The Partial Pressure of Inspired Carbon Dioxide Exposure Levels in the Extravehicular Mobility Unit.

BACKGROUND: NASA has been making efforts to assess the carbon dioxide (CO2) washout capability of spacesuits using a standard CO2 sampling protocol. This study established the methodology for determining the partial pressure of inspired CO2 (PIco2) in a pressurized spacesuit. We applied the methodology to characterize PIco2 for the extravehicular mobility unit (EMU).METHODS: We suggested an automated and mathematical algorithm to find the end-tidal CO2 and the end of inspiration. We provided objective and standardized guidelines to identify acceptable breath traces, which are essential to accurate and reproducible calculation of the in-suit inhaled and exhaled partial pressure of CO2 (Pco2). The mouth guard-based method for measurement of inhaled and exhaled dry-gas Pco2 was described. We calculated all individual concentrations of PIco2 inhaled by 19 healthy subjects classified into 3 fitness groups. The transcutaneous Pco2 was monitored as a secondary measure to validate washout performance.RESULTS: Mean and standard deviation values for the data collection performance and the CO2 metrics were presented (e.g., minimum time weighted average Pco2 at suited workloads of resting, 1000, 2000, and 3000 (BTU h1) were 4.75 1.03, 8.09 1.39, 11.39 1.26, and 14.36 1.29 (mmHg s1). All CO2 metrics had a statistically significant association and all positive slopes with increasing metabolic rate. No significant differences in CO2 metrics were found between the three fitness groups.DISCUSSION: A standardized and automated methodology to calculate PIco2 exposure level is presented and applied to characterize CO2 washout in the EMU. The EMU has been operated successfully in over 400 extravehicular activities (EVAs) and is considered to provide acceptable CO2 washout performance. Results provide a basis for establishing verifiable Pco2 requirements for current and future EVA spacesuits.Kim KJ, Bekdash OS, Norcross JR, Conkin J, Garbino A, Fricker J, Young M, Abercromby AFJ. The partial pressure of inspired carbon dioxide exposure levels in the extravehicular mobility unit. Aerosp Med Hum Perform. 2020; 91(12):923931.

Carbon Monoxide Levels in the Extravehicular Mobility Unit by Modeling and Operational Testing.

INTRODUCTION: Carbon monoxide (CO) is a toxic gas with potential for detriment to spaceflight operations. An analytical model was developed to investigate if a maximum CO contamination of 1 ppm in the oxygen (O2) supply reached dangerous levels during extravehicular activity (EVA). Occupational monitoring pre- and postsuited exposures provided supplementary data for review.METHODS: The analytical model estimated O2 and CO concentrations in the extravehicular mobility unit (EMU) based on O2 and CO flow rates into and out of the system. The model was based on 3 h of prebreathe at 15.2 psia, 8 h of EVA at 4.3 psia, and 1 h at 15.2 psia for suit doffing. The Coburn-Forster-Kane equation was used to calculate crewmember carboxyhemoglobin saturation (COHb%) as a function of time. Monitoring of hemoglobin CO saturation (Spco) with a CO-oximeter was conducted pre- and post-EVA during operations on the International Space Station and in ground-based analog environments.RESULTS: The model predicted a maximum PCO in the EMU of 0.061 mmHg and a maximum crewmember COHb% of 2.1%. Operational Spco measurements in mean ± SD during ground-based analog testing were 0.7% ± 1.8% pretest and 0.5% ± 1.5% posttest. Spco values on the ISS were 1.5% ± 0.7% pre-EVA and 1.1% ± 0.3% post-EVA.DISCUSSION: The model predicted that astronauts are not exposed to toxic levels of CO during EVA and operational measurements did not show significant differences between Spco levels between pre- and post-EVA.Makowski MS, Norcross JR, Alexander D, Sanders RW, Conkin J, Young M. Carbon monoxide levels in the extravehicular mobility unit by modeling and operational testing. Aerosp Med Hum Perform. 2019; 90(2):84-91.

A Systematic Review and Meta-Analysis of Decompression Sickness in Altitude Physiological Training.

