The risk for decompression sickness (DCS) after hyperbaric exposures (such as SCUBA diving) has been linked to the presence and quantity of vascular gas emboli (VGE) after surfacing from the dive. These VGE can be semi-quantified by ultrasound Doppler and quantified via precordial echocardiography. However, for an identical dive, VGE monitoring of divers shows variations related to individual susceptibility, and, for a same diver, dive-to-dive variations which may be influenced by pre-dive pre-conditioning. These variations are not explained by currently used algorithms. In this paper, we present a new hypothesis: individual metabolic processes, through the oxygen window (OW) or Inherent Unsaturation of tissues, modulate the presence and volume of static metabolic bubbles (SMB) that in turn act as precursors of circulating VGE after a dive.
We derive a coherent system of assumptions to describe static gas bubbles, located on the vessel endothelium at hydrophobic sites, that would be activated during decompression and become the source of VGE. We first refer to the OW and show that it creates a local tissue unsaturation that can generate and stabilize static gas phases in the diver at the surface. We then use Non-extensive thermodynamics to derive an equilibrium equation that avoids any geometrical description. The final equation links the SMB volume directly to the metabolism.
Our model introduces a stable population of small gas pockets of an intermediate size between the nanobubbles nucleating on the active sites and the VGE detected in the venous blood. The resulting equation, when checked against our own previously published data and the relevant scientific literature, supports both individual variation and the induced differences observed in pre-conditioning experiments. It also explains the variability in VGE counts based on age, fitness, type and frequency of physical activities. Finally, it fits into the general scheme of the arterial bubble assumption for the description of the DCS risk.