Lambertsen and O2: beginnings of operational physiology.
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Diving↗
Biomedical subjects
R D Vann
Publications and source records attributed to R D Vann.
Experimental trials to assess the risks of decompression sickness in flying after diving.
We conducted experimental trials of flying after diving using profiles near the no-decompression exposure limits for recreational diving. The objective was to determine the dependence of DCS occurrence during or after flight on the length of the preflight surface intervals (PFSI). One to three dives were conducted during a single day with dry, resting subjects in a hyperbaric chamber at depths of 40, 60, or 100 fsw (224, 286, 408 kPa). The dives were followed by PFSI of 3 to 17 hrs and a four-hour altitude exposure at 8,000 ft (75 kPa), the maximum permitted cabin altitude for pressurized commercial aircraft. Forty DCS incidents occurred during or after flight in 802 exposures of 495 subjects. The DCS incidence decreased as PFSI increased, and repetitive dives generally required longer PFSI to achieve low incidence than did single dives (p = 0.0159). No DCS occurred in 52 trials of a 17 hr PFSI, the longest PFSI tested. The results provide empirical information for formulating guidelines for flying in commercial aircraft after recreational diving.
Adult↗
The relative risk of decompression sickness during and after air travel following diving.
BACKGROUND: Decompression sickness (DCS) can be provoked by post-dive flying but few data exist to quantify the risk of different post-dive, preflight surface intervals (PFSI). METHODS: We conducted a case-control study using field data from the Divers Alert Network to evaluate the relative risk of DCS from flying after diving. The PFSI and the maximum depths on the last day of diving (MDLD) were analyzed from 627 recreational dive profiles. The data were divided into quartiles based on surface interval and depth. Injured divers (cases) and uninjured divers (controls) were compared using logistic regression to determine the association of DCS with time and depth while controlling for diver and dive profiles characteristics. These included PFSI, MDLD, gender, height, weight, age, and days of diving. RESULTS: The means (+/-SD) for cases and controls were as follows: PFSI, 20.7 +/- 9.6 h vs. 27.1 +/- 6.7 h; MDLD, 22.5 +/- 14 meters sea water (msw) vs. 19 +/- 11.3 msw; male gender, 60% vs. 70%; weight, 75.8 +/- 18 kg vs. 77.6 +/- 16 kg; height, 173 +/- 16 cm vs. 177 +/- 9 cm; age, 36.8 +/- 10 yr vs. 42.9 +/- 11 yr; diving > or = 3 d, 58% vs. 97%. Relative to flying > 28 h after diving, the odds of DCS (95% CI) were: 1.02 (0.61, 1.7) 24-28 h; 1.84 (1.0, 3.3) 20-24 h; and 8.5 (3.85, 18.9) < 20 h. Relative to a depth of < 14.7 msw, the odds of DCS (95% CI) were: 1.2 (0.6, 1.7) 14.7-18.5 msw; 2.9 (1.65, 5.3) 18.5-26 msw; and 5.5 (2.96, 1 0.0) > 26 msw. CONCLUSIONS: Odds ratios approximate relative risk in rare diseases such as DCS. This study demonstrated an increase in relative risk from flying after diving following shorter PFSIs and/or greater dive depths on the last day. The relative risk increases geometrically as the PFSI becomes smaller.
Adult↗
The incidence of venous gas emboli in recreational diving.
From 1989-91, the Divers Alert Network monitored recreational divers for Doppler-detected venous gas emboli (VGE) and depth-time profiles following multi-day, repetitive, multi-level exposures. A Spencer score >0 occurred in 61 of 67 subjects (91%) and 205 of 281 dives (73%). No subject developed decompression sickness (DCS) on monitored days although 102 dives (36.3%) scored at Spencer Grades 2 or 3 (High Bubble Grade, HBG). We recorded the depth-time profiles with Suunto dive computers and estimated exposure severity with a probabilistic decompression algorithm. The HBG incidence increased 53% over the range of exposure severity (p < 0.001) in the divers, was approximately 20% higher for repetitive dives than for first dives, and decreased approximately 25% over the 6-8 days of multi-day diving (p < 0.001) suggesting a phenomenon similar to DCS adaptation. The observed HBG incidence was approximately 20% higher for males than females. Older male divers had a 25% increase in observed incidence of HBG while older female divers showed a 55% increase when compared to their younger counterparts.