INTRODUCTION: A review of decompression sickness (DCS) cases associated with the NASA altitude physiological training (APT) program at the Johnson Space Center (JSC) motivated us to place our findings into the larger context of DCS prevalence from other APT centers.METHODS: We reviewed JSC records from 1999 to 2016 and 14 publications from 1968 to 2004 about DCS prevalence in other APT programs. We performed a meta-analysis of 15 APT profiles (488 cases / 385,116 exposures). We used meta-regression to evaluate the relation between estimated exposures and probability of DCS in a test group, accounting for the heterogeneity between studies.RESULTS: Our in-house review identified 6 Type I DCS (1 from an inside observer) and 1 Type II DCS. There were 6 cases in 9560 student hypobaric exposures from 3 NASA training flights; a student pooled prevalence rate of 0.44 cases / 1000 exposures compared to 1.44 cases / 1000 from 12 published APT profiles. The overall pooled DCS prevalence rate was 1.16 cases / 1000 exposures. There was substantial heterogeneity in DCS prevalence across studies. Denitrogenation time, exposure pressure, and exposure time were associated with probability of DCS in the meta-regression model.CONCLUSIONS: While the overall DCS prevalence rate is relatively low, there is marked heterogeneity among profiles. The pooled DCS prevalence rate estimate for the NASA profiles was lower than the overall rate. Variability in APT profile DCS prevalence could be further explained given student level and additional test-level covariates.Conkin J, Sanders RW, Koslovsky MD, Wear ML, Kozminski AG, Abercromby AFJ. A systematic review and meta-analysis of decompression sickness in altitude physiological training. Aerosp Med Hum Perform. 2018; 89(11):941-951.

Venous Gas Emboli and Ambulation at 4.3 psia.

INTRODUCTION: Ambulation during extravehicular activity on Mars may increase the risk of decompression sickness through enhanced bubble formation in the lower body. HYPOTHESES: walking effort (ambulation) before an exercise-enhanced denitrogenation (prebreathe) protocol at 14.7 psia does not increase the incidence of venous gas emboli (VGE) at 4.3 psia, but does increase incidence if performed after tissues become supersaturated with nitrogen at 4.3 psia. METHODS: VGE results from 45 control subjects who performed exercise prebreathe without ambulation before or during a 4-h exposure to 4.3 psia were compared to 21 subjects who performed the same prebreathe but ambulated before and during the hypobaric exposure (Group I) and to 41 subjects who only ambulated before the hypobaric exposure (Group II). Monitoring for VGE in the pulmonary artery was for 4 min at about 12-min intervals using precordial Doppler ultrasound (2.5 mHz). Detected VGE were assigned a categorical grade from I to IV. The detection of Grade III or IV was classified as "high VGE grade." RESULTS: The incidence of high VGE grade for Group I (57%) was greater than the control (17%) and Group II (15%). The incidence of pain-only decompression sickness was greater for Group I (20%) than the control (0%) and Group II (5%). CONCLUSIONS: High-grade VGE are increased by mild ambulation conducted under a supersaturated state (Group I vs. II); however, no increase was observed with mild ambulation during the saturated state alone (control vs. Group II).Conkin J, Pollock NW, Natoli MJ, Martina SD, Wessell JH III, Gernhardt ML. Venous gas emboli and ambulation at 4.3 psia. Aerosp Med Hum Perform. 2017; 88(4):370-376.

Hemoglobin Oxygen Saturation with Mild Hypoxia and Microgravity.

INTRODUCTION: Microgravity (µG) exposure and even early recovery from µG in combination with mild hypoxia may increase the alveolar-arterial oxygen (O2) partial pressure gradient. METHODS: Four male astronauts on STS-69 (1995) and four on STS-72 (1996) were exposed on Earth to an acute sequential hypoxic challenge by breathing for 4 min 18.0%, 14.9%, 13.5%, 12.9%, and 12.2% oxygen-balance nitrogen. The 18.0% O2 mixture at sea level resulted in an inspired O2 partial pressure (PIo2) of 127 mmHg. The equivalent PIO2 was also achieved by breathing 26.5% O2 at 527 mmHg that occurred for several days in µG on the Space Shuttle. A Novametrix CO2SMO Model 7100 recorded hemoglobin (Hb) oxygen saturation through finger pulse oximetry (Spo2, %). There were 12 in-flight measurements collected. Measurements were also taken the day of (R+0) and 2 d after (R+2) return to Earth. Linear mixed effects models assessed changes in Spo2 during and after exposure to µG. RESULTS: Astronaut Spo2 levels at baseline, R+0, and R+2 were not significantly different from in flight, about 97% given a PIo2 of 127 mmHg. There was also no difference in astronaut Spo2 levels between baseline and R+0 or R+2 over the hypoxic challenge. CONCLUSIONS: The multitude of physiological changes associated with µG and during recovery from µG did not affect astronaut Spo2 under hypoxic challenge.Conkin J, Wessel JH III, Norcross JR, Bekdash OS, Abercromby AFJ, Koslovsky MD, Gernhardt ML. Hemoglobin oxygen saturation with mild hypoxia and microgravity. Aerosp Med Hum Perform. 2017; 88(6):527-534.

