Incidence and risk factors for symptoms of decompression sickness among male and female dive masters and instructors--a retrospective cohort study.

UNLABELLED: The aim was to determine the incidence of symptoms of decompression sickness (DCS) in dive masters and instructors in relation to number of dives and possible risk factors. STUDY DESIGN: Retrospective cohort study of dive masters and instructors in Sweden. STUDY BASE: All dive masters and instructors listed with PADI, NAUI and CMAS in Sweden as of January 1st 1999 (2380 divers). METHODS: The dive masters and instructors received a validated questionnaire on diving activities and symptoms of DCS in 1999. 1516 men and 226 women answered, i.e. 73% of the initial study base. RESULTS: DCS symptoms were reported by 190 divers. The incidence of DCS symptoms was 1.52 for males and 1.27 for females per 1000 dives. Dive masters, divers not performing decompression-stop dives, divers not practicing advanced diving and divers with a low number of total lifetime dives had a higher proportion (p < 0.05) of DCS symptoms per 1000 dives. There were no major differences in DCS symptom incidence related to sex, age, asthma, overweight or alcohol abuse in this study.

Erythropoietin concentrations during 10 days of normobaric hypoxia under controlled environmental circumstances.

Serum erythropoietin levels (s-[epo]), haemoglobin concentration ([Hb]), haematocrit (hct), and ferritin concentration ([fer]) were measured in seven healthy male volunteers (20-23 years) exposed continuously to hypoxia (PO(2) 14 kPa) for 10 days. Serum erythropoietin concentration increased significantly from 9.5 +/- 3.51 to 33.6 +/- 11.64 U L(-1) (P < 0.05) after 2 days of hypoxia. Thereafter, s-[epo] decreased. However, after 10 days s-[epo] was 18.7 +/- 5.83 U L(-1) which was still increased above the pre-hypoxia level (P < 0.05). Serum haemoglobin concentration and hct increased over the 10 days of hypoxia, [Hb] from 152 +/- 8.9 to 168 +/- 9.2 gL(-1) (P < 0.001), and hct from 43 +/- 2.4 to 49 +/- 2.6% (P < 0.001). Ferritin concentration decreased significantly during the hypoxic exposure from 82 +/- 46.9 to 44 +/- 31.7 mmol L(-1) after 10 days (P < 0.01). In conclusion, the initial increase of s-[epo] under controlled normobaric hypoxia was marked, 353%, and levelled off after 5-10 days at 62-97% above normoxia level. There was also a significant increase in [Hb] and hct and a decrease in [fer] after 10 days of exposure to normobaric hypoxia.

Cerebrospinal fluid levels of monoamine compounds and cholecystokinin peptides after exposure to standardized barometric pressure.

BACKGROUND: Connections between mood changes and weather have been described throughout the ages, and in more recent years, there have been reports on a relationship between atmospheric pressure and neurotransmitter levels in cerebrospinal fluid. METHODS: To further investigate this issue under strictly standardized conditions, we have lumbar-punctured 8 healthy males under low (963 hPa) and high (1064 hPa) barometric pressure, using a pressure chamber. RESULTS: Under high pressure, the tyrosine concentrations in the cerebrospinal fluid (CSF) were lower, while the cholecystokinin tetrapeptide (CCK-4) levels were higher. No differences between low and high pressure were found for tryptophan, 5-hydroxyindolacetic acid (5-HIAA), dopamine (DA), and sulphated cholecystokinin octapeptide (CCK-8S). The serum level of CCK-8S was higher under high pressure. On comparing concentration ratios between the second and the first CSF fraction, we found significantly increased ratios for homovanillic acid (HVA) and 4-hydroxy-3-methoxyphenylglycol (HMPG), but a decreased ratio for tyrosine under high pressure. The difference in the concentration ratios of HVA between low and high pressure correlated negatively with age. Intraspinal pressure correlated negatively with tapping time at low pressure. CONCLUSION: Our results are in line with the hypothesis that atmospheric pressure influences CSF levels of monoamine compounds and cholecystokinin peptides.

Effects of normobaric hypoxic confinement on visual and motor performance.