Adult↗
Mountaineering oxygen mask performance at 4572 m.
BACKGROUND: Supplemental oxygen delivered by mask at high altitude is used to increase arterial oxygen saturation (SaO2) thereby mitigating physiological and cognitive dysfunction secondary to hypoxemia. Historically, mask performance has not been well documented although it may be a critical factor in determining the success of an expedition. METHODS: Three mountaineering masks were used by ten healthy, nonaltitude-acclimatized participants (eight males, two females) to compare ventilatory responses, SaO2, heart rate, and end-tidal gases. Masks tested were: Life Support Engineering Ltd. (LSEL); Zvezda Enterprise (ZE); and a prototype of our own design (Duke). Test conditions were as follows: simulated altitude at 0 and 4572 m (15,000 ft); rest and cycle exercise at 75 W; and supplemental oxygen flow at 0, 1.1 +/- 0.05, and 1.7 +/- 0.06 L x min(-1) (mean +/- SD). Statistical analysis was completed using GLM (SAS software). RESULTS: As there were no differences between the 1.1 and 1.7 L x min(-1) flow rates, the data were pooled. All three masks improved SaO2 with the ZE and Duke masks being more effective during exercise, maintaining mean SaO2 >90%. CONCLUSIONS: All three masks provided at least partial protection of physiological norms during rest and exercise at 4572 m. The ZE and Duke systems offered the best performance. The need for performance evaluation as part of system design is evident as subtle differences in design can significantly affect performance.
Adult↗
Effect of hypobaria on ventilatory and CO2 responses to short-term hypoxic exposure in cats.
The effect of hypobaria on the ventilatory response to short-term hypoxia was studied by comparing the respiratory mechanical and inspired CO2 ventilatory responses to hypobaric hypoxia (438 mmHg) with normobaric hypoxia (11.8% FIO2). Fifteen spontaneously breathing, anesthetized cats were divided into three groups of five: time control, normobaric hypoxia and hypobaric hypoxia. Measurements of ventilation, gas exchange, and responses to intermittent CO2 rebreathing were collected over a 4 h period. PaO2 fell to 44.5 +/- 2.7 mmHg, PaCO2 fell to 24.8 +/- 0.9, and pH rose to 7.49 +/- 0.01 in both hypoxic groups. Tidal volume did not change with respect to time or condition, but frequency and ventilation were significantly increased in the hypobaric hypoxic group. The slope of the CO2 response was unchanged over time or by condition. These results suggest that hypobaric hypoxia may alter the pattern of breathing responses to hypoxia but not the CO2-response. If metabolic rate remained constant, these results could be explained by a difference in dead space between hypoxic conditions.
Animals↗
Probabilistic gas and bubble dynamics models of decompression sickness occurrence in air and nitrogen-oxygen diving.
Probabilistic models of the occurrence of decompression sickness (DCS) with instantaneous risk defined as the weighted sum of bubble volumes in each of three parallel-perfused gas exchange compartments were fit using likelihood maximization to the subset of the USN Primary Air and N2-O2 database [n = 2,383, mean P(DCS) = 5.8%] used in development of the USN LE1 probabilistic models. Bubble dynamics with one diffusible gas in each compartment were modeled using the Van Liew equations with the nucleonic bubble radius, compartmental volume, compartmental bulk N2 diffusivity, compartmental N2 solubility, and the N2 solubility in blood x compartmental blood flow as adjustable parameters. Models were also tested that included the effects of linear elastic resistance to bubble growth in one, two, or all three of the modeled compartments. Model performance about the training data and separate validation data was compared to results obtained about the same data using the LE1 probabilistic model, which was independently implemented from published descriptions. In the most successful bubble volume model, BVM(3), diffusion significantly slows bubble growth in one of the modeled compartments, whereas mechanical resistance to bubble growth substantially accelerates bubble resolution in all compartments. BVM(3) performed generally on a par with LE1, despite inclusion of 12 more adjustable parameters, and tended to provide more accurate incidence-only estimates of DCS probability than LE1, particularly for profiles in which high fractional O2 gas mixes are breathed. Values of many estimated BVM(3) parameters were outside of the physiologic range, indicating that the model emerged from optimization as a mathematical descriptor of processes beyond bubble formation and growth that also contribute to DCS outcomes. Although incomplete as a mechanistic description of DCS etiology, BVM(3) remains applicable to a wider variety of decompressions than LE1 and affords a conceptual framework for further refinements motivated by mechanistic principles.
Decompression Sickness↗
The physiology of decompression illness.
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Atmospheric Pressure↗
Ascent rate, post-dive exercise, and decompression sickness in the rat.
The effects of ascent rate and post-dive exercise on the incidence of decompression sickness (DCS) were investigated in six groups of 20 rats exposed for 2 h at a pressure equivalent to 240 feet of sea water (fsw; 735 kPa). Ascent rates were 30, 45, and 60 fsw/min (92, 138, 184 kPa/min), and the rats either rested after the exposure or exercised by walking for 30 min on a treadmill at 1.6 m/min. Post-dive signs included respiratory distress, difficulty walking, paralysis, and death. DCS was scored as non-fatal at 30-min post-dive or fatal at any time. Analysis by ordinal logistic regression indicated more DCS with post-dive exercise (P = 0.0112) and at 45 (P = 0.0011) and 60 fsw/min (P = 0.0001) compared to 30 fsw/min. Survival analysis suggested earlier death at 60 fsw/min compared to 30 fsw/min (P = 0.0006). Similar effects have been reported for the less severe DCS that occurs in humans.
Animals↗
Patency and blood flow in gas denucleated arterial prostheses.
Biomaterials exposed to blood often fail due to thrombosis. Gas nuclei (air) in the material are thrombogenic and a potential cause of failure. The effects of gas nuclei on patency and blood flow were studied in 4 mm diameter arterial grafts (Gore ePTFE; Johnson and Johnson Vitagraft ePTFE; Bard ACG EXS) in the femoropopliteal position of dogs. Control and denucleated (air-free) grafts were implanted bilaterally. Grafts were denucleated by immersion in degassed saline and exposure to 4 torr vacuum and 3,000-20,000 psig pressure. Graft patency was determined at harvest in 46 dogs. Blood flow was measured with acoustic flow probes in eight dogs. Denucleated graft patency was 60% after 2 days of implant while control patency was 22% (P < .05). Measured blood flow was higher in denucleated grafts than in control grafts (P < .02) in 4 of 5 dogs which had significantly different flows. Patency and flow decreased to zero for both control and denucleated grafts over periods of up to 80 days. Air in the control grafts may have been absorbed within several days, leading to late similarity with the denucleated grafts. Thus, removing the air from 4 mm ePTFE grafts decreased acute thrombosis and increased the patency.
Animals↗
Flying after diving and decompression sickness.
Reports of 1,159 decompression sickness (DCS) incidents during recreational diving were analyzed by logistic regression for the effects of flying on the occurrence of Type II DCS, complete relief of symptoms after one recompression, and residual symptoms 3 months after treatment. The relevant diver populations were those who: 1) did not fly; 2) had symptoms before flying but flew anyhow; 3) and did not have symptoms before flying but developed symptoms during or after flight. Of the total DCS population, 13.9% had preflight symptoms while 5.6% developed symptoms during or after flight. Symptoms which occurred during or after flight were no more serious and their responses to recompression no less successful than symptoms in nonflying divers. There was a statistically significant association between divers who flew with pre-existing symptoms and Type II DCS, incomplete relief with one recompression, and residual symptoms after 3 months.
Adult↗
Absence of intravascular bubble nucleation in dead rats.
Bubble formation in the inferior vena cavae (IVC) of dead rats was investigated after 6-15-h exposures to air at 123 atm abs (12.5 MPa) and decompression to 1 atm abs at 13.6 atm/min (1.4 MPa/min). The maximum estimated air-supersaturation attained in the IVCs after decompression was 6.1-18.3 atm (0.6-1.8 MPa). Bubbles were detected by light microscopy, buoyancy, and underwater dissection. No bubbles formed in 42 blood-filled IVCs that were isolated from the circulation by ligatures, but bubbles were always observed in unisolated IVCs (P < 0.000005). Other isolated IVCs were filled with tap water, water and bubbles, or water and iron filings. Bubbles formed in 13% of the IVCs filled with tap water, in 16% of the IVCs containing water with preexisting bubbles, and in 80% of the IVCs containing water with iron filings. Results indicate that at the air supersaturations attained in the isolated IVCs a) blood is resistant to de novo bubble formation; b) preexisting bubbles are dissolved by compression; c) bubbles in water originate from preexisting gas nuclei; and d) iron filings harbor gas nuclei that are able to survive 122 atm (12.4 MPa) overpressures and form bubbles on subsequent decompression.
Air↗
The effect of interstitial air on the in vitro thrombogenicity of ePTFE vascular grafts.
Gas trapped in the interstices of the biomaterials used for vascular prostheses causes thrombosis, and the process of eliminating this gas is known as denucleation. An apparatus was developed for testing in the in vitro effects of denucleation on 4 mm I.D. expanded polytetrafluoroethylene (ePTFE) Vitagraft (Johnson and Johnson). The apparatus was designed to ensure that neither the blood nor the grafts came in contact with air. Blood from a single donor was incubated with control and denucleated grafts for 5, 10, 15, 20, and 30 minutes. The thrombus volume in the graft lumen was measured with a computer assisted videometric system. Little thrombus formed by 5 or 10 minutes, but there was less thrombus in the denucleated graft than in the control graft at all times. The differences were statistically significant at 15 and 20 minutes (p < 0.05). Denucleation nearly doubled the thrombus formation time. Thrombus was more adherent to denucleated grafts than to control grafts. These results are consistent with in vivo observations in the rat where denucleation decreased thrombus formation and increased patency duration.
Air↗
Quantification of gas denucleation and thrombogenicity of vascular grafts.
In vitro methods were developed to measure the air content of vascular graft walls and the thrombogenicity of this air. Gas content (volume %) of expanded polytetrafluoroethylene (ePTFE) grafts from different sources ranged from 75.5 +/- 0.4% to 61.8 +/- 0.3%. Exposure of Vitagraft ePTFE to a vacuum prior to saline immersion replaced 87.5% of the gas nuclei with saline (denucleation). Acetone and ethanol immersion produced 98.9% and 94.3% denucleation, respectively. Denucleation was essentially complete when vacuum exposure was followed by hydrostatic pressure treatment at 500 psig or greater. The influence of gas content on thrombogenicity was determined by immersing graft samples in whole canine blood and weighing the adherent thrombus. Denucleation significantly reduced adherent thrombus weight compared with control grafts (p less than 0.001). Air in Vitagraft walls was responsible for 84% of the adherent thrombus weight at four minutes. The described methods could be employed to assess the hemocompatibility of various biomaterials.
Adhesiveness↗
Venous gas emboli and complement activation after deep repetitive air diving.
