Search PubMed⌕ Search

Biomedical subjects

J Conkin

Publications and source records attributed to J Conkin.

At least 19 recordsLinked to original sources
PubMed2001

Lower body adynamia as a factor to reduce the risk of hypobaric decompression sickness.

BACKGROUND: We define lower body adynamia (LBA) as restricted lower body movement, particularly walking, during both the denitrogenation phase at site pressure and during the exercise phase while at altitude. HYPOTHESIS: Our null hypothesis is that subjects who are adynamic in the lower body but do upper body exercise will be at similar risk of decompression sickness (DCS) and venous gas emboli (VGE) as subjects who randomly walk but do no planned exercise while at altitude. METHODS: We selected a data set that contained 1401 altitude exposures with the following conditions: a) walking was part of the exercise at altitude; or b) there was no planned exercise done at altitude but walking was not restricted; or c) LBA was inforced, but upper body exercise was done at altitude. We used logistic regression (LR) on all 1401 exposures, a log logistic survival analysis (SA) on a subset of data from "a" and "c" (n = 234), and estimated a model for how the incidence of VGE changes through time. RESULTS: The estimated probabilities of DCS and VGE with 95% confidence intervals (Cls) from the LR with a simulation of a 3-h oxygen prebreathe, a 4-h exposure to 4.3 psia in a male, and exercise and LBA conditions as described above are: (see text). CONCLUSION: LBA that includes upper body exercise appears to be as protective against DCS and VGE as random walking by subjects who did no prescribed exercise while at altitude, and is more protective than exercise that included walking. Our conclusions are based on an assumption that we have adequately controlled, through our data selection process and the use of multivariable models, important variables in tests that were not done at the Johnson Space Center.

Cardiac Volume↗
PubMed1998

Role of metabolic gases in bubble formation during hypobaric exposures.

Our hypothesis is that metabolic gases play a role in the initial explosive growth phase of bubble formation during hypobaric exposures. Models that account for optimal internal tensions of dissolved gases to predict the probability of occurrence of venous gas emboli were statistically fitted to 426 hypobaric exposures from National Aeronautics and Space Administration tests. The presence of venous gas emboli in the pulmonary artery was detected with an ultrasound Doppler detector. The model fit and parameter estimation were done by using the statistical method of maximum likelihood. The analysis results were as follows. 1) For the model without an input of noninert dissolved gas tissue tension, the log likelihood (in absolute value) was 255.01. 2) When an additional parameter was added to the model to account for the dissolved noninert gas tissue tension, the log likelihood was 251.70. The significance of the additional parameter was established based on the likelihood ratio test (P < 0.012). 3) The parameter estimate for the dissolved noninert gas tissue tension participating in bubble formation was 19. 1 kPa (143 mmHg). 4) The additional gas tissue tension, supposedly due to noninert gases, did not show an exponential decay as a function of time during denitrogenation, but it remained constant. 5) The positive sign for this parameter term in the model is characteristic of an outward radial pressure of gases in the bubble. This analysis suggests that dissolved gases other than N2 in tissues may facilitate the initial explosive bubble-growth phase.

Air Pressure↗
PubMed1998

Information about venous gas emboli improves prediction of hypobaric decompression sickness.

HYPOTHESIS: Information about venous gas emboli (VGE) detected in the pulmonary artery such as the occurrence of VGE, Grade of VGE, the time when VGE first appear, and the time course of the Grade or occurrence of VGE, could be used to better assess the probability of decompression sickness [P(DCS)] in any hypobaric decompression. We hypothesized that these data would improve the estimate of P(DCS) since objective measurements of the decompression stress are available for the individual. METHODS: A binary correlation and survival analysis approach were used on information from 1,322 hypobaric chamber exposures to establish the relationships between VGE and DCS. RESULTS: Based on the correlation analysis, the absence of VGE is highly correlated with the absence of a DCS symptom, as evident from a negative predictive value of 0.98. However, the presence of VGE in the pulmonary artery is not highly correlated with a subsequent DCS symptom, as evident from a positive predictive value of 0.39 for Grades III and IV VGE. The correlation results suggest the presence of VGE in the pulmonary artery is a necessary, but not sufficient, condition for DCS. Based on the survival analysis, the log logistic survival model, a one-variable model with two parameters gave a log likelihood (LL) of -757. This model was expanded to include seven additional variables, including four about VGE, and the nine-parameter model gave a better LL of -481. CONCLUSION: Information about VGE plus other variables known to influence DCS is useful to better assess the P(DCS) for hypobaric decompressions.

