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PubMed1992

Nitrogen tensions in brachial vein blood of Korean ama divers.

Intravascular bubble formation and symptoms of decompression sickness have been reported during repetitive deep breath-hold diving. Therefore we examined the pattern of blood N2 kinetics during and after repetitive breath-hold diving. To study muscle N2 uptake and release, we measured brachial venous N2 partial pressure (PN2) in nine professional Korean breath-hold divers (ama) during a 3-h diving shift at approximately 4 m seawater depth and up to 4 h after diving. PN2 was determined with the manometric Van Slyke method. Diving time and depth were recorded using a backpack computer-assisted dive longer that allowed calculating the surface-to-depth time ratio to derive the effective depth. With the assumption that forearm muscle N2 kinetics follow the general Haldanian principles of compression and decompression, i.e., forearm muscle is a single compartment with a uniform tissue PN2 equal to venous PN2, PN2 data were fitted to monoexponential functions of time. In the early phase of the diving shift, PN2 rapidly increased to 640 Torr (half time = 6 min) and then slowly declined to baseline levels (half time = 36 min) after the work shift. Peak PN2 levels approximated the alveolar PN2 derived from the effective depth. We conclude that forearm muscle N2 kinetics are well described by a Haldanian single-compartment model. Decompression sickness is theoretically possible in the ama; it did not occur because the absolute PN2 remained low due to the shallow working depth of the ama we studied.

Diving↗
PubMedDate not supplied

Menstrual cycle dependent right-to-left shunting: a single-blinded transcranial Doppler sonography study.

BACKGROUND AND PURPOSE: Menstruation has been described as risk factor for neurological decompression sickness in divers. In considering this for paradoxical gas embolism, we hypothesized that there may be a link between cycle-dependent hormonal changes and the manifestation of a right-to-left shunt (RLS). METHODS: 40 women with a regular cycle of 28 days underwent transcranial Doppler sonography examinations (TCD) on day 1 and on day 15 of the menstrual cycle. Cerebral high intensity transient signs (HITS) proved a RLS. RESULTS: We found a 25% RLS incidence consistent with the literature. In 7 of 10 shunt-positive women it was detected mainly or exclusively on day 15. This difference in PFO detection rate is statistically significant (p = 0.031), indicating more RLS during the peri-ovulatory period. CONCLUSIONS: Our results do not support menstruation as a risk factor for neurological decompression sickness. The peri-ovulatory estrogen peak, which leads to systemic vasodilation, may explain our data. Factors that increase the risk for developing a RLS and thereby paradoxical embolism should be avoided, perhaps including diving during the peri-ovulatory period of the menstrual cycle. Furthermore, contrast PFO testing in fertile females may be most sensitive if conducted mid-cycle.

Adolescent↗
PubMed2002

Heat stress attenuates air bubble-induced acute lung injury: a novel mechanism of diving acclimatization.

Diving acclimatization refers to a reduced susceptibility to acute decompression sickness (DCS) in individuals undergoing repeated compression-decompression cycles. We postulated that mechanisms responsible for the acclimatization are similar to that of a stress preconditioning. In this study, we investigated the protective effect of prior heat shock treatment on air embolism-induced lung injury and on the incidence of DCS in rats. We exposed rats (n = 31) to a pressure cycle that induced signs of severe DCS in 48% of the rats, greater wet-to-dry ratio (W/D) of lung weight compared with the control group (5.48 +/- 0.69 vs. 4.70 +/- 0.17), and higher protein concentration in bronchoalveolar lavage (BAL) fluid (362 +/- 184 vs. 209 +/- 78 mg/l) compared with the control group. Rats with DCS expressed more heat shock protein 70 (HSP70) in the lungs than those without signs of disease. Prior heat shock (n = 12) increased the expression of HSP70 in the lung and attenuated the elevation of W/D of lung weight (5.03 +/- 0.17) after the identical decompression protocol. Prior heat shock reduced the incidence of severe DCS by 23%, but this failed to reach statistical significant (chi(2) = 1.94, P = 0.163). Venous air infusion (1.0 ml/40 min) caused profound hypoxemia (54.5 +/- 3.8 vs. 83.8 +/- 3.2 Torr at baseline; n = 6), greater W/D of lung weight (5.98 +/- 0.45), and high protein concentration in BAL fluid (595 +/- 129 mg/l). Prior heat shock (n = 6) did not alter the level of hypoxemia caused by air embolism, but it accelerated the recovery to normoxemia after air infusion was stopped. Prior heat shock also attenuated the elevation of W/D of lung weight (5.19 +/- 0.40) and the increase in BAL protein (371 +/- 69 mg/l) in air embolism group. Our results showed that the occurrence of DCS after rapid decompression is associated with increased expression of a stress protein (HSP70) and that prior heat shock exposure attenuates the air bubble-induced lung injury. These results suggest that bubble formation in tissues activates a stress response and that stress preconditioning attenuates lung injury on subsequent stress, which may be the mechanism responsible for diving acclimatization.

