Experiment of nitrox saturation diving with trimix excursion.
(1/67)
Depth limitations to diving operation with air as the breathing gas are well known: air density, oxygen toxicity, nitrogen narcosis and requirement for decompression. The main objectives of our experiment were to assess the decompression, counterdiffusion and performance aspect of helium-nitrogen-oxygen excursions from nitrox saturation. The experiment was carried out in a wet diving stimulator with "igloo" attached to a 2-lock living chamber. Four subjects of two teams of 2 divers were saturated at 25 msw simulated depth in a nitrogen oxygen chamber environment for 8 days, during which period they performed 32 divers-excursions to 60 or 80 msw pressure. Excursion gas mix was trimix of 14.6% oxygen, 50% helium and 35.4% nitrogen, which gave a bottom oxygen partial pressure of 1.0 bars at 60 msw and 1.3 at 80 msw. Excursions were for 70 min at 60 msw with three 10-min work periods and 40 min at 80 msw with two 10-min work periods. Work was on a bicycle ergometer at a moderate level. We calculated the excursion decompression with M-Values based on methods of Hamilton (Hamilton et al., 1990). Staged decompression took 70 min for the 60 msw excursion and 98 min for 80 msw, with stops beginning at 34 or 43 msw respectively. After the second dive day bubbles were heard mainly in one diver but in three divers overall, to Spencer Grade III some times. No symptoms were reported. Saturation decompression using the Repex procedures began at 40 msw and was uneventful: Grade II and sometimes III bubbles persisted in 2 of the four divers until 24 hr after surfacing. We conclude that excursions with mixture rich in helium can be performed effectively to as deep as 80 msw using these procedures. (+info)
A randomized two-part study was conducted in order to determine the efficacy of theophylline in the treatment of acute mountain sickness during fast ascent to altitudes >2,500 m. Fourteen healthy male subjects participated in a randomized single-blind placebo-controlled crossover study carried out in a decompression chamber (simulated altitude 4,500 m). A second randomized single-blind, placebo-controlled study was conducted at a high-altitude research laboratory (3,454 m) and included 21 healthy male subjects. The study medication was either 375 mg oral slow-release theophylline (250 mg if <70 kg) or a matched placebo tablet taken twice daily. The acute mountain sickness score (AMSS) was assessed three times a day, beginning 18 h prior to altitude exposure and continuing for 18 h after altitude exposure. In addition, measurements of respiratory frequency, pulse rate, oxygen saturation and arterial blood gas levels were performed. Acute mountain sickness was significantly reduced by theophylline during the decompression chamber study (mean+/-SD 1.2+/-0.9) with placebo versus 3.6+/-0.8 with theophylline; p=0.03). During the high-altitude study, subjects with theophylline showed a significantly lower AMSS on arrival and after 18 h at altitude (0.6 versus 2.3, p=0.03). Oxygenation was improved in both parts of the study. In conclusion, oral slow-release theophylline improves acute mountain sickness. (+info)
Management of thoracic outlet syndrome.
(3/67)
This overall management program for thoracic outlet compression syndrome is based upon experience with 153 extremities in 149 patients and the results of others. The following conclusions are documented and discussed. 1) Diagnosis is based chiefly upon history; physical signs are inconstant and often absent. 2) Major vascular problems are unusual; angiography is not always necessary. 3) Electromyography is not always critical but does aid in diagnosis of carpal tunnel syndrome. 4) Non-operative treatment relieves most patients; operative decompression is indicated for a minority. 5) Transxillary first rib resection, with removal of cervical rib is the best operation. 6) Carpal tunnel decompression should be done concomitantly when needed. 7) Operation is relatively safe. (+info)
Increasing activity of H(2)-metabolizing microbes lowers decompression sickness risk in pigs during H(2) dives.
(4/67)
The risk of decompression sickness (DCS) was modulated by varying the biochemical activity used to eliminate some of the hydrogen (H(2)) stored in the tissues of pigs (19.4 +/- 0.2 kg) during hyperbaric exposures to H(2). Treated pigs (n = 16) received intestinal injections of Methanobrevibacter smithii, a microbe that metabolizes H(2) to water and CH(4). Surgical controls (n = 10) received intestinal injections of saline, and an additional control group (n = 10) was untreated. Pigs were placed in a chamber and compressed to 24 atm abs (20.6-22.9 atm H(2)). After 3 h, the pigs were decompressed and observed for symptoms of DCS for 1 h. Pigs with M. smithii had a significantly lower (P < 0.05) incidence of DCS (44%; 7/16) than all controls (80%; 16/20). The DCS risk decreased with increasing activity of microbes injected (logistic regression, P < 0.05). Thus the supplemental tissue washout of the diluent gas by microbial metabolism was inversely correlated with DCS risk in a dose-dependent manner in this pig model. (+info)
On the likelihood of decompression sickness during H(2) biochemical decompression in pigs.
