Risk Of Decompression Sickness Research Articles

Lung collapse in the diving sea lion: hold the nitrogen and save the oxygen

Lung collapse is considered the primary mechanism that limits nitrogen absorption and decreases the risk of decompression sickness in deep-diving marine mammals. Continuous arterial partial pressure of oxygen profiles in a free-diving female California sea lion (Zalophus californianus) revealed that (i) depth of lung collapse was near 225 m as evidenced by abrupt changes in during descent and ascent, (ii) depth of lung collapse was positively related to maximum dive depth, suggesting that the sea lion increased inhaled air volume in deeper dives and (iii) lung collapse at depth preserved a pulmonary oxygen reservoir that supplemented blood oxygen during ascent so that mean end-of-dive arterial was 74 ± 17 mmHg (greater than 85% haemoglobin saturation). Such information is critical to the understanding and the modelling of both nitrogen and oxygen transport in diving marine mammals.

Approximate Explicit Nonlinear Receding Horizon Control for Decompression of Divers

This paper is based on a comprehensive dynamic mathematical model (Copernicus) of vascular bubble formation and growth during and after decompression from a dive. The model is founded on the statistical correlation between measurable venous gas emboli (VGE) and risk of severe decompression sickness (DCS) where VGE has been shown to be a reliable and sensitive predictor of decompression stress. By using the Copernicus model the diving decompression problem is formulated as a nonlinear optimal control problem, where the objective is to minimize the total ascend time subject to constraints on the maximum bubbles volume in the central venous pool. A recent study reveals that the optimal solution can be obtained by solving the optimization problem with equality constraints. Inspired by which, a simpler approach using barrier function is proposed in this paper, through which we achieve a more efficient and robust numerical implementation. To reduce the complexity of the nonlinear optimization problem this paper also studies the decompression profile parameterization and its effect. Furthermore, by applying multi-parametric nonlinear programming technique, an approximate explicit solution to the nonlinear optimization problem is obtained, which makes the practical implementation on a typical low-cost diving computer possible.

Effects of FLIRT on Bubble Growth in Man

Recompression during decompression has been suggested to possibly reduce the risk of decompression sickness (DCS). The main objective of the current study was to investigate the effects of FLIRT (First Line Intermittent Recompression Technique) on bubble detection in man. 29 divers underwent 2 simulated dives in a dry recompression chamber to a depth of 40 msw (500 kPa ambient pressure) in random order. A Buehlmann-based decompression profile served as control and was compared to an experimental profile with intermittent recompression during decompression (FLIRT). Circulating bubbles in the right ventricular outflow tract (RVOT) were monitored by Doppler ultrasound and quantified using the Spencer scoring algorithm. Heat shock protein 70 (HSP70), thrombocytes, D-Dimers and serum osmolarity were analyzed before and 120 min after the dive. Both dive profiles elicited bubbles in most subjects (range Spencer 0-4). However, no statistically significant difference was found in bubble scores between the control and the experimental dive procedure. There was no significant change in either HSP70, thrombocytes, and D-Dimers. None of the divers had clinical signs or symptoms suggestive of DCS. We conclude that FLIRT did not significantly alter the number of microbubbles and thus may not be considered superior to classical decompression in regards of preventing DCS.

Prior eccentric exercise modifies diving‐induced inflammatory gene expression in rats

