Assessment of the interaction of hyperbaric N2, CO2, and O2 on psychomotor performance in divers.

Diving narcosis results from the complex interaction of gases, activities, and environmental conditions. We hypothesized that these interactions could be separated into their component parts. Where previous studies have tested single cognitive tasks sequentially, we varied inspired partial pressures of CO2, N2, and O2 in immersed, exercising subjects while assessing multitasking performance with the Multi-Attribute Task Battery II (MATB-II) flight simulator. Cognitive performance was tested under 20 conditions of gas partial pressure and exercise in 42 male subjects meeting U.S. Navy age and fitness profiles. Inspired nitrogen (N2) and oxygen (O2) partial pressures were 0, 4.5, and 5.6 ATA and 0.21, 1.0, and 1.22 ATA, respectively, at rest and during 100-W immersed exercise with and without 0.075-ATA CO2 Linear regression modeled the association of gas partial pressure with task performance while controlling for exercise, hypercapnic ventilatory response, dive training, video game frequency, and age. Subjects served as their own controls. Impairment of memory, attention, and planning, but not motor tasks, was associated with N2 partial pressures >4.5 ATA. Sea level O2 at 0.925 ATA partially rescued motor and memory reaction time impaired by 0.075-ATA CO2; however, at hyperbaric pressures an unexpectedly strong interaction between CO2, N2, and exercise caused incapacitating narcosis with amnesia, which was augmented by O2 Perception of narcosis was not correlated with actual scores. The relative contributions of factors associated with diving narcosis will be useful to predict the effects of gas mixtures and exercise conditions on the cognitive performance of divers. The O2 effects are consistent with O2 narcosis or enhanced O2 toxicity.

Recommendations for rescue of a submerged unresponsive compressed-gas diver.

The Diving Committee of the Undersea and Hyperbaric Medical Society has reviewed available evidence in relation to the medical aspects of rescuing a submerged unresponsive compressed-gas diver. The rescue process has been subdivided into three phases, and relevant questions have been addressed as follows. Phase 1, preparation for ascent: If the regulator is out of the mouth, should it be replaced? If the diver is in the tonic or clonic phase of a seizure, should the ascent be delayed until the clonic phase has subsided? Are there any special considerations for rescuing rebreather divers? Phase 2, retrieval to the surface: What is a "safe" ascent rate? If the rescuer has a decompression obligation, should they take the victim to the surface? If the regulator is in the mouth and the victim is breathing, does this change the ascent procedures? If the regulator is in the mouth, the victim is breathing, and the victim has a decompression obligation, does this change the ascent procedures? Is it necessary to hold the victim's head in a particular position? Is it necessary to press on the victim's chest to ensure exhalation? Are there any special considerations for rescuing rebreather divers? Phase 3, procedure at the surface: Is it possible to make an assessment of breathing in the water? Can effective rescue breaths be delivered in the water? What is the likelihood of persistent circulation after respiratory arrest? Does the recent advocacy for "compression-only resuscitation" suggest that rescue breaths should not be administered to a non-breathing diver? What rules should guide the relative priority of in-water rescue breaths over accessing surface support where definitive CPR can be started? A "best practice" decision tree for submerged diver rescue has been proposed.

Common causes of open-circuit recreational diving fatalities.

Diving fatalities causes were investigated in 947 recreational open-circuit scuba diving deaths from 1992-2003. Where possible, cases were classified at each step of a four step sequence: trigger, disabling agent, disabling injury, cause of death (COD). The most frequent adverse events within each step were: (a) triggers 41% insufficient gas, 20% entrapment, 15% equipment problems; (b) disabling agents--55% emergency ascent, 27% insufficient gas, 13% buoyancy trouble; (c) disabling injuries--33% asphyxia, 29% arterial gas embolism (AGE), 26% cardiac incidents; and (d) COD--70% drowning, 14% AGE, 13% cardiac incidents. We concluded that disabling injuries were more relevant than COD as drowning was often secondary to a disabling injury. Frequencies and/ or associations with risk factors were investigated for each disabling injury by logistic regression. (The reference group for each injury was all other injuries.) Frequencies and/or associations included: (a) asphyxia--40% entrapment (Odds Ratio, OR > or = 30), 32% insufficient gas (OR = 15.9), 17% buoyancy trouble, 15% equipment trouble (OR = 4.5), 11% rough water, drysuit (OR = 4.1), female gender (OR = 2.1); (b) AGE--96% emergency ascent (OR > or = 30), 63% insufficient gas, 17% equipment trouble, 9% entrapment; (c) cardiac incidents--cardiovascular disease (OR = 10.5), age > 40 (OR = 5.9). Minimizing the frequent adverse events would have the greatest impact on reducing diving deaths.

Influence of bottom time on preflight surface intervals before flying after diving.

Previous trials of flying at 8,000 ft after a single 60 fsw, 55 min no-stop air dive found low decompression sickness (DCS) risk for a 11:00 preflight surface interval (PFSI). Repetitive 60 fsw no-stop dives with 75 and 95 min total bottom times found 16:00. Trials reported here investigated PFSIs for a 60 fsw, 40 min no-stop dive and a 60 fsw, 120 min decompression dive. The 40 min trials began with a 12:05 PFSI (USN guideline) which was incrementally reduced to 0:05 (three DCS incidents in 281 trials). The 120 min trials began with a 22:46 PFSI (USN guideline) which was reduced to 2:00 (nine incidents in 281 trials); 2:00 was rejected with six incidents. Low-risk PFSIs for the 40 min dive were nearly 12 hours shorter than for the 55 min dive, and low-risk PFSIs for the single 120 min decompression dive were 12 hours shorter than for the 75-95 min repetitive dives. With the dry, resting conditions of these dives, low-risk PFSIs appeared to be sensitive to dive profile characteristics such as bottom time, repetitive diving, and decompression stops. Whether this is so for wet, working dives is unknown.

First aid normobaric oxygen for the treatment of recreational diving injuries.

INTRODUCTION: First aid oxygen (FAO2) has been widely used as an emergency treatment for diving injuries, but there are few studies supporting its efficacy. METHODS: 2,231 sequential diving injury reports collected by the Divers Alert Network (DAN) Injury database from 1998 to 2003 were examined. RESULTS: 47% (1,045) of cases received FAO2. The median time to FAO2 treatment after surfacing was four hours and after symptom onset was 2.2 hours. Persistent complete relief (14%) or improvement (51%) was seen with FAO2 alone (65% overall response; n = 330). After one recompression treatment 67% of FAO2 patients reported complete relief compared to 58% of the no FAO2 group (OR = 1.5, 95% CI = 1.2 -1.8). FAO2 given at any time after surfacing significantly reduced the odds of multiple recompression treatments (OR = 0.83, 0.70-0.98). When FAO2 was given within 4 hours of surfacing, the OR decreased to 0.50 (0.36-0.69) yielding a number needed to treat of 6. Case severity affected urgency of FAO2 treatment. Individuals with more prominent symptoms received prompt treatment. Cardiopulmonary, skin, and serious neurological symptoms had shorter delays to FAO2 (p < 0.001). CONCLUSIONS: FAO2 increased recompression efficacy and decreased the number of recompression treatments required if given within four hours after surfacing.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.