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Introduction: The Hypobaric Decompression Sickness (DCS) Treatment Model links a decrease in computed bubble volume from increased pressure (ΔP), increased oxygen (O2) partial pressure, and passage of time during treatment to the probability of symptom resolution [P(SR)]. The decrease in offending volume is realized in two stages: 1) during compression via Boyles law; and 2) during subsequent dissolution of the gas phase via the oxygen window., Methods: We established an empirical model for the P(SR) while accounting for multiple symptoms within subjects. The data consisted of 154 cases of hypobaric DCS symptoms with ancillary information from tests on 56 men and 18 women., Results: Our best estimated model is P(SR)=1/(1+exp(-(ln(ΔP)-1.510+0.795×AMB-0.00308×Ts)/0.478)), where ΔP is pressure difference (psid); AMB=1 if ambulation took place during part of the altitude exposure, otherwise AMB=0; and Ts is the elapsed time in minutes from the start of altitude exposure to recognition of a DCS symptom., Discussion: Values of ΔP as inputs to the model would be calculated from the Tissue Bubble Dynamics Model based on the effective treatment pressure: ΔP=P2-P1|=P1×V1/V2-P1, where V1 is the computed volume of a bubble at low pressure P1 and V2 is computed volume after a change to a higher pressure P2. If 100% ground-level oxygen was breathed in place of air, then V2 continues to decrease through time at P2 at a faster rate.

Background: As is known, there are many cases when symptoms of decompression sickness (DCS) in divers appear extremely late (> 15 h after completion of diving) and there is much evidence for unsuccessful treatment of DCS by means of recompression. In this study, we have tried to gain insight into the roots of these phenomena., Methods: Using the mathematical model of extravascular gas bubble dynamics, we have analyzed the time history of such bubbles under typical air dives and recompression procedures used for DCS treatment., Results: If the parameters defining the bubble dynamics remained invariable, the bubbles formed in different body tissues would reach their maximal sizes within the well-known latency time range for DCS onset, and later these bubbles would dissolve completely during standard recompression procedures. Actually, the parameters defining the processes of bubble growth and dissolution vary with time., Conclusions: The symptoms of DCS that arise with abnormal latency may be induced by bubbles that grow a very long time in some tissues when the rate of nitrogen washout from them is reduced significantly due to vascular bubbles blocking the microcirculation. An abnormal latency of DCS onset may also appear when the negative effects of the initially asymptomatic bubbles are detected during the very slow process of their dissolution. The failure of recompression to resolve this DCS probably happens when the previously formed bubbles are large and located in tissues with less permeability so that they dissolve very slowly.

Introduction: This study investigated the influence of a far infrared-ray dry sauna-induced heat exposure before a simulated dive on bubble formation, and examined the concomitant adjustments in hemodynamic parameters., Methods: There were 16 divers who were compressed in a hyperbaric chamber to 400 kPa (30 msw) for 25 min and decompressed at 100 kPa x min(-1) with a 4-min stop at 130 kPa. Each diver performed two dives 5 d apart, one with and one without a predive sauna session for 30 min at 65 degrees C ending 1 h prior to the dive. Circulating venous bubbles were detected with a precordial Doppler 20, 40, and 60 min after surfacing, at rest, and after flexions. Brachial artery flow mediated dilation (FMD), blood pressure, and bodyweight measurements were taken before and after the sauna session along with blood samples for analysis of plasma volume (PV), protein concentrations, plasma osmolality, and plasma HSP70., Results: A single session of sauna ending 1 h prior to a simulated dive significantly reduced bubble formation [-27.2% (at rest) to 35.4% (after flexions)]. The sauna session led to an extracellular dehydration, resulting in hypovolemia (-2.7% PV) and -0.6% bodyweight loss. A significant rise of FMD and a reduction in systolic blood pressure and pulse pressure were observed. Plasma HSP70 significantly increased 2 h after sauna completion., Conclusion: A single predive sauna session significantly decreases circulating bubbles after a chamber dive. This may reduce the risk of decompression sickness. Sweat dehydration, HSP, and the NO pathway could be involved in this protective effect.