INTRODUCTION: The use of reduced oxygen levels has been suggested for fire prevention in closed spaces, such as submarines. However, if humans are to work and live in environments with reduced oxygen levels, the effect of hypoxia on human performance must be further assessed. METHODS: In 3, 11- to 14-d confinements a total of 22 subjects were exposed to different levels of normobaric hypoxia (13, 14, and 15 kPa O2), for up to 10 d, with intervening periods of normoxia. In each experiment eight subjects were divided into two teams, working in 6-h shifts around the clock. Subjects performed tests of spatial orientation, visual reaction time, parallel processing and motor skills. Performance tests and questionnaires were administered once or twice in every 24-h period. RESULTS: All of the subjects appeared to tolerate the acute reduction in oxygen partial pressure well. In many of the tests performance improved with time as a result of learning, despite reductions in the oxygen level. No reduction in performance or decrease in rate of learning was observed at any of the oxygen levels tested. CONCLUSIONS: Oxygen levels down to 14 kPa appear not to impair visual and motor performance during rest.

Effects of reduced oxygen partial pressure on cognitive performance in confined spaces.

The reduction of oxygen levels is a technique used both for fire fighting and fire protection in confined spaces. The purpose of this study was to find out if and how reduced oxygen levels affect cognitive performance in a small group of persons living in a confined space such as a submarine. In 3 separate experiments lasting for 11 to 14 days, a total of 22 men were exposed to normoxic and different levels of hypoxic normobaric atmospheres (15, 14, and 13 kPa O2). Each participant completed a cognitive test battery twice every 24-hr period in the first 2 experiments, but only once a day in the 3rd experiment. Performance in almost all tests improved with the number of test sessions performed, despite reductions of the oxygen partial pressure. Under the conditions tested, cognitive performance decrements could not be observed if inspiratory oxygen partial pressure was kept above 13 kPa.

Breathing volumes and gas exchange during simulated rapid free ascent from 100 msw.

The crew of a disabled submarine can be rescued by means of free ascent through the water to the surface. Pulmonary gas exchange was studied during simulated rapid free ascent in subjects standing immersed to the neck in a pressure chamber. The pressure was rapidly increased to 1.1 MPa [100 meters seawater (msw)] followed by decompression at 0.03 MPa/s (3 msw/s). Effective inspired tidal volume, as estimated by an Ar dilution method, fell gradually to zero during decompression from 20 to 0 msw. Directly determined expired tidal volumes were increased up to two to three times at the time of return to surface pressure compared with pre- and postdecompression volumes. End-tidal PCO2 was increased on compression and fell to a nadir of 3.4 kPa (25 Torr) at the time of return to surface pressure. Thus, intrapulmonary gas expansion caused simultaneous inspiratory hypoventilation and expiratory hyperventilation. If O2-enriched gas is to be used to reduce the risk of decompression sickness, it should be administered early during decompression to alter the intrapulmonary gas composition. The time course of arterial PCO2 changes as reflected by end-tidal values during short-lasting compression/decompression would act to promote inert gas supersaturation in the brain.

Reduced voluntary non-visual suppression of the vestibulo-ocular reflex gain during nitrous oxide narcosis.

The effect of subanesthetic nitrous oxide (N2O) narcosis (21%) on the vestibulo-ocular reflex (VOR) and on voluntary non-visual suppression of the VOR was studied in 12 subjects, using a velocity step rotational test. Gain and time constant of the VOR were calculated by computer. During tests, the subjects were required either to perform mental arithmetic or to attempt to follow an imaginary target rotating with them in the dark. Voluntary non-visual suppression of gain was significantly reduced during exposure to N2O, though there was no statistically significant effect of N2O on gain per se. The time constant was unaffected either by voluntary suppression or by N2O. The reducing effect of N2O on voluntary non-visual suppression of VOR gain is assumed to be due to reduced alertness. Reduced voluntary non-visual suppression of VOR may imply reduced visual-vestibular interaction, which might be one explanation of the complaints of dizziness associated with fatigue or with ingestion of certain sedatives.

Effects of hyperbaric pressure and temperature on atria from ectotherm animals (Rana pipiens and Anguilla anguilla).

1. Spontaneously beating atria from frogs (R. pipiens) and eels (A. anguilla) were compressed hydraulically to 10 MPa. Effects on beating frequency and twitch tension were studied. 2. At low temperatures (8-10 degrees C) compression to 10 MPa caused a slowing of the beat frequency. No effects were noted at higher temperatures (16-24 degrees C). Twitch tension was decreased by pressure at low temperatures and increased at high temperatures. 3. Differences were noted between preparations from cold and warm acclimatized frogs, and from silver and yellow eels, respectively. 4. The effect of temperature acclimatization on pressure and temperature sensitivity is discussed in relation to data on cardiac phospholipid fatty acid composition.

