Experimental trials to assess the risks of decompression sickness in flying after diving.

We conducted experimental trials of flying after diving using profiles near the no-decompression exposure limits for recreational diving. The objective was to determine the dependence of DCS occurrence during or after flight on the length of the preflight surface intervals (PFSI). One to three dives were conducted during a single day with dry, resting subjects in a hyperbaric chamber at depths of 40, 60, or 100 fsw (224, 286, 408 kPa). The dives were followed by PFSI of 3 to 17 hrs and a four-hour altitude exposure at 8,000 ft (75 kPa), the maximum permitted cabin altitude for pressurized commercial aircraft. Forty DCS incidents occurred during or after flight in 802 exposures of 495 subjects. The DCS incidence decreased as PFSI increased, and repetitive dives generally required longer PFSI to achieve low incidence than did single dives (p = 0.0159). No DCS occurred in 52 trials of a 17 hr PFSI, the longest PFSI tested. The results provide empirical information for formulating guidelines for flying in commercial aircraft after recreational diving.

Inhaled carbon monoxide and hyperoxic lung injury in rats.

Because carbon monoxide (CO) has been proposed to have anti-inflammatory properties, we sought protective effects of CO in pulmonary O(2) toxicity, which leads rapidly to lung inflammation and respiratory failure. Based on published studies, we hypothesized that CO protects the lung against O(2) by selectively increasing expression of antioxidant enzymes, thereby decreasing oxidative injury and inflammation. Rats exposed to O(2) with or without CO [50-500 parts/million (ppm)] for 60 h were compared for lung wet-to-dry weight ratio (W/D), pleural fluid volume, myeloperoxidase (MPO) activity, histology, expression of heme oxygenase-1 (HO-1), and manganese superoxide dismutase (Mn SOD) proteins. The brains were evaluated for histological evidence of damage from CO. In O(2)-exposed animals, lung W/D increased from 4.8 in normal rats to 6.3; however, only CO at 200 and 500 ppm decreased W/D significantly (to 5.9) during O(2) exposure. Large volumes of pleural fluid accumulated in all rats, with no significant CO treatment effect. Lung MPO values increased after O(2) and were not attenuated by CO treatment. CO did not enhance lung expression of oxidant-responsive proteins Mn SOD and HO-1. Animals receiving O(2) and CO at 200 or 500 ppm showed significant apoptotic cell death in the cortex and hippocampus by immunochemical staining. Thus significant protection by CO against O(2)-induced lung injury could not be confirmed in rats, even at CO concentrations associated with apoptosis in the brain.

Improved probabilistic decompression model risk predictions using linear-exponential kinetics.

Using a data base of 2,383 air and nitrogen-oxygen dives resulting in 131 cases of decompression sickness (DCS), risk functions were developed for a set of probabilistic decompression models according to survival analysis techniques. Parameters were optimized using the method of maximum likelihood Gas kinetics were either traditional exponential uptake and elimination, or an exponential uptake followed by linear elimination (LE kinetics) when calculated supersaturation was excessive. Risk functions either used the calculated relative gas supersaturation directly, or a delayed risk using a time integral of prior supersaturation. The most successful model (considering both incidence and time of onset of DCS) used supersaturation risk, and LE kinetics (in only 1 of 3 parallel compartments). Several methods of explicitly incorporating metabolic gases in physiologically plausible functions were usually found in lumped threshold terms and did not explicitly affect the overall data fit. The role of physiologic fidelity vs. empirical data fitting ability in accounting for model success is discussed.

Development and interactions of two inert gas bubbles during decompression.

A mathematical model has been developed to simulate the evolution of two inert gas bubbles in tissue. This is useful for understanding the dynamics of bubbles that presumably arise during decompression. It is assumed that they are spherical and that the tissue volume surrounding them is infinite. The total pressure in each bubble is determined by the barometric and metabolic gas pressures as well as the pressure due to surface tension. Bipolar coordinates are employed to determine the inert gas pressure distribution. Two coupled governing equations for bubble radii are then derived and solved numerically. The results demonstrate how bubble evolution is affected by the distance between bubbles and the initial bubble radii. The existence time and bubble surface flux of two equal-sized bubbles are calculated and compared with those of a single gas bubble model. The results indicate that when two bubbles are very close, it takes 20% more time for two bubbles to dissolve than for a single one, and the total surface flux of two bubbles is nearly 20% less than twice of a single bubble. When the center-to-center distance is 10 times of bubble radius, the effect of bubble interaction on bubble existence time and surface flux are about 6 and 9% changes, respectively. We conclude that if bubbles are not too small, the interactions among bubbles should be included in inert gas bubble models predicting bubble evolution.