Decompression sickness (DCS) after diving is a major risk of injury to divers, aviators and space travelers. DCS is associated with gas bubbles formed during decompression, but the processes linking bubbles to DCS are unknown. Exercise before diving reduces DCS risk. The effect of exercise on DCS could be caused by reduced bubble formation and/or to the induction of genetic pathways that affect biological responses to bubbles.Study objectiveTo examine the effects of eccentric exercise on vascular gene expression and gas bubble production after diving.MethodsThree groups of female Sprague Dawley rats were used; two diving groups with or without exercise and one control group, n=9 in each group. The exercise group did one bout of 100 min downhill treadmill running before diving, and saturation diving was simulated in an air‐filled pressure chamber at 709 kPa for 50 min. Diving‐induced stress was measured by ultrasonic detection of bubbles in the pulmonary artery and by full genome mRNA analysis of the aorta. All procedures were approved by the Animal Research Ethics Authority.ResultsDiving alone activated expression of 18 genes, whereas eccentric exercise reduced expression of 12 of these and upregulated an additional 25 genes. Specifically, elevated cytokine‐cytokine receptor expression and decreased expression of anti‐fibrinolytic Serpine1 was found in the exercise group. There were no differences in bubble formation between the groups.ConclusionsWhereas diving induces cytokine and oxygen‐responsive gene expression, the protective effect of eccentric exercise before diving may be attributed to altered expression of genes involved in inflammatory responses.This study was supported by Samarbeidsorganet HMN/NTNU, Kontaktutvalget St. Olavs Hospital/NTNU, and FUGE Midt‐ Norge, Norway.

Pre-Dive Exercise and Post-Dive Evolution of Venous Gas Emboli

Recent studies have indicated that exercise before diving significantly reduces the number of circulating bubbles and the risk of decompression sickness. However, the most effective time delay between exercise and dive is not clear; the present aim was to resolve this. In a hyperbaric chamber, 10 men were compressed to 18 m for 100 min, then decompressed as per Royal Navy Table 11. Each subject performed three dives: a control dive and two after exercise performed either 24 h or 2 h before diving. Exercise consisted of 40 min submaximal work on a cycle ergometer. Venous gas emboli (VGE) were evaluated using precordial Doppler ultrasound immediately on surfacing, with measurements made at 5-min intervals for 30 min, and at 15-min intervals for at least 2.5 h total using the Kisman Masurel (KM) scale. Exercise either 24 or 2 h prior to a dive did not reduce the median number of circulating VGE (median maximum KM grade: control, 2+; for both exercise dives, 3). Bubbles disappeared from the circulation faster after the control dive than the exercise dives. Time to median KM Doppler scores of zero were: control:120 min; 2-h group: 225 min; 24-h group: 165 min. Cycling exercise prior to diving did not reduce the number of circulating VGE in comparison to control, in contrast to recent studies. A number of factors may be responsible for these findings, including type of exercise performed, wet diving experience, and disparity in Doppler measurement techniques.

Estimated tissue and blood N2 levels and risk of decompression sickness in deep-, intermediate-, and shallow-diving toothed whales during exposure to naval sonar

Naval sonar has been accused of causing whale stranding by a mechanism which increases formation of tissue N2 gas bubbles. Increased tissue and blood N2 levels, and thereby increased risk of decompression sickness (DCS), is thought to result from changes in behavior or physiological responses during diving. Previous theoretical studies have used hypothetical sonar-induced changes in both behavior and physiology to model blood and tissue N2 tension , but this is the first attempt to estimate the changes during actual behavioral responses to sonar. We used an existing mathematical model to estimate blood and tissue N2 tension from dive data recorded from sperm, killer, long-finned pilot, Blainville’s beaked, and Cuvier’s beaked whales before and during exposure to Low- (1–2 kHz) and Mid- (2–7 kHz) frequency active sonar. Our objectives were: (1) to determine if differences in dive behavior affects risk of bubble formation, and if (2) behavioral- or (3) physiological responses to sonar are plausible risk factors. Our results suggest that all species have natural high N2 levels, with deep diving generally resulting in higher end-dive as compared with shallow diving. Sonar exposure caused some changes in dive behavior in both killer whales, pilot whales and beaked whales, but this did not lead to any increased risk of DCS. However, in three of eight exposure session with sperm whales, the animal changed to shallower diving, and in all these cases this seem to result in an increased risk of DCS, although risk was still within the normal risk range of this species. When a hypothetical removal of the normal dive response (bradycardia and peripheral vasoconstriction), was added to the behavioral response during model simulations, this led to an increased variance in the estimated end-dive N2 levels, but no consistent change of risk. In conclusion, we cannot rule out the possibility that a combination of behavioral and physiological responses to sonar have the potential to alter the blood and tissue end-dive N2 tension to levels which could cause DCS and formation of in vivo bubbles, but the actually observed behavioral responses of cetaceans to sonar in our study, do not imply any significantly increased risk of DCS.

