[Decompression disorders in conditions of decreased atmospheric pressure (Review of the literature)].
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Atmospheric Pressure↗
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[Influence of explosive decompression on blood coagulation in the rabbit].
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Animals↗
[Decompression accidents. Definition, mechanism, description, treatment].
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Accidents↗
[THE THEORY OF DECOMPRESSION AND THE CALCULATION OF DECOMPRESSION TABLES FOR DIVING WITH AIR, ACCORDING TO THE PROCEDURE OF AMERICAN AUTHORS].
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Decompression↗
Decompression: English tables.
The formulation of decompression procedures has generally been based on the observation that divers can be decompressed without stoppages to surface, from steady-state exposures of about twice the atmospheric pressure. Because decompression sickness rarely develops from this "no-stop decompression", it has been assumed that no gas is liberated. It is therefore assumed, in the calculation of the majority of decompression tables, that using a 2:1 decompression ratio allows the additional gas load from the hyperbaric exposure to be transported to the lungs in solution. Ultrasonic scanning and Doppler techniques have shown that this is not the case. Decompression tables must therefore be formulated so as to take into account the presence of gas, the critical diameter of circulating bubbles and the inherent unsaturation introduced by oxygen.
Decompression↗
Postmortem intravascular bubbling: a decompression artifact?
The relationships between drowning occurring in divers using compressed air, with subsequent recovery of the body to the surface, and the finding of intravascular gas bubbles at autopsy were studied. Guinea pigs were exposed to compressed air in a hyperbaric chamber at various depths [98, 294, and 392 kPa (1,3, and 4 atm)] for various intervals and then drowned at depth. Various decompression schedules were used in returning the drowned animals to the surface. Autopsy examination indicated that large and small intravascular gas bubbles may be found, in the absence of traumatic air embolism or decompression sickness, as a result of the process of decompression alone. Postmortem findings of intravascular bubbles bin drowned divers must be interpreted with caution and the importance of a full history of the incident, including depth and time of diving and evidence of ascent before drowning, are critical to the proper interpretation of intravascular gas bubbles.
Animals↗
Pneumoperitoneum after diving--two clinical cases and literature review.
Pneumoperitoneum after diving is a rare symptom. Diagnosis and treatment strongly depends on the primary source of the air in the abdominal cavity. There are two main sources of air entering the perineum: perforation of the gastrointestinal tract and pulmonary barotrauma. The management is different and additionally, in both cases, the decompression sickness and arterial gas embolism as consequences of inappropriate decompression phase of the diving should be included in the clinical diagnosis and treatment. The multidisciplinary team including hyperbaric physicians and surgeons is necessary for proper management of such cases. In this paper two cases of pneumoperitoneum of different origins are presented and similar cases reported in the literature are discussed.
Adult↗
Evaluation of different decompression tables by agarose gel method.
Nine different decompression tables were evaluated by the method of bubble formation in the agarose gel, the result of which is summarized as follows: 1) The number of bubbles formed in the agarose gel corresponded well with the exposed pressure. 2) The technique of this method was simple and the number of bubbles was accurately counted. 3) This method was considered useful for examining the decompression tables. 4) Using an equation obtained from the experiment with the same agarose gel, the critical number of bubbles at the end of decompression was found to be 6.6. 5) From this point of view, the R.N.P.L. Table of England and Mano's Model I Table were considered to be excellent. 6) The first stop at the deeper level during the ascent resulted in a smaller number of bubbles at the end of decompression, indicating the effectiveness of this procedure for the prevention of decompression sickness.
Atmospheric Pressure↗
Extension of oxygen tolerance in man: philosophy and significance.
The respiration of oxygen over a range of partial pressures higher than in the natural environment has expanding usefulness in health and disease. It provides for denitrogenation of the astronaut to prevent aerospace decompression sickness, it facilitates diving of many forms and improves safety in decompression after diving, and it is the key to therapy of diving and iatrogenic gas embolic diseases. In the continuum of general and hyperbaric medicine, it is essential for sustaining viability of damaged or diseased tissues not adequately oxygenated at natural oxygen pressures. Over the entire range of its clinical and operational usefulness, the pressure and duration of tolerable exposure to oxygen is limited by adverse effects on multiple chemical targets, cells, tissues, and organ functions. The rates of development and the qualitative expressions of these effects are different at different respired oxygen pressures. Successful extension of oxygen tolerance, as by slowing the rate of development of adverse effects, will further expand the medical and operational usefulness and safety of oxygen in normal, hypobaric, and hyperbaric environments. A prerequisite baseline for overall extension of oxygen tolerance is the quantitative investigation of early stages of toxic oxygen effects upon specific chemical and composite functions of multiple organ systems, including rates of development and rates of recovery. The practicality of limited oxygen tolerance extension by systematic interruption of oxygen exposure has been demonstrated and the procedure widely used. Broad present goals are both to establish oxygen tolerance for specific tissues and to optimize tolerance extension over the full range of useful oxygen pressures.