Does the time course of bubble evolution explain decompression sickness risk?

A probabilistic model of decompression sickness (DCS) risk based on linear-exponential (LE) kinetics has given the best fit of the human air and nitrox DCS database. To test the hypothesis that its success may be due to the formation of a gas phase during decompression, we developed a physiologically based bubble evolution model using a numerical solution of a partial differential equation system. Because of the computational intensity of this method, it could not be used to fully explore our hypothesis. Consequently, we compared the solution with that of a computationally simpler approximation that was previously published by Van Liew and found the two approaches gave similar results. Using the simpler model, assuming bubble densities of 1 and 1,000 bubbles/cm3, we found a tissue time constant of at least 80 min (equivalent to perfusion of 1/80 ml.g-1.min-1) was required to achieve a delay in bubble dissolution comparable to the prolonged risk of DCS predicted by the LE model. We suggest that the persistence of single bubbles in a uniformly perfused homogeneous tissue alone is unlikely to explain persistent DCS risk.

Characterization and measurement of elastance with application to underwater breathing apparatus.

The elastic loads inherent in underwater breathing apparatus (UBA) can affect diver performance. This work quantitatively examines elastance, its measurement by static tests, and its relationship to UBA. A rigid, fixed-volume container and a vertical water column with straight and parallel sides produce elastic loads that have application to closed-circuit UBA. We derived equations to describe the pressure-volume relationships of these elements from first principles and tested the equations experimentally for system pressure produced by a swept volume in a breathing machine. Our work demonstrates that simplified equations to describe elastance may not be sufficiently accurate for all situations. In addition, static measurements of elastance of a UBA or other element will not be reproducible unless all the volumes within the testing apparatus are accounted for; we provide experimental and mathematical techniques for doing so.

Management of herniated intervertebral disks during saturation dives: a case report.

During research saturation dives at 5.0 and 5.5 atm abs, 2 divers developed an acute herniation of the nucleus pulposus of the L5-S1 intervertebral disk. In both cases the pain was severe enough to require intravenous morphine or intramuscular meperidine. Although the symptoms presented by these divers are frequently considered to be an indication for immediate surgical consultation, we decided that emergency decompression posed an unacceptable risk that decompression sickness (DCS) would develop in the region of acute inflammation. In both cases strict bedrest and medical therapy were performed at depth. In the first case, 12 h was spent at depth before initiating a standard U.S. Navy saturation decompression schedule with the chamber partial pressure of oxygen elevated to 0.50 atm abs. In the second case, a conservative He-N2-O2 trimix decompression schedule was followed to the surface. In both cases, no initial upward excursion was performed. The required decompression time was 57 h 24 min from 5.5 atm abs and 55 h 38 min from 5.0 atm abs. During the course of decompression, the first diver's neurologic exam improved and he required decreasing amounts of intravenous narcotic; we considered both to be evidence against DCS. The second diver continued to have pain and muscle spasm throughout decompression, however he did not develop motor, reflex, or sphincter abnormalities. Both divers have responded well to nonsurgical therapy.

Predicting the time of occurrence of decompression sickness.

Probabilistic models and maximum likelihood estimation have been used to predict the occurrence of decompression sickness (DCS). We indicate a means of extending the maximum likelihood parameter estimation procedure to make use of knowledge of the time at which DCS occurs. Two models were compared in fitting a data set of nearly 1,000 exposures, in which greater than 50 cases of DCS have known times of symptom onset. The additional information provided by the time at which DCS occurred gave us better estimates of model parameters. It was also possible to discriminate between good models, which predict both the occurrence of DCS and the time at which symptoms occur, and poorer models, which may predict only the overall occurrence. The refined models may be useful in new applications for customizing decompression strategies during complex dives involving various times at several different depths. Conditional probabilities of DCS for such dives may be reckoned as the dive is taking place and the decompression strategy adjusted to circumstance. Some of the mechanistic implications and the assumptions needed for safe application of decompression strategies on the basis of conditional probabilities are discussed.