Complement activity has been linked to decompression sickness (DCS), but the effects of intravascular bubbles on complement activation are poorly understood. We have investigated intravascular complement activation by measuring red blood cell (RBC)-bound C3d after repetitive air diving in man. Subjects were exposed to a single, 20 min, 170 fsw (feet of sea water) dive, or to 2 such dives with a 6-h surface interval. Doppler monitoring for venous gas emboli was performed postdive. Predive blood samples were studied to determine sensitivity of complement to activation by air bubbles. Other predive and postdive venous samples were evaluated for intravascular complement activation. No cases of DCS occurred in 39 dives. Baseline complement sensitivity appeared normally distributed, thus "sensitive" and "insensitive" subjects were not clearly distinguishable. RBC-bound C3d did not increase after 1 dive but did increase after the repetitive dive (P less than 0.05). Furthermore, maximum bubble grade was independent of complement activation.
Adult↗
Hydrostatic pressure reduces thrombogenicity of polytetrafluoroethylene vascular grafts.
A prime factor in the thrombogenicity of synthetic materials in contact with blood is the blood-gas interface. Small pockets of gas, known as gas nuclei, are trapped within surface interstices. The resulting blood-gas interface denatures plasma proteins and activates clotting factors and platelets. Expanded polytetrafluoroethylene (ePTFE) vascular prostheses 1 mm in internal diameter were placed in saline under 6,000 psig hydrostatic pressure for 2 h in an attempt to dissolve all gas nuclei (i.e., to denucleate). Carotid-carotid bypasses were performed in rats using 280-mm lengths of ePTFE. All 10 control grafts lost patency in 5 min, whereas the 14 denucleated grafts had a median patency duration of 300 min (P less than 0.01). In 15-mm-long rat femoral artery interpositional ePTFE grafts, 90% of controls thrombosed within 10 min, whereas only 7% of denucleated grafts thrombosed over the duration of the 7-day observation period (P less than 0.001). Denucleation also resulted in a significant reduction (P less than 0.02) in 111In-labeled platelet adhesion to 36% of control. Scanning electron microscopy confirmed the reduced accumulation of platelets on denucleated grafts. These data suggest that the removal of trapped air with hydrostatic pressure significantly reduces the thrombogenicity of ePTFE microvascular prostheses and may have application to other clinical (catheters, valves, tubing, etc.) or experimental (micropipettes, electrodes, etc.) materials that interface with blood.
Animals↗
Mammary implants, diving, and altitude exposure.
Mammary implants were exposed to various simulated dive profiles followed by altitude exposures to stimulate aircraft travel and then were observed for bubble formation and volume changes. Minimal volume changes occurred after each dive. Numerous bubbles formed, however, reaching their maximum size in 3 hours. By comparison, when implants were exposed to high altitude following a dive exposure, significant volume changes occurred. This in vitro study showed that bubble formation and volume expansion occur after exposing implants to diving and altitude, but the circumstances required to produce these changes in vivo are extremely unlikely to occur normally.
Altitude↗
Effects of microgravity on tissue perfusion and the efficacy of astronaut denitrogenation for EVA.
The prevention of astronaut decompression sickness (DCS) during extravehicular activity (EVA) from the Shuttle Orbiter entails basic questions about how the efficacies of pre-EVA denitrogenations are affected by physiological responses and adaptations to microgravity. Many of these questions may be answered, without requiring inflight decompression experiments, when suitable inflight measurements of N2 elimination from spacecrew breathing 100% O2 can be analyzed using an N2 elimination/DCS risk correlation which has been calibrated in ground-based studies. In order to pursue this approach in our laboratory, a potentially flight-applicable, breath-by-breath method for measuring N2 elimination from human subjects breathing 100% O2 for 2-3-h periods has been developed. The present report describes this development with particular emphasis on required methodological accuracy and its achievement in view of certain properties of mass spectrometer performance. A method for the breath-by-breath analysis of errors in measured N2 elimination profiles is also described.
Adaptation, Physiological↗