Oxygen breathing or recompression during decompression from nitrox dives with a rebreather: effects on intravascular bubble burden and ramifications for decompression profiles

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.

Mobility of an Elastic Glove for Extravehicular Activity Without Prebreathing

The current U.S. extravehicular activity (EVA) suit is pressurized at 0.29 atm, which is much lower than the pressures of sea level and inside a space station. Higher pressure can reduce the risk of decompression sickness (DCS), but mobility would be sacrificed. We have demonstrated that a glove and sleeve made of elastic material increased mobility when compared with those made of nonelastic material, such as that found in the current suit. We hypothesized that an elastic glove of 0.65 atm that has no risk of DCS also has greater mobility compared with a non-elastic glove of 0.29 atm. The right hands of 10 healthy volunteers were studied in a chamber with their bare hands at normal ambient pressure, after donning a non-elastic glove with a pressure differential of 0.29 atm, and after donning an elastic glove with a pressure differential of 0.29 and 0.65 atm. Range of motion (ROM) of the index finger and surface electromyography (EMG) amplitudes during finger flexion were measured. ROM with gloves was significantly smaller than that of bare hands, but was similar between conditions of gloves regardless of elasticity and pressure differentials. However, EMG amplitudes with the elastic glove of 0.29 and 0.65 atm were significantly smaller than those with the non-elastic glove of 0.29 atm. The results suggest that mobility of the elastic glove of 0.65 atm may be better than that of the non-elastic glove of 0.29 atm, similar to that used in the current EVA suit.

A new biophysical decompression model for estimating the risk of articular bends during and after decompression

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.

Fifty Years of Decompression Sickness Research at Brooks AFB, TX: 1960–2010

INTRODUCTION, FACILITIES, AND METHODS: Decompression sickness (DCS) occurring in hypobaric environments related to aviation or spaceflight was a major focus of research at Brooks AFB/City-Base, TX, throughout the period 1960-2010. Multiple hypobaric chambers and extensive support facilities were built for research on altitude DCS using both human subjects and animal models. Areas of study included symptomatology, incidence, prediction, and prevention of DCS. High-altitude aviation, spacecraft atmospheres, and pressure suits were evaluated with various decompression and prebreathing schedules to reduce DCS risk. FACTORS AFFECTING DCS INCIDENCE: The results from these efforts were recorded in an extensive Altitude DCS Research Database which served as a resource for developing reports and exploring relationships of various parameters such as altitude, time at altitude, prebreathe time, and mode of activity while decompressed. PREVENTION AND PREDICTION OF DCS: Individual susceptibility to DCS was also evaluated in an effort to tailor preventive measures and predict susceptibility. Completion of the 26 human-use protocols provided information which was incorporated into NASA and USAF operational practices to reduce DCS risk. DCS researchers working at Brooks throughout this period produced 177 papers documenting results of thousands of subject-exposures and other experiments. An Altitude DCS Risk Assessment Computer Model was fielded in 2005. This review centers on the results of research at Brooks and notes questions about operational DCS risk that have not yet been answered.

