Pulmonary artery location during microgravity activity: Potential impact for chest-mounted Doppler during space travel

Doppler, or ultrasonic, monitoring for pain manifestations of decompression sickness (the bends) is accomplished by placing a sensor on the chest over the pulmonary artery and listening for bubbles. Difficulties have arisen because the technician notes that the pulmonary artery seems to move with subject movement in a one-g field and because the sensor output is influenced by only slight degrees of sensor movement. This study used two subjects and mapped the position of the pulmonary artery in one-g, microgravity, and two-g environments using ultrasound. The results showed that the pulmonary artery is fixed in location in microgravity and not affected by subject position change. The optimal position corresponded to where the Doppler signal is best heard with the subject in a supine position in a one-g environment. The impact of this result is that a proposed multiple sensor array on the chest proposed for microgravity use may not be necessary to monitor an astronaut during extravehicular activities. Instead, a single sensor of approximately 1 inch diameter and mounted in the position described above may suffice

Verification of an altitude decompression sickness prevention protocol for Shuttle operations utilizing a 10.s psi pressure stage

Three test series involving 173-man tess were conducted to define and verify a pre-extravehicular activity (EVA) denitrogenation procedure that would provide acceptable protection against altitude decompression sickness while minimizing the required duration of oxygen (O2) prebreathe in the suit prior to EVA. The tests also addressed the safety, in terms of incidence of decompression sickness, of conducting EVA's on consecutive days rather than on alternate days. The tests were conducted in an altitude chamber, subjects were selected as representative of the astronaut population, and EVA periods were simulated by reducing the chamber pressure to suit pressure while the subjects breathed O2 with masks and worked at EVA representative work rates. A higher than anticipated incidence of both venous bubbles (55%) and symptoms (26%) was measured following all denitrogenation protocols in this test. For the most part, symptoms were very minor and stabilized, diminished, or disappeared in the six-hour tests. Instances of clear, possible, or potential systemic symptoms were encountered only after use of the unmodified 10.2 psi protocol and not after the modified 10.2 psi protocol, the 3.5-hour O2 prebreathed protocol, or the 4.0-hour O2 prebreathe protocol. The high incidence of symptoms is ascribed to the type and duration of exercise and the sensitivity of the reporting technique to minor symptoms. Repeated EVA exposures after only 17 hours did not increase symptom or bubble incidence

Approximate Simulation of Acute Hypobaric Hypoxia with Normobaric Hypoxia

INTRODUCTION. Some manufacturers of reduced oxygen (O2) breathing devices claim a comparable hypobaric hypoxia (HH) training experience by providing F(sub I) O2 < 0.209 at or near sea level pressure to match the ambient O2 partial pressure (iso-pO2) of the target altitude. METHODS. Literature from investigators and manufacturers indicate that these devices may not properly account for the 47 mmHg of water vapor partial pressure that reduces the inspired partial pressure of O2 (P(sub I) O2). Nor do they account for the complex reality of alveolar gas composition as defined by the Alveolar Gas Equation. In essence, by providing iso-pO2 conditions for normobaric hypoxia (NH) as for HH exposures the devices ignore P(sub A)O2 and P(sub A)CO2 as more direct agents to induce signs and symptoms of hypoxia during acute training exposures. RESULTS. There is not a sufficient integrated physiological understanding of the determinants of P(sub A)O2 and P(sub A)CO2 under acute NH and HH given the same hypoxic pO2 to claim a device that provides isohypoxia. Isohypoxia is defined as the same distribution of hypoxia signs and symptoms under any circumstances of equivalent hypoxic dose, and hypoxic pO2 is an incomplete hypoxic dose. Some devices that claim an equivalent HH experience under NH conditions significantly overestimate the HH condition, especially when simulating altitudes above 10,000 feet (3,048 m). CONCLUSIONS. At best, the claim should be that the devices provide an approximate HH experience since they only duplicate the ambient pO2 at sea level as at altitude (iso-pO2 machines). An approach to reduce the overestimation is to at least provide machines that create the same P(sub I)O2 (iso-P(sub I)O2 machines) conditions at sea level as at the target altitude, a simple software upgrade

Description of the NASA Hypobaric Decompression Sickness Database (1982-1998)