Adult↗
PubMed1998

Evolved gas, pain, the power law, and probability of hypobaric decompression sickness.

The intensity of a pain-only decompression sickness (DCS) symptom with respect to time at altitude increases, peaks, and then declines in some cases. A similar pattern is also seen in a graph of the probability density function [f(t)] for DCS. The f(t) is the proportion of DCS per unit time with respect to time at altitude. The integration of f(t) with respect to time provides the cumulative probability of DCS [P(DCS)]. We suspect that the perceived intensity of pain with a given stimulus intensity is related to the P(DCS); it may be related to the intensity of the stimulus to a power (alpha). Our stimuli are defined as pressure ratio [PR = (phi P1N2/ P2)-11] or pressure difference [delta P = phi P1N2-P2], where phi P1N2 is the N2 partial pressure calculated in the 360 min half-time (t1/2) compartment or t1/2 is estimated with other parameters and P2 is ambient pressure after the ascent. Both stimuli represent a potential released volume of gas. We tested the null hypothesis that alpha > 1 was no better than alpha = 1 in PR alpha and delta P alpha in a log logistic survival analysis of 1085 exposures in hypobaric chambers. The log likelihood number increased from -1198 for alpha = 0 for the null model to -724 for PR alpha when alpha = 3.52 with a 42 min t1/2 and -714 for delta P alpha when alpha = 8.44 with a 91 min t1/2. We conclude that the improvement in our expressions for decompression dose with alpha > 1 is not by random chance and that alpha may link the physics of gas evolution to the biology of pain perception. Because of our empirical approach, we do not exclude other possible interpretations.

Altitude↗
PubMed1997

Modeling the effects of exercise during 100% oxygen prebreathe on the risk of hypobaric decompression sickness.

BACKGROUND: Several previous studies indicated that exercise during prebreathe with 100% O2 decreased the incidence of hypobaric decompression sickness (DCS). We report a meta-analysis of these investigations combined with a new study in our laboratory to develop a statistical model as a predictive tool for DCS. HYPOTHESIS: Exercise during prebreathe increases N2 elimination in a theoretical 360-min half-time compartment decreasing the incidence of DCS. METHODS: A dose-response probability tissue ratio (TR) model with 95% confidence limits was created for two groups, prebreathe with exercise (n = 113) and resting prebreathe (n = 113), using nonlinear regression analysis with maximum likelihood optimization. RESULTS: The model predicted that prebreathe exercise would reduce the residual N2 in a 360-min half-time compartment to a level analogous to that in a 180-min compartment. This finding supported the hypothesis. The incidence of DCS for the exercise prebreathe group was significantly decreased (Chi-Square = 17.1, p < 0.0001) from the resting prebreathe group. CONCLUSIONS: The results suggested that exercise during prebreathe increases tissue perfusion and N2 elimination approximately 2-fold and markedly lowers the risk of DCS. Based on the model, the prebreathe duration may be reduced from 240 min to a predicted 91 min for the protocol in our study, but this remains to be verified. The model provides a useful planning tool to develop and test appropriate prebreathe exercise protocols and to predict DCS risks for astronauts.

Clinical Protocols↗
PubMed1996

A probabilistic model of hypobaric decompression sickness based on 66 chamber tests.