Adaptation, Physiological↗
Exercise effects during diving and decompression on postdive venous gas emboli.
BACKGROUND: Exercise and diving have generally been associated with an increased risk of decompression sickness (DCS), thus accounting for the lack of studies involving exercise during decompression. However, theoretical and observational evidence contrary to this association motivated the present investigation on the effects of moderate, intermittent exercise during diving and/or during decompression on venous gas emboli (VGE) activity following a dive. HYPOTHESIS: VGE observed at both the precordium and subclavian vein sites after diving should be reduced if moderate exercise is performed during decompression vs. remaining inactive. METHODS: In a water-filled hyperbaric chamber, 39 healthy male subjects were compressed to a pressure of 450 kPa (45 msw) for 30 min followed by 55 min of staged decompression. Subjects were either active or inactive at the bottom phase (450 kPa) and/or during the decompression. Activity comprised three 5-min intervals of moderate arm or leg exercise at the bottom and five such intervals during decompression. After decompression, VGE were monitored at the precordium and subclavian vein sites using Doppler detection. Bubble activity scores were converted to various indices and analyzed using non-parametric statistics. RESULTS: VGE activity was invariant as to whether subjects were active or sedentary during the bottom phase of the dive. However, it was significantly lower for all indices examined (p < 0.05) after dives in which exercise was performed during decompression vs. inactive decompression. CONCLUSION: Moderate, intermittent physical activity during decompression decreases VGE activity after diving.
Adult↗
Pulmonary barotrauma-induced cerebral arterial gas embolism with spontaneous recovery: commentary on the rationale for therapeutic compression.
Pulmonary barotrauma-induced cerebral arterial gas embolism (CAGE) continues to complicate compressed gas diving activities. Inadequate lung ventilation secondary to inadvertent breath holding or rapid buoyant ascent can quickly generate a critical state of lung over-pressure. Pulmonary over-pressurization may also occur as a consequence of acute and chronic pulmonary pathologies. Resulting barotrauma frequently causes structural failure within the terminal distal airway. Respiratory gases are then free to embolize the systemic circulation via the pulmonary vasculature and the left heart. The brain is a common target organ. Bubbles that enter the cerebral arteries coalesce to form columns of gas as the vascular network narrows. Small amounts of gas frequently pass directly through the cerebral circulation without occlusion. Larger columns of gas occlude regional brain blood flow, either transiently or permanently, producing a stroke-like clinical picture. In cases of spontaneous redistribution, a period of apparent recovery is frequently followed by relapse. The etiology of relapse appears to be multifactoral, and chiefly the consequence of a failure of reperfusion. Prediction of who will relapse is not possible, and any such relapse is of ominous prognostic significance. It is advisable, therefore, that CAGE patients who undergo spontaneous recovery be promptly recompressed while breathing oxygen. Therapeutic compression will serve to antagonize leukocyte-mediated ischemia-reperfusion injury; limit potential re-embolization of brain blood flow, secondary to further leakage from the original pulmonary lesion or recirculation of gas from the initial occlusive event; protect against embolic injury to other organs; aid in the resolution of component cerebral edema; reduce the likelihood of late brain infarction reported in patients who have undergone spontaneous clinical recovery; and prophylax against decompression sickness in high gas loading dives that precede accelerated ascents and omitted stage decompression.
Adult↗
U.K. deep diving trials.