(5/67)
A probabilistic model was used to predict decompression sickness (DCS) outcome in pigs during exposures to hyperbaric H(2) to quantify the effects of H(2) biochemical decompression, a process in which metabolism of H(2) by intestinal microbes facilitates decompression. The data set included 109 exposures to 22-26 atm, ca. 88% H(2), 9% He, 2% O(2), 1% N(2), for 0.5-24 h. Single exponential kinetics described the tissue partial pressures (Ptis) of H(2) and He at time t: Ptis = integral (Pamb - Ptis). tau(-1) dt, where Pamb is ambient pressure and tau is a time constant. The probability of DCS [P(DCS)] was predicted from the risk function: P(DCS) = 1 - e(-r), where r = integral (Ptis(H(2)) + Ptis(He) - Thr - Pamb). Pamb(-1) dt, and Thr is a threshold parameter. Inclusion of a parameter (A) to estimate the effect of H(2) metabolism on P(DCS): Ptis(H(2)) = integral (Pamb - A - Ptis(H(2))). tau(-1) dt, significantly improved the prediction of P(DCS). Thus lower P(DCS) was predicted by microbial H(2) metabolism during H(2) biochemical decompression. (+info)
Aerobic endurance training reduces bubble formation and increases survival in rats exposed to hyperbaric pressure.
(6/67)
1. The formation of bubbles is the basis for injury to divers after decompression, a condition known as decompression illness. In the present study we investigated the effect of endurance training in the rat on decompression-induced bubble formation. 2. A total of 52 adult female Sprague-Dawley rats (300-370 g) were randomly assigned to one of two experimental groups: training or sedentary control. Trained rats exercised on a treadmill for 1.5 h per day for 1 day, or for 2 or 6 weeks (5 days per week) at exercise intervals that alternated between 8 min at 85-90% of maximal oxygen uptake (VO2,max) and 2 min at 50-60% of VO2,max. Rats were compressed (simulated dive) in a decompression chamber in pairs, one sedentary and one trained, at a rate of 200 kPa x min(-1) to a pressure of 700 kPa, and maintained for 45 min breathing air. At the end of the exposure period, rats were decompressed linearly to the 'surface' (100 kPa) at a rate of 50 kPa x min(-1). Immediately after reaching the 'surface' (100 kPa) the animals were anaesthetized and the right ventricle was insonated using Doppler ultrasound. 3. Intensity-controlled interval training significantly increased VO2,max by 12 and 60% after 2 and 6 weeks, respectively. At 6 weeks, left and right ventricular weights were 14 and 17 % higher, respectively, in trained compared to control rats. No effect of training was observed on skeletal muscle weight. Bubble formation was significantly reduced in trained rats after both 2 and 6 weeks. However, the same effect was seen after a single bout of aerobic exercise lasting 1.5 h on the day prior to decompression. All of the rats that exercised for 1.5 h and 2 weeks, and most of those that trained for 6 weeks, survived the protocol, whereas most sedentary rats died within 60 min post-decompression. 4. This study shows that aerobic exercise protects rats from severe decompression and death. This may be a result of less bubbling in the trained animals. The data showed that the increase in aerobic capacity per se was not the main mechanism, but rather an acute effect that was most notable 20 h after a single, or the last, exercise bout, with less effect after 48 h. (+info)
Hyperbaric oxygen may reduce gas bubbles in decompressed prawns by eliminating gas nuclei.
(7/67)
It is accepted that gas bubbles grow from preexisting gas nuclei in tissue. The possibility of eliminating gas nuclei may be of benefit in preventing decompression sickness. In the present study, we examined the hypothesis that hyperbaric oxygen may replace the resident gas in the nuclei with oxygen and, because of its metabolic role, eliminate the nuclei themselves. After pretreatment with oxygen, prawns were 98% saturated with nitrogen before explosive decompression at 30 m/min. Ten transparent prawns were exposed to four experimental profiles in a crossover design: 1) 10-min compression to 203 kPa with air; 2) 10-min compression with oxygen; 3) 10-min compression with oxygen to 203 kPa followed by 12 min air at 203 kPa; and 4) 10 min in normobaric oxygen followed by compression to 203 kPa with air. Bubbles were measured after explosive decompression. We found that pretreatment with hyperbaric oxygen (profile C) significantly reduces the number of bubbles and bubble volume. We suggest that hyperbaric oxygen eliminates bubble nuclei in the prawn. (+info)
Gas bubbles in rats after heliox saturation and different decompression steps and rates.
(8/67)
Effects of pressure reduction, decompression rate, and repeated exposure on venous gas bubble formation were determined in five groups (GI, GII, GIII, GIV, and GV) of conscious and freely moving rats in a heliox atmosphere. Bubbles were recorded with a Doppler ultrasound probe implanted around the inferior caval vein. Rats were held for 16 h at 0.4 MPa (GI), 0.5 MPa (GII and GIII), 1.7 MPa (GIVa), or 1.9 MPa (GIV and GV), followed by decompression to 0.1 MPa in GI to GIII and to 1.1 MPa in GIV and GV. A greater decompression step, but at the same rate (GII vs. GI and GIVb vs. GIVa), resulted in significantly more bubbles (P < 0.01). A twofold decompression step resulted in equal amount of bubbles when decompressing to 1.1 MPa compared with 0.1 MPa. The faster decompression in GII and GVa (10.0 kPa/s) resulted in significantly more bubbles (P < 0.01) compared with GIII and GVb (2.2 kPa/s). No significant difference was observed in cumulative bubble score when comparing first and second exposure. With the present animal model, different decompression regimes may be evaluated. (+info)