The availability of high-speed computers, data analysis software, and internet communication are compelling reasons to describe and make available computer databases from many disciplines. Methods: Human research using hypobaric chambers to understand and then prevent decompression sickness (DCS) during space walks has been conducted at the Johnson Space Center (JSC) from 1982 to 1998. The data are archived in the NASA Hypobaric Decompression Sickness Database, within an Access 2003 Relational Database. Results: There are 548 records from 237 individuals that participated in 31 unique tests. Each record includes physical characteristics, the denitrogenation procedure that was tested, and the outcome of the test, such as the report of a DCS symptom and the intensity of venous gas emboli (VGE) detected with an ultrasound Doppler bubble detector as they travel in the venous blood along the pulmonary artery on the way to the lungs. We documented 84 cases of DCS and 226 cases where VGE were detected. The test altitudes were 10.2, 10.1, 6.5, 6.0, and 4.3 pounds per square inch absolute (psia). 346 records are from tests conducted at 4.3 psia, the operating pressure of the current U.S. space suit. 169 records evaluate the Staged 10.2 psia Decompression Protocol used by the Space Shuttle Program. The mean exposure time at altitude was 242.3 minutes (SD = 80.6), with a range from 120 to 360 minutes. Among our test subjects, 96 records of exposures are females. The mean age of all test subjects was 31.8 years (SD = 7.17), with a range from 20 to 54 years. Discussion: These data combined with other published databases and evaluated with metaanalysis techniques would extend our understanding about DCS. A better understanding about the cause and prevention of DCS would benefit astronauts, aviators, and divers

Empirical models for use in designing decompression procedures for space operations

Empirical models for predicting the incidence of Type 1 altitude decompression sickness (DCS) and venous gas emboli (VGE) during space extravehicular activity (EVA), and for use in designing safe denitrogenation decompression procedures are developed. The models are parameterized using DCS and VGE incidence data from NASA and USAF manned altitude chamber decompression tests using 607 male and female subject tests. These models, and procedures for their use, consist of: (1) an exponential relaxation model and procedure for computing tissue nitrogen partial pressure resulting from a specified prebreathing and stepped decompression sequence; (2) a formula for calculating Tissue Ratio (TR), a tissue decompression stress index; (3) linear and Hill equation models for predicting the total incidence of VGE and DCS attendant with a particular TR; (4) graphs of cumulative DCS and VGE incidence (risk) versus EVA exposure time at any specified TR; and (5) two equations for calculating the average delay period for the initial detection of VGE or indication of Type 1 DCS in a group after a specific denitrogenation decompression procedure. Several examples of realistic EVA preparations are provided

Increase in whole-body peripheral vascular resistance during three hours of air or oxygen prebreathing

Male and female subjects prebreathed air or 100% oxygen through a mask for 3.0 hours while comfortably reclined. Blood pressures, heart rate, and cardiac output were collected before and after the prebreathe. Peripheral vascular resistance (PVR) was calculated from these parameters and increased by 29% during oxygen prebreathing and 15% during air prebreathing. The oxygen contributed substantially to the increase in PVR. Diastolic blood pressure increased by 18% during the oxygen prebreathe while stystolic blood pressure showed no change under either procedure. The increase in PVR during air prebreathing was attributed to procedural stress common to air and oxygen prebreathing

Decompression Sickness After Air Break in Prebreathe Described with a Survival Model

Data from Brooks City-Base show the decompression sickness (DCS) and venous gas emboli (VGE) consequences of air breaks in a resting 100% O2 prebreathe (PB) prior to a hypobaric exposure. METHODS: DCS and VGE survival times from 95 controls for a 60 min PB prior to 2-hr or 4-hr exposures to 4.37 psia are statistically compared to 3 break in PB conditions: a 10 min (n=40), 20 min (n=40), or 60 min break (n=32) 30 min into the PB followed by 30 min of PB. Ascent rate was 1,524 meters / min and all exposures included light exercise and 4 min of VGE monitoring of heart chambers at 16 min intervals. DCS survival time for combined control and air breaks were described with an accelerated log logistic model where exponential N2 washin during air break was described with a 10 min half-time and washout during PB with a 60 min half-time. RESULTS: There was no difference in VGE or DCS survival times among 3 different air breaks, or when air breaks were compared to control VGE times. However, 10, 20, and 60 min air breaks had significantly earlier survival times compared to control DCS times, certainly early in the exposures. CONCLUSION: Air breaks of 10, 20, and 60 min after 30 min of a 60 min PB reduced DCS survival time. The survival model combined discrete comparisons into a global description mechanistically linked to asymmetrical N2 washin and washout kinetics based on inspired pN2. Our unvalidated regression is used to compute additional PB time needed to compensate for an air break in PB within the range of tested conditions