Dynamic changes in cardiovascular function during diving and decompression at different core temperatures

Diving under cold conditions may add an additional risk for bubble production and decompression sickness. Additionally, there is sparse information regarding hemodynamic changes occurring during a dive and its effects on the outcome of a dive. Thus, detailed recordings of cardiovascular changes at different core temperatures during diving were studied. Anesthetized rats were monitored with a pressure‐volume catheter in the left ventricle and the femoral artery. Rats were randomly assigned to be normothermic controls, to perform a dry hyberbaric dive at constant core temperature (37ºC) or a dry hyperbaric dive with a core temperature of 35ºC during decompression and the early post dive period. The rats were compressed to 600 kPa, maintained for 45 min breathing air, and decompressed linearly to the surface at a rate of 50 kPa·min−1. Immediately after surfacing, right ventricle and pulmonary artery were insonated for bubble detection using ultrasound. Compression increased mean arterial pressure, pulse pressure, stroke volume, cardiac output, LV end‐systolic volume, LV end‐systolic pressure, LV dp/dt max, and total peripheral resistance in the rats. Most of these changes gradually declined and returned to baseline after decompression. However, rewarming to 37ºC after a 2ºC drop in core temperature caused a significant reduction in SV and CO, but this did not have an effect on bubble production and survival.

Decompression Sickness Risk at 6553 m Breathing Two Gas Mixtures

The risk of severe decompression sickness (DCS) increases rapidly above 6248 m (20,500 ft) and is greater when breathing higher proportions of inert gas. Contemporary aircrew may be exposed to higher cabin altitudes while breathing molecular sieve oxygen concentrator (MSOC) product gas containing variable concentrations of oxygen, nitrogen, and argon. This study assessed the risk of DCS at 6553 m (21,500 ft) breathing two simulated MSOC product gas mixtures. In a hypobaric chamber, 10 subjects each undertook 2 4-h exposures at 6553 m breathing either 75% O2:21% N2:4% Ar or 56% 02:42% N2:2% Ar. Subjects undertook regular activities simulating in-flight movements of fast jet aircrew. Venous gas emboli (VGE) "bubble" load was graded every 15 min using 2D and Doppler echocardiography by experienced operators blinded to breathing gas composition. DCS occurred in five exposures (25%), the earliest after less than 90 min at altitude. All were minor, single-site, uncomplicated limb bends that resolved with recompression. VGE occurred in 85% of exposures with some early-onset, heavy loads. Survival (Probit) analysis indicated that breathing 56% oxygen significantly decreased VGE latency relative to breathing 75% oxygen (relative potency 3.05). From 20 experimental exposures, the risk of DCS at 6553 m is estimated at 5% by 90 min and 20% at 3 h. Exploiting the negative predictive value of VGE latency as a surrogate measure of protection from DCS, at high cabin altitudes better MSOC performance (higher product gas oxygen concentrations) will protect more aircrew for longer.

Oxygen pretreatment as protection against decompression sickness in rats: pressure and time necessary for hypothesized denucleation and renucleation

Pretreatment with HBO at 300-500 kPa for 20 min reduced the incidence of decompression sickness (DCS) in a rat model. We investigated whether this procedure would be effective with lower oxygen pressures and shorter exposure, and tried to determine how long the pretreatment would remain effective. Rats were pretreated with oxygen at 101 or 203 kPa for 20 min and 304 kPa for 5 or 10 min. After pretreatment, the animals were exposed to air at 1,013 kPa for 33 min followed by fast decompression. Pretreatment at 101 or 203 kPa for 20 min and 304 kPa for 10 min significantly reduced the number of rats with DCS to 45%, compared with 65% in the control group. However, after pretreatment at 304 kPa for 5 min, 65% of rats suffered DCS. When pretreatment at 304 kPa for 20 min was followed by 2 h in normobaric air before compression and decompression, the outcome was worse, with 70-90% of the animals suffering DCS. This is probably due to the activation of "dormant" micronuclei. The risk of DCS remained lower (43%) when pretreatment with 100% O(2) at normobaric pressure for 20 min was followed by a 2 h interval in normobaric air (but not 6 or 24 h) before the hyperbaric exposure. The loss of effectiveness after a 6 or 24 h interval in normobaric air is related to micronuclei rejuvenation. Although pretreatment with hyperbaric O(2) may have an advantage over normobaric hyperoxia, decompression should not intervene between pretreatment and the dive.