Effects of hydrostatic pressure and inert gases on twitch tension.

Effect of pressure and inert gases on the twitch tension (Tmax) was measured on electrically stimulated and spontaneously beating rat atria. In stimulated preparations, pressurization to 10 MPa increased Tmax by 20-60% depending on the stimulating frequency (60-240 beats/min). The introduction of 5 MPa N2 or 5 MPa H2 at 10 MPa hydrostatic pressure decreased the Tmax by 17 +/- 6% and 13 +/- 6%, respectively. Gas effect did not depend on the stimulating frequency. Nitrous oxide (0.15 and 0.45 MPa) decreased Tmax both at "surface" and at 10 MPa. Nitrous oxide effect was slightly potentiated at pressure. In spontaneously beating preparations, compression to 10 and 15 MPa decreased beating frequency (BF) by 24 +/- 10% and 31 +/- 8% and increased Tmax by 60 +/- 35% and 105 +/- 33%, respectively. The tension increase is partly due to the direct pressure effect and partly due to the negative force-frequency relation in the rat atria. Introduction of inert gas increased BF and decreased Tmax. The potency of the gases was in the same order for both variables: He less than H2 less than N2.

Evaluation of smooth pursuit and voluntary saccades in nitrous oxide-induced narcosis.

The effect of inhaling nitrous oxide on pursuit eye movements (PEM) and voluntary saccades was studied in nine healthy subjects. Eye movements were recorded before, during, and 10 min after exposure for 15 min to normoxic mixtures of 14%, 21%, and 28% nitrous oxide. At all concentrations, there was a significant decrease in gain of PEM at a target velocity of 60 degrees/s, the decrease being of comparable magnitude at concentrations of 14% and 21%. By 10 min after exposure to nitrous oxide, the gain of PEM had recovered to pre-test values. There was also a highly significant decrease in the peak velocity of voluntary saccades at all concentrations of nitrous oxide; the decrease was more pronounced at the higher concentrations, and the existence of a dose-dependent relationship is suspected. Exposure to 21% nitrous oxide for only 2 min was enough to induce significant reduction in peak velocity of voluntary saccades. By 10 min after exposure to nitrous oxide, the peak velocity of voluntary saccades had recovered but had not reached pre-test values. The findings suggest that both PEM and voluntary saccades decrease with reduced alertness in mild narcosis. Moreover, as the effects of nitrous oxide are considered typical of inert gases in general, our findings suggest that voluntary eye movements may also be a suitable variable for use in assessing the effects of inert gas narcosis.

Effects of hydrostatic pressure, H2, N2, and He, on beating frequency of rat atria.

Hydrostatic compression to 15 MPa caused a drop in spontaneous beating frequency (BF) of isolated rat atria kept in tris solution at 37 degrees C by 30.6 +/- 7.2%. Introduction of superfusing solutions equilibrated with hydrogen (PH2: 4.9, 9, and 14 MPa, respectively), increased the BF in proportion to the hydrogen content. A hydrogen partial pressure equal to the hydrostatic pressure was calculated to reduce the bradycardia by 52.0 +/- 19.5%. Effects of nitrogen (PN2: 5 and 14 MPa) and helium (PHe: 13 and 14 MPa) were also tested. Nitrogen was found to be 1.7-2 times and helium 0.2 times as effective as hydrogen in reducing the bradycardia. Preparations compressed at 27 degrees C exhibited a more pronounced bradycardia than those kept at 37 degrees C, but 5 MPa N2 and 9 MPa H2 reversed the bradycardia to the same extent at 27 degrees C as at 37 degrees C. Tests with 4 MPa H2 showed the effect on BF to be similar, whether the gas was added during an intermediate stop in the compression (4.6 MPa) or at 10 MPa pressure. An additional hydrostatic pressure increase from 10 to 12.5 MPa eliminated the BF increase of 4 MPa hydrogen added at 10 MPa. The findings are discussed in view of the possible use of hydrogen as a breathing gas in deep sea diving.

Effects of dietary lipids on frequency and force in atrial muscle at 10 MPa.

Spontaneously beating atrial preparations, from rats fed different lipid diets, were compressed to 10 MPa. The following observations were made: Different lipid diets altered the ratio of omega-6/omega-3 polyunsaturated fatty acids of the cardiac phospholipids. Beating frequency and twitch tension at surface pressure was unaffected by the diets. Compression to 10 MPa caused a decrease in spontaneous beating frequency and an increased twitch tension in all preparations. The decrease in beating frequency was inversely related to the omega-6/omega-3 ratio. Pressure induced increase in twitch tension was not affected by the diets. N2O dissolved in the tissue bath solution partly counteracted the pressure-induced changes.