Equivalent Air Altitude and the Alveolar Gas Equation.

INTRODUCTION: It is expedient to use normobaric hypoxia (NH) as a surrogate for hypobaric hypoxia (HH) for training and research. The approach matches inspired oxygen partial pressure (P(I)o2) at the desired altitude to that at site pressure (PB) by reducing the inspired fraction of oxygen (FIo2) to <0.21 using the equation: PIo2= (PB - 47) × FIo2, where 47 mmHg is the vapor pressure of water at 37°C. The investigator then has at site pressure the equivalent PIo2 as at altitude, i.e., the NH exposure is at an "equivalent air altitude." Some accepted as fact identical signs and symptoms of hypoxia for both conditions. However, those that derived the alveolar air equation showed that the coupled alveolar oxygen (PAo2) and carbon dioxide partial pressures (PAco2) for NH and HH are not identical when PIo2is equivalent. They attribute the difference in alveolar gas composition under equivalent PIo2to a nitrogen dilution effect or, more generally, to the respiratory exchange effect. Those that use NH as a convenient surrogate for HH must concede that physiological responses to NH cannot be identical to the responses to HH given only equivalent hypoxic PIo2.

Hypobaric Decompression Sickness Treatment Model.

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.

Probability of hypobaric decompression sickness including extreme exposures.

INTRODUCTION: The fitting of probabilistic decompression sickness (DCS) models is more effective when data encompass a wide range of DCS incidence. We obtained such data from the Air Force Research Laboratory Altitude Decompression Sickness Research Database. The data are results from 29 tests comprising 708 human altitude chamber exposures (536 men and 172 women). There were 340 DCS outcomes with per-test DCS incidence ranging from 0 to 88%. The tests were characterized by direct ascent at a rate of 5000 ft x min(-1) (1524 m x min(-1)) to a range of altitudes (226 to 378 mmHg) for 4 h after prebreathe times of varying length and with varying degrees of physical activity while at altitude. METHODS: Logistic regression was used to develop an expression for the probability of DCS [P(DCS)] using the Hill equation with decompression dose as the main predictor. Here, decompression dose is defined in terms of either the tissue ratio (TR) or a bubble growth index (BGI). Other predictors in the model were gender and peak exercise intensity at altitude. RESULTS: All three predictors (decompression dose, gender, and exercise intensity) were important contributions to the model for P(DCS). DISCUSSION: Higher TR or BGI, male gender, and higher exercise intensity at altitude all increased the modeled decompression dose. Using either TR or BGI to define decompression dose provided comparable results, suggesting that a simple TR is adequate for simple altitude exposures as an abstraction of the true decompression dose. The model is primarily heuristic and limits estimates of P(DCS) to only a 4-h exposure.

Protective mechanisms in hypobaric decompression.

BACKGROUND: To reduce bubble formation and growth during hypobaric exposures, a denitrogenation or nitrogen "washout" procedure is performed. This procedure consists of prebreathing oxygen fractions as close to one as possible (oxygen prebreathe) prior to depressurization before ascending to the working altitude or low spacesuit pressures. During the NASA prebreathe reduction program (PRP), it was determined that the addition of a light arm exercise to short, individually designed, performance-based heavy exercise (dual cycle ergometry) during an abbreviated 2-h prebreathe (F1O2 - 1.0) reduced the occurrence of decompression sickness (DCS). Heavy-exercise-induced DCS reduction is likely to be related to the enhancement of the tissue nitrogen washout during the oxygen prebreathe. In addition to the heavy-exercise-induced microcirculatory adaptation, we hypothesized that the light exercise would not cause sufficient microcirculatory changes in the limbs to explain alone this further DCS protection. We evaluated microcirculatory changes as minimal by replicating the exercise characteristics of the PRP trials in 13 healthy subjects. METHODS: Noninvasive near infrared spectroscopy (NIRS) allowed observation of instantaneous variations of total, oxygenated, and deoxygenated hemoglobin/myoglobin concentrations in the microcirculatory networks (probes facing the vastus lateralis and deltoid muscles) of active limbs during dynamic exercise. RESULTS: The high-intensity leg exercise alone produced the changes in NIRS parameters; the light arm exercise induced minimal microcirculatory volume changes. However, this coupling appeared to be critical in previous altitude PRP chamber studies by reducing DCS. DISCUSSION: With only minimal microcirculatory blood volume changes, it is unlikely that light exercise alone causes significant nitrogen tissue washout. Therefore, our results suggest that in addition to nitrogen tissue washout, another unknown exercise-induced effect may have further enhanced the DCS protection, possibly mediated via the anti-inflammatory effect of exercise, gas micronuclei reduction, NO pathways, or other molecular mechanisms.

