Johnny Conkin

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.

Comments on Point: Counterpoint: Hypobaric hypoxia induces/does not induce different responses from normobaric hypoxia.

112:1788-1794, 2012. ; J Appl Physiol Joshua C. Weavil, Peter Bartsch and Charles F. Nelatury Samuel Verges, Patrick Levy, Eric M. Snyder, Bruce D. Johnson, Jonathon L. Stickford, Y. Millet, Benjamin D. Levine, James H. Wessel III, Bernard Wuyam, Renaud Tamisier, MacInnis, Michael S. Koehle, Thomas Rupp, Marc Jubeau, Stephane Perrey, Guillaume Laymon, Jack A. Loeppky, Matiram Pun, Kai Schommer, Mary C. Vagula, Martin J. S. Chapman, Johnny Conkin, Hugo Nespoulet, Darren P. Casey, Bryan J. Taylor, Abigail Olivier Girard, Michael S. Koehle, Jordan A. Guenette, Samuel Verges, Robert F. normobaric hypoxia induces/does not induce different responses from Comments on Point:Counterpoint: Hypobaric hypoxia

Blood biochemical factors in humans resistant and susceptible to formation of venous gas emboli during decompression

SummaryBlood biochemical parameters were measured in 12 male human subjects before and after exposure to a staged decompression protocol, with simulated extravehicular activity, during 3 days. Following the exposure, significant changes occurred in several parameters, including increases in blood urea nitrogen, inorganic phosphate, potassium, and osmolality, and decreases in uric acid and creatinine. Pre-exposure blood samples from subjects who were susceptible to formation of venous gas emboli (VGE) during decompression exhibited significantly greater levels of total cholesterol, high density lipoprotein cholesterol, potassium, inorganic phosphate, calcium, and magnesium. The results indicate that, following this decompression profile, small but significant (P<0.05) changes occur in several blood biochemical parameters, and that levels of certain blood factors may be related to susceptibility to VGE formation during decompression.

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.

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.

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.

Fifteen-minute Extravehicular Activity Prebreathe Protocol Using NASA's Exploration Atmosphere (8.2 psia/ 34% 02)

A TBDM DCS probability model based on an existing biophysical model of inert gas bubble growth provides significant prediction and goodness-of-fit with 84 cases of DCS in 668 human altitude exposures. 2. Model predictions suggest that 15-minute O2 prebreathe protocols used in conjunction with suit ports and an 8.2 psi, 34% O2, 66% N2 atmosphere may enable rapid EVA capability for future exploration missions with the risk of DCS 12%. EVA could begin immediately at 6.0 psi, with crewmembers decreasing suit pressure to 4.3 psi after completing the 15-minute in-suit prebreathe. 3. Model predictions suggest that intermittent recompression during exploration EVA may reduce decompression stress by 1.8% to 2.3% for 6 hours of total EVA time. Savings in gas consumables and crew time may be accumulated by abbreviating the EVA suit N2 purge to 2 minutes (20% N2) compared with 8 minutes (5% N2) at the expense of an increase in estimated decompression risk of up to 2.4% for an 8-hour EVA. Increased DCS risk could be offset by IR or by spending additional time at 6 psi at the beginning of the EVA. Savings of 0.48 lb of gas and 6 minutes per person per EVA corresponds to more than 31 hours of crew time and 1800 lb of gas and tankage under the Constellation lunar architecture. 6. Further research is needed to characterize and optimize breathing mixtures and intermittent recompression across the range of environments and operational conditions in which astronauts will live and work during future exploration missions. 7. Development of exploration prebreathe protocols will begin with definition of acceptable risk, followed by development of protocols based on models such as ours, and, ultimately, validation of protocols through ground trials before operational implementation.

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.

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.

Hemoglobin O2 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.