One consequence of the NASA tissue ratio (TR) model is that calculated probability of decompression sickness [P(DCS)] is constant in tests at different ambient pressures so long as the ratio of P1N2 to P2 is the same in each test; P1N2 is N2 pressure in the 360 minute half-time compartment, and P2 is ambient pressure after decompression. We test the hypothesis that constant P(DCS) is better described by TRs that decrease as P2 decreases. Data were from 66 NASA and USAF hypobaric chamber tests resulting in 211 cases of DCS in 1075 exposures. The response variable was presence or absence of DCS while at P2. Explanatory variables were P1N2, P2, exercise at P2, (yes or no), time to DCS (failure time), and time to end of test in those without DCS (censored time). Probability models were fitted using techniques from survival analysis. The log likelihood for the two parameter log logistic survival model was -846 with only failure and censored times, -801 when TR [P1N2/P2] plus exercise were added, and -663 when modified TR [(((P1N2+cl)/P2)-1)c2] plus exercise were added, where c1 and c2 are fitted parameters in the five parameter model. Constant P(DCS) was better described by TRs that decrease as P2 decreases; a conclusion supported by additional empirical observations, and bubble growth models that are independent of DCS data. Exercise increased the P(DCS) at P2. As a description of decompression "dose", the modified TR was superior to TR over a wider range of experimental conditions.

Adult↗
PubMed1996

Relationship of the time course of venous gas bubbles to altitude decompression illness.

The correlation is low between the occurrence of gas bubbles in the pulmonary artery, called venous gas emboli (VGE), and subsequent decompression illness (DCI). The correlation improves when a "grade" of VGE is considered; a zero to four categorical classification based on the intensity and duration of the VGE signal from a Doppler bubble detector. Additional insight about DCI might come from an analysis of the time course of the occurrence of VGE. Using the NASA Hypobaric Decompression Sickness Databank, we compared the time course of the VGE outcome between 322 subjects who exercised and 133 Doppler technicians who did not exercise to evaluate the role of physical activity on the VGE outcome and incidence of DCI. We also compared 61 subjects with VGE and DCI with 110 subjects with VGE but without DCI to identify unique characteristics about the time course of the VGE outcome to try to discriminate between DCI and no-DCI cases. The VGE outcome as a function of time showed a characteristic short lag, rapid response, and gradual recovery phase that was related to physical activity at altitude and the presence or absence of DCI. The average time for DCI symptoms in a limb occurred just before the time of the highest fraction of VGE in the pulmonary artery. It is likely, but not certain, that an individual will report a DCI symptom if VGE are detected early in the altitude exposure, the intensity or grade of VGE rapidly increases from a limb region, and the intensity or grade of VGE remains high.

Adult↗
PubMed1996

Testing of hypotheses about altitude decompression sickness by statistical analyses.

This communication extends a statistical analysis of forced-descent decompression sickness at altitude in exercising subjects (J Appl Physiol 1994; 76:2726-2734) with a data subset having an additional explanatory variable, rate of ascent. The original explanatory variables for risk-function analysis were environmental pressure of the altitude, duration of exposure, and duration of pure-O2 breathing before exposure; the best fit was consistent with the idea that instantaneous risk increases linearly as altitude exposure continues. Use of the new explanatory variable improved the fit of the smaller data subset, as indicated by log likelihood. Also, with ascent rate accounted for, replacement of the term for linear accrual of instantaneous risk by a term for rise and then decay made a highly significant improvement upon the original model (log likelihood increased by 37 log units). The authors conclude that a more representative data set and removal of the variability attributable to ascent rate allowed the rise-and-decay mechanism, which is expected from theory and observations, to become manifest.

Altitude↗
PubMed1994

Probabilistic model of altitude decompression sickness based on mechanistic premises.