Testing of revised unlimited-duration upward excursions during helium-oxygen saturation dives.

As originally published in 1978, the U.S. Navy Unlimited-Duration Saturation Excursion Limits were found to result in an occasional case of vestibular decompression sickness (DCS) after upward excursions from storage depths in the 800-1000 feet of seawater (fsw) range. A series of dives was undertaken to revise these limits. Fifty divers performed a total of 164 man-excursions during 9 saturation dives with maximum storage depths of 36 to 1100 fsw. All excursions tested were upward excursions taken after saturation at the initial storage depth. A total of 130 man-excursions were at or greater than the maximum limits, which were calculated according to the empirical relationship: UEXD = [(0.1574.D1 + 6.197)0.5 - 1]/(0.0787) where UEXD is the upward excursion distance and D1 is the pre-excursion storage depth in fsw. During testing, 9 cases of DCS occurred that were all type 1. All of these cases occurred 8 h or more into the saturation decompression, which was begun immediately after some of the upward excursions. None of these cases of DCS were ascribed to the excursion itself, but rather to a saturation decompression rate that was too fast. As a result of the described testing, excursions computed according to the above formula were accepted for operational use in 1987. The theoretical aspects of the excursion distance calculation are discussed, including the compatibility with some current decompression models.

Central nervous system oxygen toxicity in closed circuit scuba divers II.

Central nervous system oxygen toxicity is currently the limiting factor in underwater swimming/diving operations using closed-circuit oxygen equipment. A dive series was conducted at the Navy Experimental Diving Unit in Panama City, FL, to determine whether these limits can be safely extended and also to evaluate the feasibility of making excursions to increased depth after a previous transit at a shallower depth for various lengths of time. A total of 465 man-dives were conducted on 14 different experimental profiles. In all, 33 episodes of oxygen toxicity were encountered, including 2 convulsions. Symptoms were classified as probable, definite, or convulsion. Findings were as follows: symptom classification is a useful tool in evaluating symptoms of oxygen toxicity; safe exposure limits should generally be adjusted only as a result of definite symptoms or convulsions; the following single-depth dive limits are proposed: 20 fsw (6.1 msw)--240 min, 25 fsw (7.6 msw)--240 min, 30 fsw (9.1 msw)--80 min, 35 fsw (10.7 msw)--25 min, 40 fsw (12.2 msw)--15 min, 50 fsw (15.2 msw)--10 min; a pre-exposure of up to 4 h at 20 fsw causes only a slight increase in the probability of an oxygen toxicity symptom on subsequent downward excursions; a pre-exposure depth of 25 fsw will have a more adverse effect on subsequent excursions than will 20 fsw; a return to 20 fsw for periods of 95-110 min seems to provide an adequate recovery period from an earlier excursion and enables a second excursion to be taken without additional hazard; nausea was the most commonly noted symptom of oxygen toxicity, followed by muscle twitching and dizziness; dives on which oxygen toxicity episodes were noted had a more rapid rate of core temperature cooling than dives without toxicity episodes; several divers who had passed the U.S. Navy Oxygen Tolerance Test were observed to be reproducibly more susceptible to oxygen toxicity than the other experimental divers.

Report of an isolated mid-frequency hearing loss following inner ear barotrauma.

A case describing an isolated mid-frequency hearing loss as a result of inner ear barotrauma is presented. The onset of symptoms was insidious but progressed to a profound total-range hearing loss in the right ear. This loss resolved rapidly with cessation of diving activity, bed rest, and head elevation, leaving only an isolated 20-dB hearing decrement at 1000 Hz. Since the diver was participating in evaluation of experimental decompression tables, differentiation had to be made between barotrauma and inner ear decompression sickness.

Hindrance to diffusive gas mixing in the lung in hyperbaric environments.