Acclimatization↗
PubMed2000

Computation of decompression tables using continuous compartment half-lives.

There is no consensus on the number of compartments and the half-lives (T1/2) used in the calculation of inert gas exchange and decompression sickness (DCS) boundary in existing dive tables and decompression computers. We propose the use of a continuous variable for the tissue half-lives, allowing the simulation of an infinite number of compartments and reducing the discrepancy between different algorithms to a single DCS boundary expression. Our computational method is based on the premise that M-values can be expressed in terms of T1/2 and ambient pressure (D). We combined the surfaces defined by M(D,T1/2) and tissue tension H(t,T1/2) to plan decompression. The efficiency and applicability of the method is investigated with four different DCS boundaries. The first two utilize the M-value relations proposed by Bühlmann and Wienke to derive no-D limits for sea level. The third boundary is defined by a surface fitted to the empirical M-values of US Navy, Bühlmann tables, US Air Force, and our altitude diving data. This expression was used to design the decompression procedure for a multilevel dive at 11,429-ft altitude and was used in six man dives in the Kaçkar Mountains, Turkey. Although precordial bubbles were observed in two dives, there were no cases of DCS. The fourth DCS boundary is constructed with the addition of a constraint that forces calculated M-values to stay below the available M-values. This constraint aims the highest degree of "conservatism". As an application of the new boundary, the method is used to derive decompression stop diving schedules for 11,429-ft altitude. The concept of continuous tissue half-lives is applicable to different types of gas exchange and DCS boundary functions or to a combination of different models with a desired level of conservatism. It has proved to be a useful tool in planning decompression for undocumented modes of diving such as decompression stop diving or multilevel diving at altitude. The algorithm can easily be incorporated into dive computers.

Algorithms↗
PubMed1991

Decompression comparison of N2 and O2 in rats.

We have previously reported that O2 in the breathing gas mixture contributed significantly to the risk of decompression sickness (DCS) in rats after rapid (less than 10 s) decompression to the surface from depth. The rate of O2 uptake was extremely fast (less than 1 min estimated for equilibrium after a pressure change) compared to much slower rates for He and N2. To further define the role that O2 plays in diving, the present investigation examined decompression outcome in unanesthetized male albino rats after 60-min N2-O2 dives (1-3 atm abs O2, depth 6.26 or 7.26 atm abs). Slower decompression profiles were used to determine the elimination rates of N2 and O2 as pressure was reduced and included "stops" of up to 20 min. The probability of DCS was modeled using the maximum likelihood technique. O2 again contributed significantly to the risk of DCS, although O2 was eliminated very rapidly during decompression; the washout of N2 was considerably longer. These findings support the view that O2 can add significantly to decompression risk. However, this phenomenon may not normally be encountered during human diving operations where relatively slower decompression and lower PO2's are used.

Animals↗
PubMed1983

A five-year survey of hypobaric chamber physiological incidents in the Canadian Forces.