To develop a predictive equation and to test ideas about the mechanisms involved in hypobaric decompression sickness, we performed statistical analyses on published results of 7,023 exercising O2-breathing men subjected to one-step decompressions in altitude chambers. The dependent variable was signs or symptoms so severe that the person's trial was terminated (forced descent). The three independent variables were 1) duration of 100% O2 breathing at ground level (prebreathing), 2) atmospheric pressure after ascent, and 3) exposure duration. The best model, chosen from trial-and-error combinations of premises about bubble behavior, indicates that decompression sickness outcome depends on 1) prebreathing time, but with an unexpectedly long washout half time for N2; 2) time at altitude, as if bubbles grow; and 3) the estimated difference, raised to the fifth power, between the partial pressure of N2 in tissue before and that in bubbles after decompression, perhaps an index of the number of bubbles generated. We expect the model to provide accurate predictions for decompressions matching those of the bulk of the data; the mechanistic cues should be considered hypotheses for further investigation.

Altitude Sickness↗
PubMed1993

The oxygen window and decompression bubbles: estimates and significance.

The "oxygen window" causes a partial pressure difference of inert gas between the inside and outside of decompression bubbles. Estimates of Po2 and Pco2 in tissue are necessary for O2 window calculations and any calculations about growth or decay of decompression sickness bubbles, but the estimates involve many uncertainties. Using simplifying assumptions, we estimated the O2 window over a broad range of environments for tissues having a wide range of O2 extractions. The results were as follows: a) the window increases with ambient pressure, but levels off at very high pressure; b) the window is only 1 or 2 kPa for air breathing at extreme altitudes, and 200 kPa or more in hyperbaric environments; c) when O2 is breathed instead of air, the window is as much as 50 times larger at altitude but only about 10 times larger in hyperbaric environments; d) changes in bubble size due to the window decrease as barometric pressure increases; and e) there are seven additional factors which may supplement or oppose the action of the oxygen window.

Altitude↗
PubMed1992

Failure of the straight-line DCS boundary when extrapolated to the hypobaric realm.

The lowest pressure (P2) to which a diver can ascend without developing decompression sickness (DCS) after becoming equilibrated at some higher pressure (P1) is described by a straight line with a negative y-intercept. We tested whether extrapolation of such a line also predicts safe decompression to altitude. We substituted tissue nitrogen pressure (P1N2) calculated for a compartment with a 360-min half-time for P1 values; this allows data from hypobaric exposures to be plotted on a P2 vs. P1N2 graph, even if the subject breathes oxygen before ascent. In literature sources, we found 40 reports of human exposures in hypobaric chambers that fell in the region of a P2 vs. P1N2 plot where the extrapolation from hyperbaric data predicted that the decompression should be free of DCS. Of 4,576 exposures, 785 persons suffered decompression sickness (17%), indicating that extrapolation of the diver line to altitude is not valid. Over the pressure range spanned by human hypobaric exposures and hyperbaric air exposures, the best separation between no DCS and DCS on a P2 vs. P1N2 plot seems to be a curve which approximates a straight line in the hyperbaric region but bends toward the origin in the hypobaric region.

Altitude↗
PubMed1992

A computerized databank of decompression sickness incidence in altitude chambers.

This report describes a hypobaric decompression sickness databank (HDSD) for use with personal computers. The databank consolidates some of the decompression sickness (DCS) information that has accumulated from altitude chamber tests from 1942 to the present. The information was transcribed to a data collection form, screened for accuracy and duplication, and then added to the databank through a computer keyboard. The databank consists of two files; 63 fields contain details of the test conditions in the altitude chamber, the outcome of the test in terms of DCS and venous gas emboli, the physical characteristics of the group of subjects who underwent the test, and the denitrogenation procedures prior to decompression. The HDSD currently contains 378 records that represent 130,012 altitude exposures from 80 sources: scientific journal articles, government and contractor reports, and chapters from books.

Atmosphere Exposure Chambers↗
PubMed1989

Pulmonary hemodynamics, extravascular lung water and residual gas bubbles following low dose venous gas embolism in dogs.

