Just to follow up a bit more. The natural question is, “if helium is taken up faster than nitrogen into the inner ear fluid space faster, why doesn’t this impose a helium penalty, whereby the inner ear imposes a deeper first stop if diving heliox than trimix or nitrox?” This is a complicated issue, and indeed inner ear DCS does sometimes onset during decompression, characteristically not long after a helium-to-nitrogen switch, indicating either that the helium-to-nitrogen switch is implicated, or that the decompression up to that time (including obviously the deeper stops) was insufficient. I happen to believe the latter is the more important factor - so why no helium penalty? There are two issues to consider. First is because inner ear DCS during decompression typically occurs from dives deeper than 300 fsw (and unusually much deeper), which are conducted with mostly helium and probably inconsequential amounts of nitrogen, so there is no scope for a helium penalty to manifest – i.e. no one is conducting 400 fsw air dives to find out if they can get away with a bit shallower first stop than a comparable heliox dive.
Second, the inner ear might not be the “leading” tissue that imposes the first decompression stops. Much of my thinking about inner ear DCS is summarized in Mitchell and Doolette, Pathophysiology of inner ear decompression sickness: potential role of the persistent foramen ovale. Diving and Hyperbaric Medicine 2015;45:105-110. Here we summarize the data about inner ear DCS occurring following air and nitrox diving, where inner ear DCS is not uncommon and there is a lot of data. These data show that there is a strong associating with persistent (patent) foramen ovale (PFO) / right-to-left shunt of bubbles (RLS). More than 80% of the divers with inner ear DCS have RLS, compared to about 25% in the general population. This (and other circumstantial evidence) suggests that RLS of VGE through a PFO is the culprit in most inner ear DCS occurring after surfacing from these sort of dives. In that paper, we hypothesize that this same PFO mechanism might be the cause of inner ear DCS occurring during decompression from technical dives. So whereas supersaturation by decompression (with perhaps a small contribution from ICD) in the inner ear is important, you need to seed the inner ear with bubbles by RLS. There still is not enough data to confirm that hypothesis, but a paper published since showed that in five of eight (63%) technical divers who had inner ear DCS tested positive for PFO/RLS (Guenzani et al. Inner-ear decompression sickness in nine trimix recreational divers. Diving and Hyperbaric Medicine 2016;46:111-116.) If VGE are the culprit, then it may be that the tissues from which the VGE arise (that may not manifest any helium penalty), not the inner ear itself, that are the “leading” tissues during the relevant part of decompression.
It is noteworthy that inner ear DCS is usually associated with relatively aggressive decompression, whether it follows air / nitrox dives or occurs during decompression from deeper helium-based dives. When conducting deeper dives, my recommendation is to use conservative decompression and not assume that the levels of conservatism you use for say a 200 fsw dive are going to be adequate.
David Doolette