Introduction: Immune reactivity, stress responses, and inflammatory reactions may all contribute to pathogenic mechanisms associated with decompression sickness (DCS). Currently, there are no biomarkers for DCS. This research examined if DCS is associated with increased levels of biomarkers associated with vascular function, early/non-specific stress responses, and hypothalamic-pituitary-adrenal (HPA) axis stress responses., Methods: Rats undergoing a test dive to 175 ft of seawater (fsw) (6.2 ATA) for 60 min with a rapid decompression were observed for DCS (ambulatory deficit). Animals exercised on a rotating cage (approximately 3 m x min(-1)) throughout the dive and subsequent 30-min observation period. All animals were euthanized and blood and tissue samples (brain, liver, lung) were collected for analysis of CRP and ET-1 by ELISA and stress markers by PCR., Results: HO-1 and HSP-70 increased in the brain, and HO-1, Egr-1, and iNOS increased in the lungs of animals with DCS. There was no difference in any stress marker in the liver, or in serum levels of CRP or ET-1., Conclusions: The results demonstrate that < 30 min after surfacing, there are genomic changes in animals with DCS compared with animals not showing signs of DCS. Identification of specific markers of DCS may permit use of such biomarkers as predictors of DCS susceptibility and/or occurrence.

Objective: The objectives of this preliminary work were to evaluate the distribution of an ultrasound contrast agent (UCA) (microbubbles) in different arterial regions (brain, kidney, lower limbs) using the Doppler spectrum brightness analysis and to discuss the results in the context of decompression physiology., Method: There were four patients who instrumented with two pulsed Doppler sensors in order to monitor in real-time the spectrum of the middle cerebral femoral arteries. Renal arteries were investigated using an echo-Doppler probe handled by a sonographer. Measurements of the systolic mean, diastolic frequencies, qualitative, and quantitative analysis of the spectrum brightness intensity were performed before and after intravenous injection of a UCA., Results: All of the systolic mean and diastolic arterial frequencies remained constant during the experiment. Some seconds after the first injection, the cerebral spectrum was heterogeneously enhanced with strong flashes over the entire spectrum. The renal and femoral spectrums were homogeneously reinforced. The spectrum brightness patterns did not change during the first 10 min., Discussion: This work shows that the distribution of the UCA microbubbles within the vessel sections changed according to the distance from the heart, as suggested by the spectrum recorded at different sites. By mixing the blood, the heart could re-aggregate the UCA particles, even when they returned from the distal vascular regions where they were homogeneously distributed. The circulating microbubbles and their distribution within the arteries should be considered in decompression procedures with repetitive dives.

Background: Evidence for a causal relationship between decompression sickness (DCS) and leukocyte sequestration was assessed in a rat model based on the effects of interventions which impede cell-to-cell adherence, including hyperbaric oxygen therapy (HBO2)., Hypothesis: We hypothesized that leukocyte adhesion to vessels may play a role in DCS., Methods: Rats were subjected to decompression stress and their ability to ambulate on a rotating drum was assessed to quantify functional neurological deficits. Leukocyte adherence in the brain was measured by a myeloperoxidase (MPO) radioimmunoassay. Interventions included infusion of antibodies to render rats neutropenic or to inhibit leukocyte beta2 integrin adhesion molecules. Tissue gas bubbles were imaged and quantified using a transmission ultrasound camera., Results: Decompressed rats manifested a deficit in their ability to ambulate and a five-fold elevation in concentration of MPO in brain. Neutropenic rats, and those infused with antibody fragments to inhibit leukocyte beta2 integrins, did not exhibit brain MPO elevations, nor a deficit in ambulatory function. HBO2 was used in a prophylactic manner to address its ability to inhibit leukocyte beta2 integrin-mediated adherence without reducing the presence of decompression-induced bubbles. Prophylactic HBO2 prevented cerebral leukocyte sequestration and the performance deficit., Conclusions: The results implicate beta2 integrin-mediated leukocyte adhesion in neurological deterioration after decompression stress, and offer new insight into the therapeutic action of HBO2. Immunomodulatory approaches, including prophylactic HBO2, may improve the safety of decompression procedures in undersea and space exploration.