Using a breathing medium of 40 kPa oxygen, remainder helium, 18 volunteer subjects participated in a series of 15 exposures to pressures equivalent to depths of 180-540 m s.w. The time of exposure at these pressures was mostly 2 days, except for the 540 m s.w. exposure, when 6 days were spent at full pressure. Compression procedures, based upon placing 'stages' at 60 m s.w. intervals, evolved with experience and proved to be a highly successful way of achieving acceptable pressure-time courses. Decompression combined slow linear release of pressure with overnight halts for sleep. On one occasion a depth of 660 m s.w. was reached by breathing 40 kPa oxygen, 10% nitrogen, remainder helium. Throughout all exposures, teams of investigators followed the changes in cardiovascular, respiratory, haematological, neurophysiological and metabolic status, and mental performance of the volunteers. Some major findings were that the neurophysiological and behavioural changes could be assigned to the motor, or vestibular, or cerebral, or autonomic systems, and were mainly first observed during compression. The subjects suffered, apparently from severe nitrogen narcosis, when breathing 10% (by volume) nitrogen in oxygen-helium at 420 m s.w. Lung ventilation was remarkably adaptable to the oxygen requirements of exercise at all depths, but cardiac output was adversely affected at 540 m s.w., particularly for heavier workloads. Ventilatory responses to carbon dioxide were significantly elevated after diving. Thermal balance was seen to be precarious, but nevertheless it was achieved by the normal subjective assessments of comfort. Water loss was affected by diminished evaporation from the skin. Skin temperature sensitivity was changed and took many days after the dives to return to normal. Energy requirements increased for work purposes, but basal metabolic rate was undisturbed. Body chemistry altered at pressures in excess of 300 m s.w., for example thyroid hormone and nitrogen balances were affected. No decompression sickness was encountered until the pressures were low, but marked haematological changes could occur during decompression. Every change that occurred during these dives reverted to normal, mostly before the end of the decompression. It is concluded that diving with oxygen-helium breathing mixtures to depths as great as 540 m s.w. can be effective and safe. An attempt is made to assess the physiological significance of the principal findings.
Adult↗
No changes in lung function after a saturation dive to 2.5 MPa with intermittent reduction in Po2 during decompression.
Decompression stress and exposure to hyperoxia may cause a reduction in transfer factor of the lung for carbon monoxide and in maximal aerobic capacity after deep saturation dives. In this study lung function and exercise capacity were assessed before and after a helium-oxygen saturation dive to a pressure of 2.5 MPa where the decompression rate was reduced compared with previous deep dives, and the hyperoxic exposure was reduced by administering oxygen intermittently at pressures of 50 and 30 kPa during decompression. Eight experienced divers of median age 41 years (range 29-48) participated in the dive. The incidence of venous gas microemboli was low compared with previous deep dives. Except for one subject having treatment for decompression sickness, no changes in lung function or angiotensin converting enzyme, a marker of pulmonary endothelial cell damage, were demonstrated. The modified diving procedures with respect to decompression rate and hyperoxic exposure may have contributed to the lack of changes in lung function in this dive compared with previous deep saturation dives.
Adult↗
[Analysis of decompression safety during extravehicular activity of astronauts in the light of probability theory].
Objectives of the study were comparative assessment of the risk of decompression sickness (DCS) in human subjects during shirt-sleeve simulation of extravehicular activity (EVA) following Russian and U.S. protocols, and analysis of causes of the difference between real and simulated EVA decompression safety. To this end, DCS risk during exposure to a sing-step decompression was estimated with an original method. According to the method, DCS incidence is determined by distribution of nucleation efficacy index (z) in the worst body tissues and its critical values (zm) as a function of initial nitrogen tension in these tissues and final ambient pressure post decompression. Gaussian distribution of z values was calculated basing on results of the DCS risk evaluation on the U.S. EVA protocol in an unsuited chamber test with various pre-breath procedures (Conkin et al., 1987). Half-time of nitrogen washout from the worst tissues was presumed to be 480 min. Calculated DCS risk during short-sleeve EVA simulation by the Russian and U.S. protocols with identical physical loading made up 19.2% and 23.4%, respectively. Effects of the working spacesuit pressure, spacesuit rigidity, metabolic rates during operations in EVA space suit, transcutaneous nitrogen exchange in the oxygen atmosphere of space suit, microgravity, analgesics, short compression due to spacesuit leak tests on the eye of EVA are discussed. Data of the study illustrate and advocate for high decompression safety of current Russian and U.S. EVA protocols.
Astronauts↗
Hyperbaric oxygen may reduce gas bubbles in decompressed prawns by eliminating gas nuclei.
It is accepted that gas bubbles grow from preexisting gas nuclei in tissue. The possibility of eliminating gas nuclei may be of benefit in preventing decompression sickness. In the present study, we examined the hypothesis that hyperbaric oxygen may replace the resident gas in the nuclei with oxygen and, because of its metabolic role, eliminate the nuclei themselves. After pretreatment with oxygen, prawns were 98% saturated with nitrogen before explosive decompression at 30 m/min. Ten transparent prawns were exposed to four experimental profiles in a crossover design: 1) 10-min compression to 203 kPa with air; 2) 10-min compression with oxygen; 3) 10-min compression with oxygen to 203 kPa followed by 12 min air at 203 kPa; and 4) 10 min in normobaric oxygen followed by compression to 203 kPa with air. Bubbles were measured after explosive decompression. We found that pretreatment with hyperbaric oxygen (profile C) significantly reduces the number of bubbles and bubble volume. We suggest that hyperbaric oxygen eliminates bubble nuclei in the prawn.