Oxygen Consumption at Altitude as a Risk Factor for Altitude Decompression Sickness

The existence of a general influence of exercise on the incidence of decompression sickness (DCS) has been known for more than a half-century. However, quantification of the effect has not been done for several reasons, including isolation of exercise as the only variable. The DCS database at Brooks City-Base, TX, contains detailed physiologic information on over 3000 altitude exposures. The purpose of this study was to measure Vo2 during the activities performed during those exposures to retrospectively determine if Vo2, a quantifiable index of exercise intensity, was related to the level of reported DCS. Ground-level activity was designed to duplicate the standardized activity during the altitude exposures. Breath-by-breath Vo2 was determined for each activity using a COSMED metabolic measurement system. Comparison of the Vo2 during four levels of activity performed under otherwise comparable conditions allowed a determination of correlation between Vo2 and DCS risk observed during the altitude exposures. Four previous altitude exposure profiles at 8992 m to 9144 m (29,500 to 30,000 ft; 231 to 226 mmHg) for 4 h following a 1-h prebreathe resulted in 38-86% DCS. This study provided the Vo2 of activities during those studies. The correlation between DCS incidence and the highest 1-min Vo2 of activity was 0.89. The highest 1-min Vo2 showed a high correlation with level of DCS risk. Future exposures involving lower levels of activity could provide data that would allow improvement in modeling of DCS risk.

Air Break During Preoxygenation and Risk of Altitude Decompression Sickness

To reduce the risk of decompression sickness (DCS), current USAF U-2 operations require a 1-h preoxygenation (PreOx). An interruption of oxygen breathing with air breathing currently requires significant extension of the PreOx time. The purpose of this study was to evaluate the relationship between air breaks during PreOx and subsequent DCS and venous gas emboli (VGE) incidence, and to determine safe air break limits for operational activities. Volunteers performed 30 min of PreOx, followed by either a 10-min, 20-min, or 60-min air break, then completed another 30 min of PreOx, and began a 4-h altitude chamber exposure to 9144 m (30,000 ft). Subjects were monitored for VGE using echocardiography. Altitude exposure was terminated if DCS symptoms developed. Control data (uninterrupted 60-min PreOx) to compare against air break data were taken from the AFRL DCS database. At 1 h of altitude exposure, DCS rates were significantly higher in all three break in prebreathe (BiP) profiles compared to control (40%, 45%, and 47% vs. 24%). At 2 h, the 20-min and 60-min BiP DCS rates remained higher than control (70% and 69% vs. 52%), but no differences were found at 4 h. No differences in VGE rates were found between the BiP profiles and control. Increased DCS risk in the BiP profiles is likely due to tissue renitrogenation during air breaks not totally compensated for by the remaining PreOx following the air breaks. Air breaks of 10 min or more occurring in the middle of 1 h of PreOx may significantly increase DCS risk during the first 2 h of exposure to 9144 m when compared to uninterrupted PreOx exposures.

Hypoxia Awareness Training for Aircrew: A Comparison of Two Techniques

Major hazards associated with hypoxia awareness training are the risks of decompression sickness, barotrauma, and loss of consciousness. An alternate method has been developed which combines exposure to a simulated altitude of 10,000 ft (3048 m) with breathing of a gas mixture containing 10% oxygen and 90% nitrogen. The paradigm, called Combined Altitude and Depleted Oxygen (CADO), places the subjects at a physiological altitude of 25,000 ft (7620 m) and provides demonstration of symptoms of hypoxia and the effects of pressure change. CADO is theoretically safer than traditional training at a simulated altitude of 25,000 ft (7620 m) due to a much lower risk of decompression sickness (DCS) and has greater fidelity of training for fast jet aircrew (mask-on hypoxia). This study was conducted to validate CADO by comparing it with hypobaric hypoxia. There were 43 subjects who were exposed to two regimens of hypoxia training: hypobaric hypoxia (HH) at a simulated altitude of 25,000 ft (7620 m) and CADO. Subjective, physiological, and performance data of the subjects were collected, analyzed, and compared. There were no significant differences in the frequency and severity of the 24 commonly reported symptoms, or in the physiological response, between the two types of hypoxia exposure. CADO is similar to HH in terms of the type and severity of symptoms experienced by subjects, and appears to be an effective, useful, and safe tool for hypoxia training.