Introduction: Exposure to 35,000 ft without preoxygenation (breathing 100% oxygen prior to decompression) can result in severe decompression sickness (DCS). Exercise while decompressed increases the incidence and severity of symptoms. Clarification of the level of activity vs. time to symptom onset is needed to refine recommendations for current operations requiring 35,000-ft exposures. Currently, the U.S. Air Force limits these operations to 30 min following 75 min of preoxygenation. The objective of this study was to determine the effect of exercise intensity on DCS incidence and severity at 35,000 ft., Methods: Following 75 or 90 min of ground-level preoxygenation, 54 male and 38 female subjects were exposed to 35,000 ft for 3 h while performing strenuous exercise, mild exercise, or seated rest. The subjects were monitored for venous gas emboli (VGE) with an echo-imaging system and observed for signs and symptoms of DCS., Results: Exposures involving strenuous and mild exercise resulted in higher incidence (p < 0.05) and earlier onset of symptoms (p < 0.05) of DCS than exposure at rest. Mild and strenuous exercise during exposure did not differ in incidence or rate of onset. Incidence at 30 min of exposure was 8% at rest and 23% while exercising., Conclusion: The results showed that current guidelines for 35,000-ft exposures keep DCS risk below 10% at rest. Exercise, even at mild levels, greatly increases the incidence and rate of onset of DCS.

To gain insight into the special nature of gas bubbles that may form in astronauts, aviators and divers, we developed a mathematical model which describes the following: 1) the dynamics of extravascular bubbles formed in intercellular cavities of a hypothetical tissue undergoing decompression; and 2) the dynamics of nitrogen tension in a thin layer of intercellular fluid and in a thick layer of cells surrounding the bubbles. This model is based on the assumption that, due to limited cellular membrane permeability for gas, a value of effective nitrogen diffusivity in the massive layer of cells in the radial direction is essentially lower compared to conventionally accepted values of nitrogen diffusivity in water and body tissues. Due to rather high nitrogen diffusivity in intercellular fluid, a bubble formed just at completion of fast one-stage reduction of ambient pressure almost instantly grows to the size determined by the initial volume of the intercellular cavity, surface tension of the fluid, the initial nitrogen tension in the tissue, and the level of final pressure. The rate of further bubble growth and maximum bubble size depend on comparatively low effective nitrogen diffusivity in the cell layer, the tissue perfusion rate, the initial nitrogen tension in the tissue, and the final ambient pressure. The tissue deformation pressure performs its conservative action on bubble dynamics only in a limited volume of tissue (at a high density of formed bubbles). Our model is completely consistent with the available data concerning the random latency times to the onset of decompression sickness (DCS) symptoms associated with hypobaric decompressions simulating extravehicular activity. We believe that this model could be used as a theoretical basis for development of more adequate methods for the DCS risk prediction.

Unlabelled: To gain insight into the special features of bubbles that may form in aviators and astronauts, we simulated the growth and decay of bubbles in two hypobaric decompressions and a hyperbaric one, all with the same tissue ratio (TR), where TR is defined as tissue PN2 before decompression divided by barometric pressure after. We used an equation system which is solved by numerical methods and accounts for simultaneous diffusion of any number of gases as well as other major determinants of bubble growth and absorption. We also considered two extremes of the number of bubbles which form per unit of tissue., Results: A) Because physiological mechanisms keep the partial pressures of the "metabolic" gases (O2, CO2, and H2O) nearly constant over a range of hypobaric pressures, their fractions in bubbles are inversely proportional to pressure and their large volumes at low pressure add to bubble size. B) In addition, the large fractions facilitate the entry of N2 into bubbles, and when bubble density is low, enhance an autocatalytic feedback on bubble growth due to increasing surface area. C) The TR is not closely related to bubble size; that is when two different decompressions have the same TR, metabolic gases cause bubbles to grow larger at lower hypobaric pressures. We conclude that the constancy of partial pressures of metabolic gases, unimportant in hyperbaric decompressions, affects bubble size in hypobaric decompressions in inverse relation to the exposure pressure.

The "oxygen window" causes a partial pressure difference of inert gas between the inside and outside of decompression bubbles. Estimates of Po2 and Pco2 in tissue are necessary for O2 window calculations and any calculations about growth or decay of decompression sickness bubbles, but the estimates involve many uncertainties. Using simplifying assumptions, we estimated the O2 window over a broad range of environments for tissues having a wide range of O2 extractions. The results were as follows: a) the window increases with ambient pressure, but levels off at very high pressure; b) the window is only 1 or 2 kPa for air breathing at extreme altitudes, and 200 kPa or more in hyperbaric environments; c) when O2 is breathed instead of air, the window is as much as 50 times larger at altitude but only about 10 times larger in hyperbaric environments; d) changes in bubble size due to the window decrease as barometric pressure increases; and e) there are seven additional factors which may supplement or oppose the action of the oxygen window.

