Indices of Increased Decompression Stress Following Long-Term Bed Rest.

Human extravehicular activity (EVA) is essential to space exploration and involves risk of decompression sickness (DCS). On Earth, the effect of microgravity on physiological systems is simulated in an experimental model where subjects are confined to a 6° head-down bed rest (HDBR). This model was used to investigate various resting and exercise regimen on the formation of venous gas emboli (VGE), an indicator of decompression stress, post-hyperbaric exposure. Eight healthy male subjects participating in a bed rest regimen also took part in this study, which incorporated five different hyperbaric exposure (HE) interventions made before, during and after the HDBR. Interventions i-iv were all made with the subjects lying in 6° HD position. They included (C1) resting control, (C2) knee-bend exercise immediately prior to HE, (T1) HE during the fifth week of the 35-day HDBR period, (C3) supine cycling exercise during the HE. In intervention (C4), subjects remained upright and ambulatory. The HE protocol followed the Royal Navy Table 11 with 100 min spent at 18 m (280 kPa), with decompression stops at 6 m for 5 min, and at 3 m for 15 min. Post-HE, regular precordial Doppler audio measurements were made to evaluate any VGE produced post-dive. VGE were graded according to the Kisman Masurel scale. The number of bubbles produced was low in comparison to previous studies using this profile [Kisman integrated severity score (KISS) ranging from 0-1], and may be because subjects were young, and lay supine during both the HE and the 2 h measurement period post-HE for interventions i-iv. However, the HE during the end of HDBR produced significantly higher maximum bubble grades and KISS score than the supine control conditions (p < 0.01). In contrast to the protective effect of pre-dive exercise on bubble production, a prolonged period of bed rest prior to a HE appears to promote the formation of post-decompression VGE. This is in contrast to the absence of DCS observed during EVA. Whether this is due to a difference between hypo- and hyperbaric decompression stress, or that the HDBR model is a not a good model for decompression sensitivity during microgravity conditions will have to be elucidated in future studies.

Submarine 'safe to escape' studies in man.

The Royal Navy requires reliable advice on the safe limits of escape from a distressed submarine (DISSUB). Flooding in a DISSUB may cause a rise in ambient pressure, increasing the risk of decompression sickness (DCS) and decreasing the maximum depth from which it is safe to escape. The aim of this study was to investigate the pressure/depth limits to escape following saturation at raised ambient pressure. Exposure to saturation pressures up to 1.6 bar (a) (160 kPa) (n = 38); escapes from depths down to 120 meters of sea water (msw) (n = 254) and a combination of saturation followed by escape (n = 90) was carried out in the QinetiQ Submarine Escape Simulator, Alverstoke, United Kingdom. Doppler ultrasound monitoring was used to judge the severity of decompression stress. The trials confirmed the previously untested advice, in the Guardbook, that if a DISSUB was lying at a depth of 90 msw, then it was safe to escape when the pressure in the DISSUB was 1.5 bar (a), but also indicated that this advice may be overly conservative. This study demonstrated that the upper DISSUB saturation pressure limit to safe escape from 90 msw was 1.6 bar (a), resulting in two cases of DCS.

Oxygen or carbogen breathing before simulated submarine escape.

Raised internal pressure in a distressed submarine increases the risk of bubble formation and decompression illness after submarine escape. The hypothesis that short periods of oxygen breathing before submarine escape would reduce decompression stress was tested, using Doppler-detectable venous gas emboli as a measure. Twelve goats breathed oxygen for 15 min at 0.1 MPa before exposure to a simulated submarine escape profile to and from 2.5 MPa (240 m/seawater), whereas 28 control animals underwent the same dive without oxygen prebreathe. No decompression sickness (DCS) occurred in either of these two groups. Time with high bubble scores (Kisman-Masurel >or=3) was significantly (P < 0.001) shorter in the prebreathe group. In a second series, 30 goats breathed air at 0.2 MPa for 6 h. Fifteen minutes before escape from 2.5 MPa, animals were provided with either air (n = 10), oxygen (n = 12), or carbogen (97.5% O(2) and 2.5% CO(2)) gas (n = 8) as breathing gas. Animals breathed a hyperoxic gas (60% O(2)-40% N(2)) during the escape. Two animals (carbogen group) suffered oxygen convulsions during the escape but recovered on surfacing. Only one case of DCS occurred (carbogen group). The initial bubble score was reduced in the oxygen group (P < 0.001). The period with bubble score of Kisman-Masurel >or=3 was also significantly reduced in the oxygen group (P < 0.001). Oxygen breathing before submarine escape reduces initial bubble scores, although its significance in reducing central nervous system DCS needs to be investigated further.

Magnetic resonance imaging and neuropathology findings in the goat nervous system following hyperbaric exposures.

Divers may be at risk of long-term CNS damage from non-symptomatic hyperbaric exposure. We investigated the effect of severe, controlled hyperbaric exposure on a group of healthy goats with similar histories. Thirty goats were exposed to various dive profiles over a period of 5 years, with 17 experiencing decompression sickness (DCS). Brains were scanned using magnetic resonance (MR) imaging techniques. The animals were then culled and grossly examined, with the brain and spinal cord sent for neuropathological examination. No significant correlation was found between age, years diving, DCS or exposure to pressure with MR-detectable lesions in the brain, or with neuropathological lesions in the brain or spinal cord. However, spinal scarring was noted in 3 animals that had suffered from spinal DCS.

The effect of breathing hyperoxic gas during simulated submarine escape on venous gas emboli and decompression illness.

Raised internal pressure in a distressed submarine rapidly increases the risk of decompression sickness (DCS) following submarine escape. The hypothesis that breathing a hyperoxic gas during escape may reduce the risk of DCS was tested using goats. Shallow air saturation and simulated submarine escape dives were carried out either singularly or in combination (saturation, escape, or saturation followed by escape) using air or 60% / 40% oxygen (O2) / nitrogen (N2) mixture as breathing gas during the escapes. Post-surfacing, animals were observed for signs of DCI and O2 toxicity. Precordial Doppler ultrasound was used to score venous gas emboli (VGE) using the Kisman Masurel (KM) scale. Following escape from 2.5 MPa, the rate at which VGE disappeared in the hyperoxic group (n = 8) was significantly faster(p < 0.05) than the air group (n = 7). One case of pulmonary barotrauma with arterial gas embolism occurred in the air group, but no cases of DCS were observed. After saturation at 0.18 MPa followed by escape from 2.5 MPa, DCS occurred in four of 15 animals in the air group and in two of 16 animals in the hyperoxic group. The rate of disappearance of VGE was significantly faster (p < 0.01) in the hyperoxic group. O2 toxicity was not discernible in any of the animals.