that the route of the gas bubbles is through pulmonary shunts), that is, though blood vessels larger than lung capillaries. This is based on the observation that PFO bubbles are in the left ventricle in one or two heartbeats, while with pulmonary shunts, it requires five or more heat beats.
WKPP and Arterialization
The observation that individuals who re-dive are at risk for DCS is an important one. What I was debating was whether the mechanism was one of passage through the lungs with repressurization. I did not doubt the observation that DCS occurred. Laboratory trials indicate that passage does not occur. HOWEVER, evidence collected since 1995 by clinicians (regarding so-called paradoxical stroke = stroke from clots originating on the venous side of the circulatory system) implicate Valsalva-like maneuvers to a large degree. This is somewhat different than the laboratory studies of the 1980s. In these studies, Valsalva-like maneuvers were not performed. Neither were straining maneuvers performed when reaching surface after a very short dive. This might color the outcome and is what makes this forum interesting for me; I receive information that I would not otherwise find.
Microbubbles and Repetitive Dives
I am more a proponent of the microbubbles-through-hydrodynamic-cavitation hypothesis. The concepts of Dr Wienke stress these changes less, most likely because they are less deterministic (= more random) and not as easily modeled. The concepts that I present were developed more to explain decompression risk in a gravity-free environment with its attendent reduced level of musculoskeletal activity. In addition, prior compression is not involved in hypobaric activity as it is in diving.
During the initial descent, I have little reason to doubt that the micronuclei are compressed. It is during the surface interval that musculoskeletal activity will make its being appearance with respect to microbubbles. Here we see not only microemboli formation, but also growth while tissues are in a state of supersaturation. Repetitive decompression while under these conditions is apparently very harmful.
Laboratory Experiments
It is obvious that experiments with humans would be very difficult to perform for many of these questions to be answered. It would involve exposing people to situations where arterialization would be provoked and made to occur. While the proper setting could be obtained to virtually assure subject safety, it is still not totally risk free. There are questions involved regarding the necessity of doing this study as well as questions of subject compensation if something horrible comes about that can not be reversed with pressure therapy.:boom:
In the absence of direct trials, recourse can sometimes be made to research work in the field of vein-to-artery (paradoxical) stroke. Here we have studies where the individuals are at a greater risk if nothing is done. I have taken some of these studies and imposed the results on the diving situation. At the present, that is the best information that we will obtain.
Dr Deco :doctor:
