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Butler, B. D.

Publications and source records attributed to Butler, B. D..

16 records
All sourcesNASA NTRSDOE OSTI
NASA NTRS2000

Design of a 2-Hour Prebreathe Protocol for Space Walks (EVAs) from the International Space Station (ISS)

The majority of extravehicular activities (EVAs) performed from the shuttle use a 10.2 psi staged decompression. The International Space Station (ISS) will operate at 14.7 psi, requiring crews to "campout" in the airlock at 10.2 psi. The constraints associated with campout (crew isolation, oxygen usage, and waste management), provided the rationale to develop a 2-hour prebreathe protocol from 14.7 psi. Previous studies on the affect of microgravity and exercise during prebreathe suggested the feasibility of this approach. Various combinations of adynamia (nonwalking subjects), prebreathe exercise doses, and space suit donning options (10.2 vs. 14.7 psi) were analyzed against timeline and consumable constraints. Prospective decompression sickness (DCS) and venous gas emboli (VGE) accept/reject criteria were defined from statistical analysis of historical DCS data, combined with risk management of DCS under ISS mission circumstances. Maximum operational DCS levels were defined based on protecting for EVA capability with two crew members at 95% confidence, throughout ISS lifetime (within the constraints of NASA DCS disposition policy JPG 1800.3). The accept / reject limits were adjusted for greater safety (including Grade IV VGE criteria) based on analysis of related medical factors. Monte-Carlo simulation was performed to design a closed sequential, multi-center laboratory trial, including the capability of rejecting the primary protocol and testing at least one alternate exercise dose, within the 2-hour prebreathe. The 2-hour protocol incorporates 0, breathing for 5 0 min at 14.7 psi, including 10 min dual cycle ergometry at 75%VO(2max). It requires an additional 30 minO2breathing during depress from 14.7 to 10.2 psi, followed by a 30-60 min suit donning break at 10.2 psi/26.5% O2. It concludes with a 40 min in-suit O2 prebreathe. The protocol would be accepted for operations, if the incidence of DCS was less than 15% and Grade IV VGE less than 20%, both at 95% confidence. The above protocol and accept/reject limits were implemented in a multi-center study.

Gernhardt, M. L.↗
NASA NTRS2000

Relationship of Exercise, Age, and Gender on Decompression Sickness and Venous Gas Emboli During 2-Hour Oxygen Prebreathe Prior to Hypobaric Exposure

We evaluated four 2-hour oxygen prebreathe protocols combining adynamia (non-walking) and 4 different amounts of exercise for potential use with extravehicular activity (EVA) on the International Space Station. Phase I: upper and lower body exercises using dual-cycle ergometry (75% VO2 max for 10 min). Phase 11: same ergometry plus 24 min of light exercise that simulated space suit preparations. Phase III: same 24 min of light exercise but no ergometry, and Phase IV: 56 min of light exercise without ergometry. After 80 min on 100% O2, the subjects breathed 26.5% O2 - 73.5% N2 for 30 min at 10.2 psi. All subjects performed a series of upper body exercises from a recumbent position for 4 hrs at 4.3 psi to simulate EVA work. Venous gas emboli (VGE) were monitored every 12 min using precordial Doppler ultrasound. The 39 female and 126 male exposures were analyzed for correlations between decompression sickness (DCS) or VGE, and risk variables. The duration and quantity of exercise during prebreathe inversely relates to DCS and VGE incidence. The type and distribution of the 19 cases of DCS were similar to historical cases. There was no correlation of age, gender, body mass index, or fitness level with greater incidence of DCS or all VGE. However there were more Grade IV VGE in males > 40 years (10 of 19) than in those =< 40 years (3 of 107), with p<0.01 from Fisher's Exact Chi square The latency time for VGE was longer (103 min +/- 56 SD, n = 15 versus 53 min +/- 31, n =13) when the ergometry occurred about 15 min into the prebreathe than when performed at the start of the prebreathe, but the order of the ergometry did not influence the overall DCS and VGE incidence. An increasing amount of exercise during prebreathes reduced the risk of DCS during subsequent exposures to 4.3 psi. Age, gender, or fitness level did not correlate with the incidence of DCS or VGE (combination of Grades I-IV). However males greater than 40 years had a higher incidence of Grade IV VGE.

Conkin, J.↗
NASA NTRS2000

Design and Testing of a 2-Hour Oxygen Prebreathe Protocol for Space Walks from the International Space Station

To develop and test a 2-hour prebreathe protocol for performing extravehicular activities (EVAs) from the International Space Station (ISS). Combinations of adynamia (non-walking), prebreathe exercise, and space suit donning options (10.2 vs. 14.7 psi) were evaluated, against timeline and consumable contraints to develop an operational 2- hour prebreathe protocol. Prospective accept/reject criteria were defined for decompression sickness (DCS) and venous gas emboli (VGE) from analysis of historical DCS data, combined with risk management of DCS under ISS mission circumstances. Maximum operational DCS levels were defined based on protecting for EVA capability with two crew-members at 95% confidence, throughout ISS lifetime (within the constraints of NASA DCS disposition policy JPG 1800.3). The accept/reject limits were adjusted for greater safety based on analysis of related medical factors. Monte-Carlo simulation was performed to design a closed sequential, multi-center human trial. Protocols were tested with 4 different prebreathe exercises (Phases I-IV), prior to exposure to 4.3 psi for 4 hrs. Subject selection, Doppler monitoring for VGE, test termination criteria, and DCS definitions were standardized. Phase I: upper and lower body exercises using dual-cycle ergometry (75% VO2 max for 10 min). Phase II: ergometry plus 24 min of light exercise (simulating space-suit preparations). Phase III: same 24 min of light exercise but no ergometry, and Phase IV: 56 min of light exercise without ergometry. A prebreathe procedure was accepted if, at 95% confidence, the incidence of DCS was less than 15% (with no Type II DCS), and Grade IV VGE was less than 20%.

Gernhardt, Michael L.↗
NASA NTRS1999

Role of Inflammatory Reponse in Experimental Decompression Sickness

Decompression to altitude can result in gas bubble formation both in tissues and in the systemic veins. The venous gas emboli (VGE) are often monitored during decompression exposures to assess risk for decompression sickness (DCS). Astronauts are at risk for DCS during extravehicular activities (EVA), where decompression occurs from the Space Shuttle or Space Station atmospheric pressure of 14.7 pounds per square inch (PSI) to that of the space suit pressure of 4.3 PSI. DCS symptoms include diffuse pain, especially around joints, inflammation and edema. Pathophysiological effects include interstitial inflammatory responses and recurring injury to the vascular endothelium. Such responses can result in vasoconstriction and associated hemodynamic changes.The granulocyte cell activation and chemotaxin release results in the formation of vasoactive and microvascular permeability altering mediators, especially from the lungs which are the principal target organ for the venous bubbles, and from activated cells (neutrophils, platelets, macrophages). Such mediators include free arachidonic acid and the byproducts of its metabolism via the cyclooxygenase and lipoxygenase pathways (see figure). The cyclooxygenase pathway results in formation of prostacyclin and other prostaglandins and thromboxanes that cause vasoconstriction, bronchoconstriction and platelet aggregation. Leukotrienes produced by the alternate pathway cause pulmonary and bronchial smooth muscle contraction and edema. Substances directly affecting vascular tone such as nitric oxide may also play a role in the respose to DCS. We are studying the role and consequent effects of the release inflammatory bioactive mediators as a result of DCS and VGE. More recent efforts are focused on identifying the effects of the body's circadian rhythm on these physiological consequences to decompression stress. al

Butler, B. D.↗
NASA NTRS1997

Dibutyryl cAMP effects on thromboxane and leukotriene production in decompression-induced lung injury

Decompression-induced venous bubble formation has been linked to increased neutrophil counts, endothelial cell injury, release of vasoactive eicosanoids, and increased vascular membrane permeability. These actions may account for inflammatory responses and edema formation. Increasing the intracellular cAMP has been shown to decrease eicosanoid production and edema formation in various models of lung injury. Reduction of decompression-induced inflammatory responses was evaluated in decompressed rats pretreated with saline (controls) or dibutyryl cAMP (DBcAMP, an analog of cAMP). After pretreatment, rats were exposed to either 616 kPa for 120 min or 683 kPa for 60 min. The observed increases in extravascular lung water ratios (pulmonary edema), bronchoalveolar lavage, and pleural protein in the saline control group (683 kPa) were not evident with DBcAMP treatment. DBcAMP pretreatment effects were also seen with the white blood cell counts and the percent of neutrophils in the bronchoalveolar lavage. Urinary levels of thromboxane B2, 11-dehydrothromboxane B2, and leukotriene E4 were significantly increased with the 683 kPa saline control decompression exposure. DBcAMP reduced the decompression-induced leukotriene E4 production in the urine. Plasma levels of thromboxane B2, 11-dehydrothromboxane B2, and leukotriene E4 were increased with the 683-kPa exposure groups. DBcAMP treatment did not affect these changes. The 11-dehydrothromboxane B2 and leukotriene E4 levels in the bronchoalveolar lavage were increased with the 683 kPa exposure and were reduced with the DBcAMP treatment. Our results indicate that DBcAMP has the capability to reduce eicosanoid production and limit membrane permeability and subsequent edema formation in rats experiencing decompression sickness.

Non-NASA Center↗
NASA NTRS1997

Effect of body repositioning after venous air embolism. An echocardiographic study

BACKGROUND: Current therapy for massive venous air embolism (VAE) may include the use of the left lateral recumbent (LLR) position, although its effectiveness has been questioned. This study used transesophageal echocardiography to evaluate the effect of body repositioning on intracardiac air and acute cardiac dimension changes. METHODS: Eighteen anesthetized dogs in the supine position received a venous air injection of 2.5 ml/kg at a rate of 5 ml/ s. After 1 min the dogs were repositioned into either the LLR, LLR 10 degrees head down (LLR-10 degrees), right lateral recumbence, or remained in the supine position. RESULTS: Repositioning after VAE resulted in relocation of intracardiac air to nondependent areas of the right heart. Peak right ventricular (RV) diameter increase and mean arterial pressure decrease were greater in the repositioned animals compared with those in the supine position (P < 0.05). Right ventricular diameter and mean arterial pressure showed an inverse correlation (r = 0.81). Peak left atrial diameter decrease was greater in the LLR and LLR-10 degrees positions compared with the supine position (P < 0.05). Repositioning did not influence peak pulmonary artery pressure increase, and no correlation was found between RV diameter and pulmonary artery pressure. All animals showed electrocardiogram and echocardiographic changes reconcilable with myocardial ischemia. CONCLUSIONS: In dogs, body repositioning after VAE provided no benefit in hemodynamic performance or cardiac dimension changes, although relocation of intracardiac air was demonstrated. Right ventricular air did not appear to result in significant RV outflow obstruction, as pulmonary artery pressure increased uniformly in all groups and was not influenced by the relocation of intracardiac air. The combination of increased RV afterload and arterial hypotension, possibly with subsequent RV ischemia rather than RV outflow obstruction by an airlock appeared to be the primary mechanism for cardiac dysfunction after VAE.

NASA Discipline Environmental Health↗
NASA NTRS1996

Cardiopulmonary Changes with Moderate Decompression in Rats

Sprague-Dawley rats were compressed to 616 kPa for 120 min then decompressed at 38 kPa/min to assess the cardiovascular and pulmonary responses to moderate decompression stress. In one series of experiments the rats were chronically instrumented with Doppler ultrasonic probes for simultaneous measurement of blood pressure, cardiac output, heart rate, left and right ventricular wall thickening fraction, and venous bubble detection. Data were collected at base-line, throughout the compression/decompression protocol, and for 120 min post decompression. In a second series of experiments the pulmonary responses to the decompression protocol were evaluated in non-instrumented rats. Analyses included blood gases, pleural and bronchoalveolar lavage (BAL) protein and hemoglobin concentration, pulmonary edema, BAL and lung tissue phospholipids, lung compliance, and cell counts. Venous bubbles were directly observed in 90% of the rats where immediate post-decompression autopsy was performed and in 37% using implanted Doppler monitors. Cardiac output, stroke volume, and right ventricular wall thickening fractions were significantly decreased post decompression, whereas systemic vascular resistance was increased suggesting a decrease in venous return. BAL Hb and total protein levels were increased 0 and 60 min post decompression, pleural and plasma levels were unchanged. BAL white blood cells and neutrophil percentages were increased 0 and 60 min post decompression and pulmonary edema was detected. Venous bubbles produced with moderate decompression profiles give detectable cardiovascular and pulmonary responses in the rat.

Robinson, R.↗
NASA NTRS1995

Cardiovascular Pressures with Venous Gas Embolism and Decompression

Venous gas embolism (VGE) is reported with decompression to a decreased ambient pressure. With severe decompression, or in cases where an intracardiac septal defect (patent foramen ovale) exists, the venous bubbles can become arterialized and cause neurological decompression illness. Incidence rates of patent foramen ovale in the general population range from 25-34% and yet aviators, astronauts, and deepsea divers who have decompression-induced venous bubbles do not demonstrate neurological symptoms at these high rates. This apparent disparity may be attributable to the normal pressure gradient across the atria of the heart that must be reversed for there to be flow potency. We evaluated the effects of: venous gas embolism (0.025, 0.05 and 0.15 ml/ kg min for 180 min.) hyperbaric decompression; and hypobaric decompression on the pressure gradient across the left and right atria in anesthetized dogs with intact atrial septa. Left ventricular end-diastolic pressure was used as a measure of left atrial pressure. In a total of 92 experimental evaluations in 22 dogs, there were no reported reversals in the mean pressure gradient across the atria; a total of 3 transient reversals occurred during the peak pressure gradient changes. The reasons that decompression-induced venous bubbles do not consistently cause serious symptoms of decompression illness may be that the amount of venous gas does not always cause sufficient pressure reversal across a patent foramen ovale to cause arterialization of the venous bubbles.

Butler, B. D.↗
NASA NTRS1995

Transesophageal Echocardiographic Study of Decompression-Induced Venous Gas Emboli

Transesophageal echo-cardiography was used to evaluate venous bubbles produced in nine anesthetized dogs following decompression from 2.84 bar after 120 min at pressure. In five dogs a pulsed Doppler cuff probe was placed around the inferior vena cava for bubble grade determination. The transesophageal echo images demonstrated several novel or less defined events. In each case where the pulmonary artery was clearly visualized, the venous bubbles were seen to oscillate back and forth several times, bringing into question the effect of coincidental counting in routine bubble grade analysis using precordial Doppler. A second finding was that in all cases, extensive bubbling occurred in the portal veins with complete extraction by the liver sinusoids, with one exception where a portal-to-hepatic venous anastomosis was observed. Compression of the bowel released copious numbers of bubbles into the portal veins, sometimes more than were released into the inferior vena cava. Finally, large masses of foam were routinely observed in the non-dependent regions of the inferior vena cava that not only delayed the appearance of bubbles in the pulmonary artery but also allowed additional opportunity for further reaction with blood products and for coalescence to occur before reaching the pulmonary microcirculation. These novel observations are discussed in relation to the decompression process.

Butler, B. D.↗
NASA NTRS1994

Body position does not affect the hemodynamic response to venous air embolism in dogs

Current therapy for massive venous air embolism (VAE) includes the use of the left lateral recumbent (LLR) position. This recommendation is based on animal studies, conducted 50 yr ago, which looked primarily at survival. Little is known, however, about the concomitant hemodynamic response after VAE in various body positions. The purpose of this study was to investigate the hemodynamic and cardiovascular changes in various body positions after VAE. Twenty-two mechanically ventilated supine mongrel dogs received a venous air infusion of 2.5 mL/kg at a rate of 5 mL/s. One minute after the infusion, 100% oxygen ventilation was commenced and the body position of the dogs was changed to either the LLR (n = 6), the LLR with the head 10 degrees down (LLR-10 degrees; n = 6) or the right lateral recumbent (RLR; n = 5) position. Five dogs were maintained in the supine position (SUP; n = 5). One dog died in every group except in the SUP group, where all the dogs recovered. There were no significant differences among the various body positions in terms of heart rate, mean arterial pressure, pulmonary artery pressure, central venous pressure, left ventricular end-diastolic pressure, or cardiac output. The acute hemodynamic changes occurring during the first 5-15 min after VAE recovered to 80% of control within 60 min. Our data suggest that body repositioning does not influence the cardiovascular response to VAE. Specifically, our data do not support the recommendation of repositioning into the LLR position for the treatment of VAE.

Non-NASA Center↗
NASA NTRS1991

Doppler detection of decompression bubbles with computer assisted digitization of ultrasonic signals

The use of an inexpensive, commercially available audio digitizer in conjunction with a PC to digitize Doppler bubble signals for visual and electronic evaluation is reported. This device can be operated simultaneously with Doppler audio monitoring. Precordial and arterial Doppler recordings of gas bubbles were obtained from anesthetized dogs after intravascular infusion or following decompression. Additional evaluations were conducted on Doppler bubble recordings obtained from human decompression studies. The device can be used in real-time or for later signal analysis. Accompanying menu-driven software provides for numerous signal modification options and visual displays. This device can provide a simultaneous visual display of Doppler signals normally available only for audio evaluation.

Butler, B. D.↗
NASA NTRS1989

Venous gas embolism - Time course of residual pulmonary intravascular bubbles

A study was carried out to determine the time course of residual pulmonary intravascular bubbles after embolization with known amounts of venous air, using an N2O challenge technique. Attention was also given to the length of time that the venous gas emboli remained as discrete bubbles in the lungs with 100 percent oxygen ventilation. The data indicate that venous gas emboli can remain in the pulmonary vasculature as discrete bubbles for periods lasting up to 43 + or - 10.8 min in dogs ventilated with oxygen and nitrogen. With 100 percent oxygen ventilation, these values are reduced significantly to 19 + or - 2.5 min.

Butler, B. D.↗
NASA NTRS1989

Effect of lysophosphatidylcholine on the filtration coefficient in intact dog lungs

Lysophosphatidylcholine (lyso-Pc) is a lysophospholipid normally found in low concentrations in the lung. At high concentrations lyso-Pc, instilled into the airways, causes pulmonary edema. The hypothesis was tested that the edema caused by lyso-Pc was due to an increase in pulmonary microvascular membrane permeability. In 11 anesthetized dogs, the left lower lobes (LLL) were continuously weighed while lyso-Pc (20 mM) was instilled into the LLL airways. After 30 min, the microvascular membrane fluid filtration coefficient (Kf) was determined from the relationship between the rate of LLL weight gain and the pulmonary microvascular pressure. Kf was not significantly different between the lyso-Pc-treated lobes vs control lobes. The data do not support the hypothesis that lyso-Pc, instilled into the airways, causes an increase in pulmonary microvascular permeability.

Butler, B. D.↗
NASA NTRS1988

Vascular pressures and passage of gas emboli through the pulmonary circulation

Doppler technique was used to measure the pulmonary vascular pressure gradients in dogs that received venous air emboli (VAE) at the rate of 0.35 ml/kg per min, at which the spillover of bubbles into the systemic arteries occur. It was found that, in 60 percent of dogs, venous bubbles spilled over into the arterial circulation at the pulmonary vascular pressure gradient of about 34.7 mm Hg. When the pulmonary vascular pressure gradient was raised to about 52 mm Hg, the spillover of venous bubbles occurred 100 percent of time. It is concluded that venous bubbles can cross the lungs of anesthetized dogs when the driving pressures are sufficient to overcome the normal filtering function.

Butler, B. D.↗
NASA NTRS1985

Transpulmonary passage of venous air emboli

Twenty-seven paralyzed anesthetized dogs were embolized with venous air to determine the effectiveness of the pulmonary vasculature for bubble filtration or trapping. Air doses ranged from 0.05 to 0.40 ml/kg min in 0.05-ml increments with ultrasonic Doppler monitors placed over arterial vessels to detect any microbubbles that crossed the lungs. Pulmonary vascular filtration of the venous air infusions was complete for the lower air doses ranging from 0.05 to 0.30 ml/kg min. When the air doses were increased to 0.35 ml/kg min, the filtration threshold was exceeded with arterial spillover of bubbles occurring in 50 percent of the animals and reaching 71 percent for 0.40 ml/kg min. Significant elevations were observed in pulmonary arterial pressure and pulmonary vascular resistance. Systemic blood pressure and cardiac output decreased, whereas left ventricular end-diastolic pressure remained unchanged. The results indicate that the filtration of venous bubbles by the pulmonary vasculature was complete when the air infusion rates were kept below a threshold value of 0.30 ml/kg min.

Butler, B. D.↗