Diffusivity of a gas is inversely proportional to atmospheric pressure. We studied pulmonary gas mixing in hyperbaric environments (5.5 and 9.5 ATA) as a means of understanding the role played by diffusion in normal situations and also as a means of determining whether persons in hyperbaric environments will be handicapped by poor diffusive mixing. Our subjects took single breaths of a mixture of indicator gases (5% each of SF6, Ar, Ne, and He; 20% O2, balance N2). Recordings of expired volumes and concentrations showed that heavier indicators were less well mixed than lighter ones, as evidenced by a slower fall during the transition between dead space and "alveolar" gas and a steeper slope of the alveolar plateau. Differences between light and heavy gases increased as pressure increased. Amounts of the indicators retained in the functional residual capacity (FRC) or residual volume after a single breath had a weak positive relation to diffusivity; the amounts (A) in the FRC (as fraction of inspired amounts) were well fitted by a simple equation. ARFC/AI = 0.55 - (0.0010/D), where D is molecular diffusivity. We conclude that the changes of distribution of inspired gas that occur with large changes of diffusivity have only a minor effect on the amount of gas exchanged between the inspirate and residual gas in the FRC.

Metabolic response to respiratory heat loss-induced core cooling.

To study the phenomenon of isolated core cooling, four resting men breathed cooled helium-oxygen (T in = 14 +/- 2 degrees C, 40-60% relative humidity) in a warm hyperbaric chamber at pressures equivalent to 640, 1,000, and 1,400, and 1,800 ft seawater (fsw). Rectal temperature (T re) fell by 0.43 +/- 0.13 degrees C at 640 fsw to 0.98 +/- 0.15 degrees C at 1,800 fsw after 60 min. The rate at which T re fell was linearly related to the product of inspired gas density times specific heat. The metabolic response (VO2) to this isolated core cooling was more closely related to the rate of fall in T re than to the magnitude of this fall. A distinct threshold temperature, below which a rise in VO2 would occur, was not demonstrable. However, when the rate of fall of T re exceeded 0.70 degrees C . h-1, VO2 increased above base line, in spite of high skin temperatures that may have blunted the VO2 response. When VO2 did increase, its net benefit on thermal homeostasis was negated by the associated rise in pulmonary ventilation and its attendant increase in respiratory heat loss. Breathing cool helium-oxygen under hyperbaric conditions can rapidly lower deep body temperature, even in the presence of a warm body surface.

Thermal responses in humans exposed to cold hyperbaric helium-oxygen.

The relationship of metabolic heat production to skin and core temperatures, cutaneous heat flow, and respiratory heat loss was measured in 10 male subjects cooled in hyperbaric helium at 20.7 ATA and 15 or 20 degrees C for 60-120 min. Under these conditions, metabolic heat production tended to compensate for the sum of convective and radiant heat losses from the skin but did not increase sufficiently to compensate for additional respiratory heat losses. There was a positive correlation between respiratory heat loss and fall in rectal temperature. Individual variability in ventilatory response to cold hyperbaric helium exposure as shown by a wide range of minute ventilation-to-oxygen consumption ratios (VE/VO2) was similar to that reported during cold water immersion. Subjects with high VE/VO2 had low mean physiological shell insulation values and lost more heat through the skin as well as through the respiratory tract than subjects with low VE/VO2.

Prolonged oxygen exposures in immersed exercising divers at 25 fsw (1.76 ATA).

Twenty-four oxygen exposures lasting 80 to 271 min were performed by six immersed exercising subjects at 25 fsw (1.76 ATA) in both warm and cold water. Two types of exercise were performed, moderate work (50 watts) for long periods of time, and graded exercise (25-150 watts) lasting 85 min. In 21 degrees C water, moderate exercise lasted 228 +/- 39 min, with a mean VO2 of 1.72 +/- 0.11 liter/min. In 4 degree C water, the duration was 163 +/- 22 min, with a mean VO2 of 1.83 +/- 0.16 liter/min. The differences in duration of oxygen exposure in warm and cold water reflect termination at an inspired PCO2 of 7.6 mmHg, a level reached earlier in cold water because of CO2 absorbent exhaustion. In 21 degrees C water, the VO2 for graded exercise ranged from 1.51 to 3.00 liter/min and in 4 degrees C water, from 2.00 to 3.16 liter/min. Central nervous system oxygen toxicity was not observed during these exposures, although two divers had clinical and spirometric evidence of early pulmonary oxygen toxicity. The absence of CNS oxygen toxicity is attributed to low resistance and minimization of dead space, which caused a low inspired PCO2, although the divers' experience with oxygen diving and their excellent physical condition may have contributed as well.

