No abstract

Preventive measures to reduce the risk of decompression sickness can involve several procedures such as oxygen breathing during in-water decompression. Theoretical predictions also suggest that brief periods of recompression during the course of decompression could be a method for controlling bubble formation. The aim of this study was to get clearer information about the effects of different experimental ascent profiles (EAPs) on bubble reduction, using pure oxygen or recompression during decompression for nitrox diving. Four EAPs were evaluated using bubble monitoring in a group of six military divers using Nitrox 40% O(2) breathing with a rebreather. For EAP 1 and 2, 100% O(2) was used for the end stage of decompression, with a 30% reduction of decompression time in EAP 1 and 50% in EAP 2, compared to the French navy standard schedule. For EAP 3 and 4, nitrox 40% O(2) was maintained throughout the decompression stage. EAP 3 is based on an air standard decompression schedule, whereas EAP 4 involved a brief period of recompression at the end of the stop. We found that EAP 1 significantly reduced bubble formation, whereas high bubble grades occurred with other EAPs. No statistical differences were observed in bubbles scores between EAP 3 and 4. One diver developed mild neurological symptoms after EAP 3. These results tend to demonstrate that the "oxygen window" plays a key role in the reduction of bubble production and that breathing pure oxygen during decompression stops is an optimal strategy to prevent decompression sickness for nitrox diving.

Recent advances in submarine rescue systems have allowed a transfer under pressure of crew members being rescued from a disabled submarine. The choice of a safe decompression procedure for pressurised rescuees has been previously discussed, but no schedule has been validated when the internal submarine pressure is significantly increased i.e. exceeding 2.8 bar absolute pressure. This study tested a saturation decompression procedure from hyperbaric exposures up to 6 bar, the maximum operating pressure of the NATO submarine rescue system. The objective was to investigate the incidence of decompression sickness (DCS) and clinical and spirometric indices of pulmonary oxygen toxicity. Two groups were exposed to a Nitrogen-Oxygen atmosphere (pO2 = 0.5 bar) at either 5 bar (N = 14) or 6 bar (N = 12) for 12 h followed by 56 h 40 min resp. 60 h of decompression. When chamber pressure reached 2.5 bar, the subjects breathed oxygen intermittently, otherwise compressed air. Repeated clinical examinations, ultrasound monitoring of venous gas embolism and spirometry were performed during decompression. During exposures to 5 bar, 3 subjects had minor subjective symptoms i.e. sensation of joint discomfort, regressing spontaneously, and after surfacing 2 subjects also experienced joint discomfort disappearing without treatment. Only 3 subjects had detectable intravascular bubbles during decompression (low grades). No bubbles were detected after surfacing. About 40% of subjects felt chest tightness when inspiring deeply during the initial phase of decompression. Precordial burning sensations were reported during oxygen periods. During decompression, vital capacity decreased by about 8% and forced expiratory flow rates decreased significantly. After surfacing, changes in the peripheral airways were still noticed; Lung Diffusion for carbon monoxide was slightly reduced by 1% while vital capacity was normalized. The procedure did not result in serious symptoms of DCS or pulmonary oxygen toxicity and may be considered for use when the internal submarine pressure is significantly increased.

The biophysical models that intend to predict the risk of decompression sickness after a change of pressure are not numerous. Few approaches focus in particular on joints as target tissues, with the aim to describe properly the mechanisms inducing pain. Nevertheless, for this type of decompression incidents, called articular bends, no model proved to fit the empirical results for a broad range of exposures and decompression procedures. We present here an original biophysical decompression model for describing the occurrence of articular bends. A target joint is broken down into two parts that exchange inert gases with the blood by perfusion and with each other by diffusion over distances of a few millimetres. This diffusion pathway allows the slow amplification of microbubbles growing during and after decompression, consistent with the possible delayed occurrence of bends. The diffusion coefficients introduced into this model are larger than those introduced into most modern decompression models. Their value remains physical (#10(-9)m(2)/s). Inert gas exchanges and the formation, amplification and resorption of microbubbles during and after decompression were simulated. We used a critical gas volume criterion for predicting the occurrence of bends. A risk database extracted from COMEX experience and other published studies were used for the correlation of model parameters not known a priori. We considered a large range of exposure, and the commonly used inert gases nitrogen and helium. This correlation phase identified the worst biophysical conformations most likely to lead to the formation, in tissues such as tendons, of a large number of microbubbles recruited from pre-existing gas nuclei during decompression. The risk of bends occurrence was found to be linked to the total separated gas volume generated during and after decompression. A clamping phenomenon occurs soon after the start of decompression, greatly slowing the gas exchanges controlled especially by the oxygen window. This model, which reproduces many empirical findings, may be considered both descriptive and predictive.

From a preliminary analysis, the proposed denitrogenation procedure proved to be adequate compared to other methods. An investigation of the method demonstrated that the system accuracy can be improved. A validation phase using more subjects may support the use of this new technology.