PH2O and simulated hypobaric hypoxia.

Some manufacturers of reduced oxygen (O2) breathing devices claim a comparable hypobaric hypoxia (HH) training experience by providing F1O2 < 0.209 at or near sea level pressure to match the ambient oxygen partial pressure (iso-PO2) of the target altitude. I conclude after a review of literature from investigators and manufacturers that these devices may not properly account for the 47 mmHg of water vapor partial pressure that reduces the inspired partial pressure of oxygen (P1O2), which is substantial at higher altitude relative to sea level. Consequently, some devices claiming an equivalent HH experience under normobaric conditions would significantly overestimate the HH condition, especially when simulating altitudes above 10,000 ft (3048 m). 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. An approach to reduce the overestimation and standardize the operation is to at least provide machines that create the same P1O2 conditions at sea level as at the target altitude, a simple software upgrade.

Decompression sickness after air break in prebreathe described with a survival model.

INTRODUCTION: A perception exists in aerospace that a brief interruption in a 100% oxygen prebreathe (PB) by breathing air has a substantial decompression sickness (DCS) consequence. The consequences of an air break during PB on the subsequent hypobaric DCS outcomes were evaluated. The hypothesis was that asymmetrical and not symmetrical nitrogen (N2) kinetics was best to model the distribution of subsequent DCS survival times after PBs that included air breaks. METHODS: DCS survival times from 95 controls for a 60-min PB prior to 2- or 4-h exposures to 4.37 psia (9144 m; 30,000 ft) were analyzed along with 3 experimental conditions: 10-min air break (N = 40), 20-min air break (N = 40), or 60-min air break (N = 32) 30 min into the PB followed by 30 min of PB. Ascent rate was 1524 m x min(-1) and all 207 exposures included light exercise at 4.37 psia. Various computations of decompression dose were evaluated; either the difference or ratio of P1N2 and P2, where P1N2 was computed tissue N2 pressure to account for the PB and P2 was altitude pressure. RESULTS: Survival times were described with an accelerated log logistic model with asymmetrical N2 kinetics defining P1N2--P2 as best decompression dose. Exponential N2 uptake during the air break was described with a 10-min half time and N2 elimination during PB with a 60-min half time. CONCLUSION: A simple conclusion about compensation for air break is not possible because the duration and location of a break in a PB is variable. The resulting survival model is used to compute additional PB time to compensate for an air break in PB within the range of tested conditions.

Air break during preoxygenation and risk of altitude decompression sickness.

INTRODUCTION: 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. METHODS: 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. RESULTS: 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. DISCUSSION: 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.

Critique of the equivalent air altitude model.

The adverse effects of hypoxic hypoxia include acute mountain sickness (AMS), high altitude pulmonary edema, and high altitude cerebral edema. It has long been assumed that those manifestations are directly related to reduction in the inspired partial pressure of oxygen (P(I)O2). This assumption underlies the equivalent air altitude (EAA) model, which holds that combinations of barometric pressure (P(B)) and inspired fraction of O2 (F(I)O2) that produce the same P(I)O2 will result in identical physiological responses. However, a growing body of evidence seems to indicate that different combinations of P(B) and P(I)O2 may produce different responses to the same P(I)O2. To investigate this question with respect to AMS, we conducted a search of the literature using the terms hypobaric hypoxia, normobaric hypoxia, and hypobaric normoxia. The results suggest that the EAA model provides only an approximate description of isohypoxia, and that P(B) has an independent effect on hypoxia and AMS. A historical report from 1956 and 15 reports from 1983 to 2005 compare the same hypoxic P(I)O2 at different P(B) with respect to the development of hypoxia and AMS. These data provide evidence for an independent effect of P(B) on hypoxia and AMS, and thereby invalidate EAA as an ideal model of isohypoxia. Refinement of the EAA model is needed, in particular for applications to high altitude where supplemental O2 is inadequate to prevent hypoxic hypoxia. Adjustment through probabilistic statistical modeling to match the current limited experimental observations is one approach to a better isohypoxic model.

A latent class model to assess error rates in diagnosis of altitude decompression sickness.