This study was conducted to examine the effects of exercise prior to decompression on the incidence of altitude decompression sickness (DCS). In a balanced, two-period, crossover trial, 39 healthy individuals (29 males, 10 females) of mean (S.D.) age 32.5 (7.7) years and body mass index 23.7 (3.4) were each exposed twice, without denitrogenation, to an altitude of 6,400 m (21,000 ft) in a hypobaric chamber. Under the experimental condition, subjects exercised at their predetermined anaerobic threshold levels for 30 min each day for 3 d prior to altitude exposure; the other condition was a non-exercise control. Under both conditions, subjects performed exercise simulating space extravehicular activities at altitude for a period of 3 h, while breathing 100% oxygen. There were nine preferences (untied responses) for DCS, four under control and five under experimental conditions; all were Type I, pain-only bends. No carryover effect between exposures was detected, and the test for treatment differences showed p = 0.56 (95% confidence interval = 0.34-0.58) for symptoms. No significant difference in DCS preferences was found after subjects exercised up to their anaerobic threshold levels during the days prior to decompression.

Intracardial gas bubbles, detected with Doppler ultrasound, and symptoms of decompression sickness were registered at 9,000 m simulated altitude within 12, 18, and 24 h of exposures to 15 or 39 m simulated water depth allowing no stage decompression. With a time interval of 12 h between diving and flying, the earliest intracardial bubbles were found in some subjects already during the first minutes at altitude, and the earliest symptoms of decompression sickness some minutes afterwards. With an 18-h interval, the earliest bubbles and symptoms as well as their average time onsets appeared somewhat later. With a 24-h interval, the earliest bubbles and symptoms were detected slightly later, i.e. after 17 min and 23 min, respectively. Thus, a safe time interval between no-stage decompression dives and flying at 9,000 m cabin altitude for a maximum of 15 min appears to be 24 h. For prolonged such flights, a longer time interval seems to be necessary.

A case of altitude decompression chokes in a subject is described, which occurred unintentionally in an experimental series dealing with safe time intervals between diving and flying at 9,000 m of altitude. Before the development of the first signs of chokes, intracardial gas bubbles could be registered during 65 min and heavy showers of bubbles during 38 min with the precordial Doppler ultrasound technique. The intracardial bubbles and symptoms partly continued after recompression to surface pressure. After 10 min of hyperbaric oxygen treatment, the symptoms disappeared completely. The same subject, as well as others, did not develop chokes with similar durations of heavy showers of intracardial gas bubbles in other experiments.

Incidence of lethal bends and intravascular bubbles has been studied in the eel (Anguilla anguila L.) submitted to hyperbaric air decompressions at temperatures of 17 and 27 degrees C. The fish was an accurate model to seek the nature of the inert gas transport limiting process (diffusion or perfusion) because an increase in temperature considerably influences the rate of perfusion whereas the properties of gases vary in relatively lower proportions. Qualitative and quantitative analysis of the results are consistent with the hypothesis of a diffusion limited nitrogen transport through the tissues of the decompressed eel.

Extensive data concerning the incidence of decompression sickness among workers participating in the deepest caisson operation in Japan to date have been collected and analyzed for the period April through August, 1976. When the bottom pressure was between 3.0 and 3.2 ATA, the incidence of decompression sickness was 3.05%; subsequently, the incidence was only 0.96% between 3.2 and 3.4 ATA. The man lock (i.e., decompression chamber) had never been ventilated during the former group of decompressions and the level of CO2 had ranged between 1.8 and 2.3% (v/v); in the latter group of decompressions, the CO2 level ranged between 0.3 and 0.8% with ventilation. All other conditions, including the decompression table used, were the same. Moreover, based upon the nature of the muscular activity required of the caisson workers just prior to decompression, their most common site of affliction was found to lie within the body region where the highest tissue tensions of CO2 would be expected during decompression.