Decompression Sickness in Breath-hold Diving, and Its Probable Connection to the Growth and Dissolution of Small Arterial Gas Emboli
Authors: Saul Goldman, J. M. Solano-Altamirano
DOI / Source: 10.1016/j.mbs.2015.01.001
Date: 05 January 2015
Reading level: Intermediate
Why This Matters for Freedivers
This paper gives a very clear “how could DCS happen in freediving” explanation that goes beyond rules of thumb. The practical message is simple: tiny bubbles can survive long enough to reach sensitive areas (brain/inner ear), and repetitive diving with short surface intervals can make that risk much bigger—while longer surface intervals can reduce it dramatically.
Synopsis
Freedivers often hear two ideas that seem to clash: “DCS is a scuba thing,” but also “Taravana is real.” This paper tries to bridge that gap with a simple but powerful concept: small arterial gas emboli—tiny bubbles that make it into the arterial side of circulation—can act like “seeds.” Most of the time those seeds disappear quickly, because surface tension makes small bubbles want to shrink and dissolve. So far, so reassuring.
The interesting part is what happens if a seed bubble doesn’t fully dissolve in time and ends up lodged in the tiny capillaries that feed the brain or inner ear. After a dive, those tissues can be temporarily loaded with extra nitrogen (they “lag behind” the fast changes happening in the lungs and arterial blood). If the tissue around the capillary is still nitrogen-rich, nitrogen can diffuse into the trapped bubble and inflate it, making it more capable of blocking blood flow in a very narrow vessel. In the authors’ model, that’s a plausible pathway for neurological DCS and inner ear DCS in breath-hold diving.
To explore this, the authors build a mathematical model of bubble growth/shrinkage using diffusion physics (solving the Laplace equation for a simplified “bubble + surrounding medium” setup). Then they run the model on two real-world patterns: - Single very deep, competitive-style dives, where the exposure is short but intense. - Repetitive commercial-style dives (like traditional pearl diving), where each dive is moderate but the session is long and the dives are frequent.
The most useful takeaway for everyday freedivers comes from the repetitive-diving scenario: surface interval matters a lot. When the break on the surface is short, nitrogen doesn’t have time to wash out, and the model predicts a much higher chance that these tiny arterial bubbles could grow in the brain/inner ear environment. When the surface interval is much longer (they highlight ~15 minutes as a big step-change in their modeled scenarios), the predicted risk drops sharply because tissue nitrogen has time to fall.
You don’t need to follow the math to benefit from the logic: this paper supports the idea that freediving risk isn’t just about “max depth,” but about the whole session profile—how repetitive it is, how short the rests are, and how long you keep the day going.
Abstract
We solved the Laplace equation for the radius of an arterial gas embolism (AGE), during and after breath-hold diving. We used a simple three-region diffusion model for the AGE, and applied our results to two types of breath-hold dives: single, very deep competitive-level dives and repetitive shallower breath-hold dives similar to those carried out by indigenous commercial pearl divers in the South Pacific. Because of the effect of surface tension, AGEs tend to dissolve in arterial blood when in arteries remote from supersaturated tissue. However if, before fully dissolving, they reach the capillary beds that perfuse the brain and the inner ear, they may become inflated with inert gas that is transferred into them from these contiguous temporarily supersaturated tissues. By using simple kinetic models of cerebral and inner ear tissue, the Nitrogen tissue partial pressures during and after the dive(s) were determined. These were used to theoretically calculate AGE growth and dissolution curves for AGEs lodged in capillaries of the brain and inner ear. From these curves it was found that both Cerebral and Inner Ear Decompression Sickness are expected to occur occasionally in single competitive-level dives. It was also determined from these curves that for the commercial repetitive dives considered, the duration of the surface interval (the time interval separating individual repetitive dives from one another) was a key determinant, as to whether Inner Ear and/or Cerebral decompression sickness arose. Our predictions both for single competitive-level and repetitive commercial breath-hold diving were consistent with what is known about the incidence Cerebral and Inner Ear Decompression Sickness in these forms of diving.