Pulmonary hemodynamic responses, extravascular lung water and bubble longevity times were studied in halothane anesthetized dogs receiving low dose venous gas infusions. Dogs in one group (23.3 +/- 4.3 kg, n = 6) were embolized with air (0.05 ml.kg-1.min -1) for 60 min followed by a recovery period lasting 70 min. During the recovery the ventilatory gases were intermittently switched from nitrogen (68-69%)/oxygen (30%) to nitrous oxide (68-69%)/oxygen (30%) to expand any residual pulmonary vascular bubbles. Subsequent changes in pulmonary artery pressure, pulmonary vascular resistance, end-tidal carbon dioxide and arterial carbon dioxide tensions were used to indicate the presence of remaining bubbles that would have expanded in volume with the nitrous oxide ventilation. This embolization sequence was repeated three times to simulate repetitive exposure of the pulmonary circulation to venous gas emboli. In a second group of dogs (20.2 +/- 2.7 kg, n = 8) the venous gas infusions (0.05 ml.kg-1.min-1) were continuous for 180 min, followed by recovery with intermittent nitrous oxide/oxygen challenges to determine bubble longevity. Pulmonary hemodynamic and carbon dioxide data were significantly changed from baseline following each embolization. These differences as well as the development of extravascular lung water (edema formulation) were not significant when comparisons were made between the Repetitive gas embolism group after 180 min. Residual pulmonary vascular bubbles were indicated (mean +/- S.E.M.) 26.9 +/- 2.3 min following the 180 min Continuous venous gas infusion and 39.5 +/- 5.3, 46.4 +/- 5.0 and 55.5 +/- 4.4 min, respectively, following the three 60 min Repetitive venous gas infusions.

Animals↗
PubMed1987

The effect of extended O2 prebreathing on altitude decompression sickness and venous gas bubbles.

The purpose of this study was to determine the effect of extended O2 prebreathing on symptom and bubble incidence during decompressions simulating extravehicular activity. The 38 subjects breathed O2 for a 6-h period prior to decompression to 4.3 psi. The subjects performed upper body exercise for 6 h. Subjects were monitored with a Doppler bubble detector and were encouraged to report all symptoms. Eight subjects were exposed to the same protocol after an 8-h prebreathe. Venous bubbles were detected in 18 of 38 subjects decompressed after the 6-h prebreathe. Four of these subjects reported symptoms of altitude decompression sickness. No symptoms or bubbles were detected in the eight subjects who had prebreathed 8 h. The incidence of symptoms and bubbles when combined with prior data on 3.5- and 4.0-hour prebreathes showed an inverse correlation to pre-breathing time. The incidence of symptoms was higher than has been reported for subjects exposed to decompression of shorter duration with less activity.

Adult↗
PubMed1986

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

Blood 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 less than 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.

Adult↗
PubMed1983

Decrease of ether induction time after exposure to dysbaric conditions in rat.

In 22 adult male albino rats (means = 565 g) it was consistently observed that the time required to anesthetize them with 5 ml of diethyl ether after a hyperbaric exposure of 6 ATA using compressed air decreased depending on the severity of the animals' post-decompression reaction to the compression-decompression exposure. Monitoring the time required to lightly anesthetize adult male rats with diethyl ether to a point of losing the righting reflex after a particular compression-decompression exposure provided an indication of the rats' post-exposure state of health. This technique aided in correctly establishing if a rat developed a degree of decompression sickness that may have otherwise gone unnoticed. The loss of resistance to ether induction as a result of decompression sickness may be related to alterations in the blood-brain barrier, blood perfusion inequities, or changes in cardiopulmonary mechanics due to the presence of gaseous emboli. Rats that survived the compression-decompression exposures showed a marked resistance to ether induction after 24 h of recovery.

Animals↗
PubMed1982

Investigation of the combined effects of bedrest and mild hypoxia.

Subjects were exposed to an 8-h mild hypoxia exposure (8000 ft. equivalent, 2438 m) with and without a 28-h period of 6 degrees headdown bedrest. Anticipated responses to the bedrest and the hypoxia were observed. There was no indication that bedrest affected the arterial oxygenation or the oxygen gradient across the lungs of the subjects undergoing mild hypoxia. It is concluded that there is no evidence that would preclude an alveolar O2 pressure as low as 69 torr during contingency spacecraft operation.

Adult↗