BACKGROUND: Prospective testing of denitrogenation protocols to reduce the risk of decompression sickness (DCS) in astronauts requires pre-defined accept and reject criteria. We assume that the end-point of a test, the presence or absence of signs and symptoms attributable to DCS, is unequivocal. However, diagnosis of DCS is not perfect, nor is there is a gold standard to assess diagnosis error rates. These error rates could cause consistent bias in the decision to accept or reject proposed protocols. We used a Latent Class Model (LCM) incorporating inter-rater agreement to estimate false-positive and negative rates of DCS diagnosis for each of six symptomatic (covariate) strata. METHODS: Case descriptions from 135 reports collected since 1982 were available with 103 diagnosed as DCS (73.1%). There were 3 subsets of 45 descriptions that were randomly selected, information about the original diagnosis omitted, and were sent to 15 physicians (raters), all experts in altitude DCS. Subsets were diagnosed for DCS by either four, five, or six raters. We then used a LCM to estimate false-positive and false-negative error rates for the original NASA test diagnosis, even though a gold standard was not available. RESULTS: Estimates of false-positive rates in the NASA diagnoses ranged from 13% to 83% and from 1% to 32% for false-negative rates over the six strata of symptomatic response variables. CONCLUSIONS: Our findings suggest that use of current DCS diagnostic outcomes as if they were error free would likely produce an inflated rejection rate of acceptable protocols in future testing if adjustments are not made.

Age affects severity of venous gas emboli on decompression from 14.7 to 4.3 psia.

INTRODUCTION: Variables that define who we are, such as age, weight and fitness level influence the risk of decompression sickness (DCS) and venous gas emboli (VGE) from diving and aviation decompressions. We focus on age since astronauts that perform space walks are approximately 10 yr older than our test subjects. Our null hypothesis is that age is not statistically associated with the VGE outcomes from decompression to 4.3 psia. METHODS: Our data are from 7 different NASA tests where 188 men and 50 women performed light exercise at 4.3 psia for planned exposures no less than 4 h. Prebreathe (PB) time on 100% oxygen ranged from 150-270 min, including ascent time, with exercise of different intensity and length being performed during the PB in four of the seven tests with 150 min of PB. Subjects were monitored for VGE in the pulmonary artery using a Doppler ultrasound bubble detector for a 4-min period every 12 min. There were six design variables; the presence or absence of lower body adynamia and five PB variables; plus five concomitant variables on physical characteristics: age, weight height, body mass index, and gender that were available for logistic regression (LR). We used LR models for the probability of DCS and VGE, and multinomial logit (ML) models for the probability of Spencer VGE Grades 0-IV at exposure times of 61, 95, 131, 183 min, and for the entire exposure. RESULTS: Age was significantly associated with VGE in both the LR and ML models, so we reject the null hypothesis. Lower body adynamia was significant for all responses. CONCLUSIONS: Our selection of tests produced a wide range of the explanatory variables, but only age, lower body adynamia, height, and total PB time was helpful in various combinations to model the probability of DCS and VGE.

Improved pulmonary function in working divers breathing nitrox at shallow depths.

INTRODUCTION: There is limited data about the long-term pulmonary effects of nitrox use in divers at shallow depths. This study examined changes in pulmonary function in a cohort of working divers breathing a 46% oxygen enriched mixture while diving at depths less than 12 m. METHODS: A total of 43 working divers from the Neutral Buoyancy Laboratory (NBL), NASA-Johnson Space Center completed a questionnaire providing information on diving history prior to NBL employment, diving history outside the NBL since employment, and smoking history. Cumulative dive hours were obtained from the NBL dive-time database. Medical records were reviewed to obtain the diver's height, weight, and pulmonary function measurements from initial pre-dive, first year and third year annual medical examinations. RESULTS: The initial forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) were greater than predicted, 104% and 102%, respectively. After 3 yr of diving at the NBL, both the FVC and FEV1 showed a significant (p < 0.01) increase of 6.3% and 5.5%, respectively. There were no significant changes in peak expiratory flow (PEF), forced mid-expiratory flow rate (FEF(25-75%)), and forced expiratory flow rates at 25%, 50%, and 75% of FVC expired (FEF25%, FEF50%, FEF75%). Cumulative NBL dive hours was the only contributing variable found to be significantly associated with both FVC and FEV1 at 1 and 3 yr. CONCLUSIONS: NBL divers initially belong to a select group with larger than predicted lung volumes. Regular diving with nitrox at shallow depths over a 3-yr period did not impair pulmonary function. Improvements in FVC and FEV1 were primarily due to a training effect.