Optimal Decompression Through Multi-parametric Nonlinear Programming

Recently, a comprehensive dynamic mathematical model named Copernicus has been established to discover the mechanism of the vascular bubble formation and growth during and after decompression from a dive. The model uses Venous Gas Emboli (VGE) as a measurement and connects it to the risk of severe Decompression Sickness (DCS). Being validated by a series of diving tests, Copernicus model is believed to be suitable and efficient to predict DCS hence generate optimal decompression profiles for the divers. This paper is based on the Copernicus model and presents a nonlinear model predictive control approach, where multi-parametric nonlinear programming is used to construct an explicit solution for the ease of implementation on a typical low-cost diving computer.

Preconditioning Methods and Mechanisms for Preventing the Risk of Decompression Sickness in Scuba Divers: A Review

Scuba divers are at risk of decompression sickness due to the excessive formation of gas bubbles in blood and tissues following ascent, with potentially subsequent neurological injuries. Since nonprovocative dive profiles are no guarantor of protection against this disease, novel means are required for its prevention including predive procedures that could induce more resistance to decompression stress. In this article, we review the recent studies describing the promising preconditioning methods that might operate on the attenuation of bubble formation believed to reduce the occurrence of decompression sickness. The main practical applications are simple and feasible predive measures such as endurance exercise in a warm environment, oral hydration, and normobaric oxygen breathing. Rheological changes affecting tissue perfusion, endothelial adaptation with nitric oxide pathway, up-regulation of cytoprotective proteins, and reduction of preexisting gas nuclei from which bubbles grow could be involved in this protective effect.

Use of heart rate monitoring for an individualized and time-variant decompression model

Individual differences, physiological pre-conditions and in-dive conditions like workload and body temperature have been known to influence bubble formation and risk of decompression sickness in diving. Despite this fact, such effects are currently omitted from the decompression algorithms and tables that are aiding the divers. There is an apparent need to expand the modeling beyond depth and time to increase safety and efficiency of diving. The present paper outlines a mathematical model for how heart rate monitoring in combination with individual parameters can be used to obtain a customized and time-variant decompression model. We suggest that this can cover some of the individual differences and dive conditions that are affecting bubble formation. The model is demonstrated in combination with the previously published Copernicus decompression model, and is suitable for implementation in dive computers and post dive simulation software for more accurate risk analysis.

Activation of Platelets and Fibrinolysis Induced by Saturated Air Dives

The Doppler technique is currently the usual method for detection of bubbles in the circulation following decompression. However, cases of decompression sickness (DCS) frequently occur in the absence of detectable bubbles, so that other markers for increasing risk of DCS would be welcome. This study assessed the hemostatic effects of compressed-air saturation dives that conformed to the "safe" limits of accepted decompression tables. We measured coagulation times, thrombin generation, platelets, and fibrinolysis in 21 male divers who were subjected to saturated hyperbaric exposures to 0.28-0.3 MPa (corresponds to 18-20 msw). Each diver did one dive. Pooled before- and after-dive data for all exposures showed after decompression, statistically significant changes included decrease of the mean platelet count after, increased induced platelet aggregation and number of platelet aggregates, increased number of P-selectin (CD62P) positive platelets and CD62P density on platelets, increase of platelet derived microparticles in the blood of the divers, decrease of factor XII, X, and fibrinogen concentrations, and marked increase of plasmin-antiplasmin complex concentration. Thrombin activation markers and coagulation times did not change significantly. Saturated hyperbaric exposures followed by nominally safe decompression led to activation of platelets and the fibrinolytic system. The probable mechanism for the activation of platelets and fibrinolysis is contact with the surface of evolved bubbles in the divers' circulation.