Diffusion-dependence of pulmonary gas mixing at 5.5 and 9.5 ATA.

Gas-phase diffusivity is inversely proportional to pressure, so mixing of inspired gas in the lung can be expected to be poor in hyperbaric environments. Subjects performed multiple-breath wash-in of a mixture (4% each of SF6, Ar, Ne, and He; 21% O2, 63% N2) at 1.5, 5.5, and 9.5 ATA. At the higher pressures there were marked differences of concentrations between the indicator gases, measured by mass spectrometer at the mouth during a single expiration. Compared to heavier gases, light gases fell from dead space concentration to the "alveolar" level sooner, had a flatter plateau, and had a lower average expired concentration, indicating that more of the light gases were retained in the Functional Residual Capacity (FRC) after the breath. However, wash-in rates for the indicators were about the same; a rapid initial rate for He diminished so that it was about the same as the SF6 rate, because in later breaths a back pressure developed for He. The findings illustrate the basic principle that the amount of gas that diffuses from one location to another in a container depends not only on diffusivity, but also in an interdependent manner on concentration gradient, time for diffusion, and configuration of the container.

Effects of immersion and static lung loading on submerged exercise at depth.

The effects of static lung loading in the range +20 cmH2O to -20 cmH2O was investigated in 3 male subjects breathing air during submerged exercise in the prone position at pressures ranging from 1.45 ATA to 6.76 ATA. Both maximal and submaximal exercise was performed and dry controls were done at 1.45 ATA. A low-resistance bag-in-a-box breathing apparatus (less than 1.25 cmH2O/liter/s at 8 g/liter density) was used. Static lung loading had little effect on maximal or submaximal VO2, VCO2, VE, heart rate, or end-tidal PCO2, while increased breathing gas density did affect these parameters to a larger extent. Imersion per se reduced the VE at a given level of VO2 and increased both the VT and VA at a given VE. Increasingly positive static lung load increased VC and ERV both during rest and exercise. Exercise-induced dyspnea was experienced and scored. At submaximal VO2 levels up to 2.5 liter/min this dyspnea did not limit exercise at any depth, but during maximal exertion at 6.76 ATA (VO2 from 3.45--3.77 liter/min), dyspnea became work limiting in several cases. Static load had a marked effect on dyspnea and a load of +10 cmH2O produced the least dyspnea, enabling all subjects to perform maximal exertions for 5 min at 6.76 ATA. The 15-s MVV was performed at all depths and static loads and neither it nor the VE/MVV ratio correlated with the degree of dyspnea.

Chamber-based system for physiological monitoring of submerged exercising subjects.

A system has been designed which allows for measurement of cardiorespiratory parameters in the fully submerged subject performing graded exercise. It consists of a horizontal wet chamber; a waterproofed, electrically braked bicycle ergometer; and a low-resistance "bag-in-a-box" breathing apparatus. Chamber and breathing apparatus design allow for a great deal of flexibility in both positioning of the subject and instrumentation. The 200-liter "bag-in-a-box" configuration provides the subject with humidified gas through 2.5 in. i.d. tubing. A rolling seal spirometer provides the lung counter volume. Provision is made for breath-by-breath gas analysis with a mass spectrometer. Hydrostatic pressure on the diver's thorax relative to chamber pressure can be easily and reproducibly varied over a wide range of positive and negative static lung loads. This system has been used on over 100 man-dives to depths equivalent to 6.5 ATA with oxygen consumptions up to 4.0 liters/min.

Development of unlimited duration excursion tables and procedures for helium-oxygen saturation diving.

Excursion ascents were performed during a series of experimental helium-oxygen saturation dives ranging between 150 and 1000 fsw to study the limits of multiple and extended duration excursions both deeper and shallower than the saturation depth. The distance a diver can safely ascend without decompression following saturation was found to be a function of depth, increasing from 75 ft at a saturation depth of 225 fsw to 180 ft at 1000 fsw. Initiation of saturation decompression immediately after an excursion was found to be safe. This information is incorporated into new U.S. Navy Unlimited Duration Excursion Tables and Procedures for Saturation Diving.