Effect of hydration on nitrogen washout in human subjects

Five subjects were tested to assess the influence of drinking hypotonic water (distilled water) on whole body tissue nitrogen washout. During the test, the subjects breathed aviators' oxygen for three hours. Each subject performed two baseline nitrogen washouts in a two-week period. The third washout, in the third week, was done under a transient hydrated condition. This was accomplished by having the subjects drink 1.5 liters of hypotonic water 30 minutes before the washout. Five-minute plots of tissue nitrogen removal from the three separate washouts were analyzed to ascertain if the hydration technique had any effect. Our results clearly indicate that the hydration technique did not alter the tissue nitrogen washout characteristics to any degree over three hours. An increase in tissue nitrogen washout under a transient hydrated condition using hypotonic fluid was not demonstrated to be the mechanism responsible for the reported benefit of this technique in preventing Type I altitude decompression pain in man

Exploiting Aerobic Fitness to Reduce Risk of Hypobaric Decompression Sickness

Decompression sickness (DCS) is multivariable. But we hypothesize an aerobically fit person is less likely to experience hypobaric DCS than an unfit person given that fitness is exploited as part of the denitrogenation (prebreathe, PB) process prior to an altitude exposure. Aerobic fitness is peak oxygen uptake (VO2pk, ml/kg/min). Treadmill or cycle protocols were used over 15 years to determine VO2pks. We evaluated dichotomous DCS outcome and venous gas emboli (VGE) outcome detected in the pulmonary artery with Doppler ultrasound associated with VO2pk for two classes of experiments: 1) those with no PB or PB under resting conditions prior to ascent in an altitude chamber, and 2) PB that included exercise for some part of the PB. There were 165 exposures (mean VO2pk 40.5 plus or minus 7.6 SD) with 25 cases of DCS in the first protocol class and 172 exposures (mean VO2pk 41.4 plus or minus 7.2 SD) with 25 cases of DCS in the second. Similar incidence of the DCS (15.2% vs. 14.5%) and VGE (45.5% vs. 44.8%) between the two classes indicates that decompression stress was similar. The strength of association between outcome and VO2pk was evaluated using univariate logistic regression. An inverse relationship between the DCS outcome and VO2pk was evident, but the relationship was strongest when exercise was done as part of the PB (exercise PB, coef. = -0.058, p = 0.07; rest or no PB, coef. = -0.005, p = 0.86). There was no relationship between VGE outcome and VO2pk (exercise PB, coef. = -0.003, p = 0.89; rest or no PB, coef. = 0.014, p = 0.50). A significant change in probability of DCS was associated with fitness only when exercise was included in the denitrogenation process. We believe a fit person that exercises during PB efficiently eliminates dissolved nitrogen from tissues

The effect of exercise on venous gas emboli and decompression sickness in human subjects at 4.3 psia

The contribution of upper body exercise to altitude decompression sickness while at 4.3 psia after 3.5 or 4.0 hours of 100% oxygen prebreathing at 14.7 psia was determined by comparing the incidence and patterns of venous gas emboli (VGE), and the incidence of Type 1 decompression sickness (DCS) in 43 exercising male subjects and 9 less active male Doppler Technicians (DT's). Each subject exercised for 4 minutes at each of 3 exercise stations while at 4.3 psia. An additional 4 minutes were spent monitoring for VGE by the DT while the subject was supine on an examination cot. In the combined 3.5 and 4.0 hour oxygen prebreathe data, 13 subjects complained of Type 1 DCS compared to 9 complaints from DT's. VGE were detected in 28 subjects compared to 14 detections from DT's. A chi-square analysis of proportions showed no statistically significantly difference in the incidence of Type 1 DCS or VGE between the two groups; however, the average time to detect VGE and to report Tyep 1 DCS symptoms were statistically different. It was concluded that 4 to 6 hours of upper body exercise at metabolic rates simulating EVA metabolic rates hastens the initial detection of VGE and the time to report Type 1 DCS symptoms as compared to DT's