Abstract

We derive the conditions under which an arterial gas embolus—an AGE—either grows or contracts while being carried by arterial blood, and the role of this in decompression sickness (DCS) in scuba diving and in DCS-like conditions in breath-hold diving. The AGEs are presumed to have arisen by arterializations of venous gas emboli through a right/left shunt, which can be either a cardiac shunt such as a patent foramen ovale (PFO) or a pulmonary shunt such as an arterial-venous anastomosis (AVA). A key calculation is to compare transit times of an AGE from the left heart to the head, for an AGE that was arterialized through a PFO or an AVA. We find that for arterializations through a PFO and an AGA, respectively, AGEs generated at 100 fsw with corresponding initial radii of <(4.5–6) μ and <(6–8) μ will tend to dissolve (and therefore do no harm) before reaching the head. But AGEs larger than this will survive the trip before dissolving and may (depending on their size and the degree of contiguous tissue supersaturation) become significantly inflated. We also find that both for competitive-level single breath-hold dives and for repetitive commercial breath-hold dives—such as in pearl diving in the South Pacific—both inner ear DCS (IEDCS) and cerebral DCS (CDCS) can be expected to occur. This is because in both, the degree of supersaturation of the brain and inner ear can be sufficient to significantly inflate AGEs lodged in nearby capillaries. For repetitive commercial breath-hold diving, the duration of the surface interval between consecutive dives was found to be crucial, with surface intervals of at least 15min being sufficient to largely prevent CDCS and IEDCS.

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