Animals↗
Evaluation of different decompression schedules by an agarose gel bubble technique.
It is well known that diving decompression schedules vary according to country and that Navy schedules are often different from civilian ones. Furthermore, it is difficult to compare them effectively, because the bends incidence for each schedule is rarely known accurately. We have evaluated various decompression schedules by an agarose gel bubble technique in which the appearance of bubbles in a dry chamber at a controlled temperature was used, and we report this as a useful method of evaluating decompression tables. It is generally accepted that decompression sickness symptoms are due to bubble formation and the body's subsequent physiological reaction. Individual differences and physical conditions are also influential factors. However, bubble formation appears to be the most important factor in initiating symptoms. As the number of bubbles is influenced by the physical decompression ratio, it can be estimated which decompression schedule is more likely to minimize the number of bubbles. Nine decompression schedules were studied in this experiment: U.S. Navy Table, French Navy Table, Japanese Standard Decompression Schedule Numbers 1 and 2, Royal Naval Physiological Laboratory Table, French Ministry of Labor Table, Model 1 Table by Mano et al., Washington State Table, and Blackpool Table.
Decompression↗
[Fatty acid composition of the lipids in human blood plasma and erythrocyte membranes during simulation of extravehicular activities of cosmonauts].
Dynamics of the lipoacidic content of total plasma lipids and erythtocyte membranes was studied in 32 experiments with ten apparently healthy male subjects aged 27 to 41 years who were exposed to repeated decompression from the normal ground down to 40-35 kPa. For two hours of exposure to lowered pressure the subjects were breathing pure oxygen in mask and performing incremental physical work mimicking loading of the upper extremities of cosmonauts doing extravehicular activities (EVA) at the energy cost of 3 kcal/min. Decompression sessions were repeated with intervals from 3 to 5 days. In seven experiments, the subjects developed symptoms of the decompression sickness (DCS). Penetration of gas bubbles (GB) into the pulmonary artery was registered in 27 cases (84.4%). In 24 cases maximal intensity of the US signals from GB reached 3 to 4 Spencer's points. No changes in the lipidoacidic content of blood plasma or erythrocyte membranes were determined following the first exposure to decompression. BY the onset of repeated decompression, total number of lipids in erythrocyte membranes decreased from 54.6 to 40.4 mg% in the group of subjects who had not displayed DCS symptoms (n = 5) and from 51.2 to 35.2 mg% (p < 0.05) in the group of subjects with DCS symptoms (n = 5). In the subjects with DCS, polyunsaturated linoleic acid (18:2) tended to decrease against the upward trend of saturated fatty acids (16:0, 18:0). In these subjects, arachidonic acid in erythrocyte membranes (20:4) decreased following each decompression exposure and significantly increased (p < 0.05) in-between. In both groups, blood plasma showed slight fluctuations in the lipoacidic contents. These data suggest that exposure to the variety of the EVA-simulating factors may entail quite distinct but reversible modifications in the lipid metabolism in blood and the structural/functional state of erythrocyte membranes. The most marked alterations were observed in the subjects with the DCS symptoms during high intensity of US signals from GB in the venous blood flow.
Adult↗
Pressure reduction limits for rats subjected to various time/pressure exposures.
The impact of the combined effects of exposure time and hydrostatic pressure on pressure reduction is explored in this study. In Phase I of the study, excursion dives were made to 10, 20, and 30 ATA for 5, 10, 20, 40, or 80 min. In Phase II, the animals were saturated at 1.3, 10, or 20 ATA for 60 min; each saturation exposure was followed by a 10-atm excursion dive of either 1, 5, 10, 20, or 40 min. The chamber gas mixture during all pressure exposures was 0.51 ATA oxygen, 0.79 ATA nitrogen, and the remainder helium. The subjects were 655 rats; during each pressure exposure 5 rats were exercised in a rotating cage. After each exposure, the rats were abruptly decompressed to a lesser pressure for observation and tabulation of the decompression sickness incidence. Results suggest that neither the starting saturation pressure nor the differential excursion pressure alters the time required for an animal to reach equilibrium with the surrounding environment. Pressure-reduction values, however, vary with both the exposure pressure and exposure time. These results will have a direct impact on the formulation of future decompression models.
Animals↗