C S Olstad | PubMed Health

PubMed1992

Susceptibility of divers in open water to motion sickness.

Several aspects of the environment of divers should increase their susceptibility to motion sickness: a) sensory conflicts, b) body fluid redistribution, and c) nitrogen narcosis. We tested motion sickness susceptibility by placing subjects on a rotating platform and having them perform stylized heat movements that produced cross-coupled angular accelerations in vestibular end organs until nausea developed. This test was performed once each day on 9 consecutive days while subjects were immersed at the end of 3-4 h of diving. The test was also carried out while subjects were nonimmersed with no preceding diving on the day immediately before and after this 9-day period. Compared with nonimmersed conditions, significantly fewer head movements were required to elicit nausea while immersed (P less than 0.01). We conclude that individuals are more susceptible to motion sickness while immersed in open water than while on dry land.

Coriolis Force↗

PubMed1991

Ethanol and venous bubbles after decompression in humans.

We exposed 34 subjects to a 48-h, 6.25-msw dive, and administered ethanol (0.5-1.0 ml pure ethanol.kg-1 body weight) orally to 11 of them immediately after direct decompression. Doppler monitoring of both precordial and subclavian sites for 24 h postsurfacing revealed that all subjects from both groups had detectable bubbles, and that there was no difference in timing or magnitude between the 2 groups. These results do not support the recently suggested role for ethanol in the treatment of decompression sickness.

Decompression Sickness↗

PubMed1990

Human dose-response relationship for decompression and endogenous bubble formation.

The dose-response relationship for decompression magnitude and venous gas emboli (VGE) formation in humans was examined. Pressure exposures of 138, 150, and 164 kPa (12, 16, and 20.5 ft of seawater gauge pressure) were conducted in an underwater habitat for 48 h. The 111 human male volunteer subjects then ascended directly to the surface in less than 5 min and were monitored for VGE with a continuous-wave Doppler ultrasound device over the precordium or the subclavian veins at regular intervals for a 24-h period. No signs or symptoms consistent with decompression sickness occurred. However, a large incidence of VGE detection was noted. These data were combined with those from our previously reported experiments at higher pressures, and the data were fit to a Hill dose-response equation with nonlinear least-squares or maximum likelihood routines. Highly significant fits of precordial VGE incidences were obtained with the Hill equation (saturation depth pressure at which there is a 50% probability of detectable VGE [D(VGE)50] = 150 +/- 1.2 kPa). Subclavian monitoring increased the sensitivity of VGE detection and resulted in a leftward shift [D(VGE)50 = 135 +/- 2 kPa] of the best-fit curve. We conclude that the reduction in pressure necessary to produce bubbles in humans is much less than was previously thought; 50% of humans can be expected to generate endogenous bubbles after decompression from a steady-state pressure exposure of only 135 kPa (11 ft of seawater). This may have significant implications for decompression schedule formulation and for altitude exposures that are currently considered benign. These results also imply that endogenous bubbles arise from preexisting gas collections.

Adult↗