Hypobaric chamber training forms an integral part of the Canadian Forces (CF) Aeromedical Training Programme (AMTP). There are four standard types of runs (Type I, II, III, IV) in which personnel are exposed to the reduced atmospheric pressures ranging from ground level (GL) to 43,000 ft (13,106 m) (0.16 ATA). Physiological incidents involving trapped gases in the hollow body organs resulting from exposure to these reduced atmospheric pressures are considered "normal" during chamber runs and are managed by well established procedures. Altitude decompression sickness (DCS) on the other hand is a potentially life-threatening disorder and must be managed accordingly. This report is a summary of all physiological incidents occurring in CF hypobaric chambers during the period 1 January, 1977-31 December, 1981, and emphasizes significant trends in the incidence of altitude DCS at these chambers.

Aerospace Medicine↗
PubMed1989

[Comparison of the readings of the digital decompression meter with hyperbaric chamber tests].

An estimation of the risk incurred through the use of digital decompression computers used by the diver must be based on comparisons with hyperbaric chamber tests. We compared the decompression indications displayed by different commercial devices to depth/bottom time profiles for which hyperbaric chamber experiments have given us the relevant information on types and frequency of decompression sickness.

Decompression↗
PubMed1991

Ethanol and venous bubbles after decompression in humans.

We exposed 34 subjects to a 48-h, 6.25-msw dive, and administered ethanol (0.5-1.0 ml pure ethanol.kg-1 body weight) orally to 11 of them immediately after direct decompression. Doppler monitoring of both precordial and subclavian sites for 24 h postsurfacing revealed that all subjects from both groups had detectable bubbles, and that there was no difference in timing or magnitude between the 2 groups. These results do not support the recently suggested role for ethanol in the treatment of decompression sickness.

Decompression Sickness↗
PubMed2003

Age affects severity of venous gas emboli on decompression from 14.7 to 4.3 psia.

INTRODUCTION: Variables that define who we are, such as age, weight and fitness level influence the risk of decompression sickness (DCS) and venous gas emboli (VGE) from diving and aviation decompressions. We focus on age since astronauts that perform space walks are approximately 10 yr older than our test subjects. Our null hypothesis is that age is not statistically associated with the VGE outcomes from decompression to 4.3 psia. METHODS: Our data are from 7 different NASA tests where 188 men and 50 women performed light exercise at 4.3 psia for planned exposures no less than 4 h. Prebreathe (PB) time on 100% oxygen ranged from 150-270 min, including ascent time, with exercise of different intensity and length being performed during the PB in four of the seven tests with 150 min of PB. Subjects were monitored for VGE in the pulmonary artery using a Doppler ultrasound bubble detector for a 4-min period every 12 min. There were six design variables; the presence or absence of lower body adynamia and five PB variables; plus five concomitant variables on physical characteristics: age, weight height, body mass index, and gender that were available for logistic regression (LR). We used LR models for the probability of DCS and VGE, and multinomial logit (ML) models for the probability of Spencer VGE Grades 0-IV at exposure times of 61, 95, 131, 183 min, and for the entire exposure. RESULTS: Age was significantly associated with VGE in both the LR and ML models, so we reject the null hypothesis. Lower body adynamia was significant for all responses. CONCLUSIONS: Our selection of tests produced a wide range of the explanatory variables, but only age, lower body adynamia, height, and total PB time was helpful in various combinations to model the probability of DCS and VGE.

Adolescent↗
PubMed1997

Improved probabilistic decompression model risk predictions using linear-exponential kinetics.

Using a data base of 2,383 air and nitrogen-oxygen dives resulting in 131 cases of decompression sickness (DCS), risk functions were developed for a set of probabilistic decompression models according to survival analysis techniques. Parameters were optimized using the method of maximum likelihood Gas kinetics were either traditional exponential uptake and elimination, or an exponential uptake followed by linear elimination (LE kinetics) when calculated supersaturation was excessive. Risk functions either used the calculated relative gas supersaturation directly, or a delayed risk using a time integral of prior supersaturation. The most successful model (considering both incidence and time of onset of DCS) used supersaturation risk, and LE kinetics (in only 1 of 3 parallel compartments). Several methods of explicitly incorporating metabolic gases in physiologically plausible functions were usually found in lumped threshold terms and did not explicitly affect the overall data fit. The role of physiologic fidelity vs. empirical data fitting ability in accounting for model success is discussed.

Decompression Sickness↗
PubMed1983

Postmortem computed tomography in a diving fatality.

Determination of the exact cause of death in diving casualties is usually difficult at autopsy. In such cases, formation of gas in various organs is sometimes supposed to be causative, and thus establishment of the exact distribution of gas is crucial. This is not possible by conventional autopsy techniques. In the head of a 20-year-old navy diver who died during a dive to a maximum depth of 43 m, it was possible to demonstrate the distribution of gas by cerebral computed tomography. Gas was also found by conventional X-ray examination of the right ventricle and by pulmonary angiography in the pulmonary arteries. It seems probable that the attempted resuscitation was unsuccessful because of ongoing decompression sickness.

Accidents, Occupational↗
PubMed1976

Decompression-induced decrease in nitrogen elimination rate in awake dogs.

Formulation of safe decompression procedures still requires unproven assumptions regarding both gas equilibration rates and the associated ascent criteria. Although the assumption of symmetry of uptake and elimination rates has been suspect for several years, few data are available. Measurements of actual mixed venous blood nitrogen content [vN2] during compression and following decompression in chronically catheterized awake dogs have clearly demonstrated that desaturation is markedly slower than saturation, and that this effect can be imposed by decompression. The disappearance of arteriovenous nitrogen concentration differences during desaturation following a decompression that produced decompression sickness indicates that cardiopulmonary and cardiovascular changes induced by mechanisms associated with decompression per se can potentiate its deleterious effects. Current US practices do not provide for such asymmetry, while those used in the UK have incorporated this in their models for the last decade.

Animals↗
PubMed1985

Complications of saturation diving.

The experience of 458 man-dives with 731 excursions between 50 m and 300 m carried out by Royal Navy saturation divers is summarized. During saturation decompression there were 6 treated bends and 33 reported niggles. Two bends occurred in dives deeper than 249 m and the remaining 4 bends occurred in dives where decompression began in much less than the saturation stop time after completion of downward excursions. There was one case of vestibular system decompression sickness after an excursion to 300 m. It is concluded that the decompression table is effective in use shallower than 150 m but that the risk increases with greater depth. There is, however, only limited experience in the deeper range. There is no evidence that chamber compression with air to 10 m adversely affects decompression from deeper than 50 m. An account of the medical and physiological conditions affecting divers in these dives is given.

Decompression Sickness↗
PubMed2002

[Effects of fast decompression on prostaglandins content in cerebral tissue of guinea pigs].

Objective. To investigate the effect of fast decompression on prostaglandins in cerebral tissue. Method. 26 guinea pigs were divided into 2 groups randomly. The animals in group FDC (group 1) were treated with fast decompression and formed decompression sickness, but those in control group (group 2) were not treated with decompression. The contents of prostaglandin E2 (PGE2), 6-keto-prostaglandin F1a (6-K-PGF1a) and thromboxane B2 (TXB2) in cerebral tissue of the animals were determined by enzyme immunoassay. Result. The content of PGE2 in cerebral tissue of FDC animals was twice as much as that in control animals. The content of TXB2 in cerebral tissue of FDC animals was 3 times as high as that in control animals, and that of 6-K-PGF1a in cerebral tissue of FDC animals was 2.6 times as that in control animals. It showed very significant differences as compared with control group (P<0.01). Conclusion. The content of PGs in cerebral tissue increased markedly after fast decompression, and may cause cerebral injury.

6-Ketoprostaglandin F1 alpha↗