Pressure equilibration of the middle ear during ascent.

The capacity to equilibrate the middle ear with the ambient pressure depends on different factors. During descent when the clearing is active the technique is the most important factor. During ascent when the clearing is passive the status of the mucosal membranes lining the eustachian tube is believed to be of major importance. Horizontal position in air and head-up immersion in water to the neck have in earlier investigations shown to decrease the passive clearing capacity compared to vertical, head-up position in air. It was found in this study that a change from head-up position in water to prone in water did not change in clearing capacity, while head-down position in water gave a significant decrease of the clearing capacity. The results are discussed in terms of venous pressure in the neck veins in the different positions.

Effects of high hydrostatic pressure on rat atrial muscle.

Muscle preparations from rat atria were hydraulically compressed in circulating Tris-buffered solution kept at 37 degrees C. Spontaneously beating preparations decreased their beating frequency with 37.3 +/- 13.5 beats/min (22.3% +/- 6.7%, P less than 0.001) and increased their force with 2.3 +/- 1.1 mN (48.6% +/- 17.5%, P less than 0.001) when they were compressed to 10 MPa (100 atm). Decompression gave values not significantly different from precompression control values. The increase in force could in part be explained by the hyperbaric bradycardia and negative force-frequency relation. The remaining force increase seemed to be an effect of the increase in hydrostatic pressure. Changes in action potential duration and Ca2+ availability for the contractile machinery are discussed as possible mechanisms. Electrically driven preparations increased their contraction force at compression if the stimulus strength was at least 175% of the threshold. At lower stimulus levels just above threshold and at higher frequencies, inconsistent results were obtained at pressure.

Hyperbaric chamber for evaluating hydrostatic pressure effects on tissues and cells.

A chamber system is described for the study of pure hydrostatic pressure effects on tissues and cells. The small chamber has an internal volume of 7.6 liters and is rated for working pressures up to 400 ATA. Sliding doors at each end permit easy access and quick sealing. A cam-driven pump provides constant flow of physiological solution to the tissue bath containing the preparation. Connections to the pump allow a variety of test solutions to be used in the course of an experiment. The tissue bath is designed to prevent chamber gas from diffusing in to the perfusate, thus allowing for pure hydrostatic compression of the bath contents. The bath is coupled to a motorized stage to facilitate placement of recording devices once the bath is placed inside the chamber. Temperature is controlled within 0.05 degrees C of set point by thermoelectric modules coupled to a feedback amplifier. This system has been used for electrical and mechanical studies of cardiac muscle, but its versatility makes it suitable for a wide range of other biomedical applications.

Spontaneous activity of rat portal vein at normal and elevated hydrostatic pressure.

The effects of high hydrostatic pressure on the spontaneous contractile activity of isolated rat portal veins were studied. During compression, an increase of activity was seen, whereas stable elevated hydrostatic pressure gave a decrease of both frequency and time-integrated force. Decompression further reduced the activity, but all changes were reversible upon return to control pressure. During sustained high pressure the frequency of contractions was reduced by 15.9% at 25 atm, 26.4% at 50 atm, and 45.8% at 100 atm. The corresponding reductions in integrated active force were 13.7%, 16.7%, and 40.7%, respectively. Contractions caused by electrical stimulation of nerve endings left in the preparation were reduced by 44.1%, and potassium contractures were reduced by only 15.3% at 100 atm. It is concluded that inhibition of activity in rat portal vein at high hydrostatic pressure is due in part to effects on the smooth muscle membrane.

Rate of pressure change and hyperbaric bradycardia in the mouse sinus node.

Sinus node preparations from mice were hydraulically compressed at 10, 100, and 500 atm x min-1 in Tyrode's solution at 27 degrees C. At the highest compression rate, both a delay and a more pronounced beating frequency response to pressure was seen. The delayed reaction is ascribed to either adiabatic effects or a time-delay in conformational changes in the pacemaker cell membrane. The potentiating effect of a high compression rate could be eliminated by autonomic blockade (atropine and practolol).

Influence of nitrous oxide, nitrogen, neon, and helium on the beating frequency of the mouse sinus node at high pressure.

The beating frequency (BF) reducing effect of 150 atm of hydrostatic pressure on mammalian cardiac pacemaker tissue (hyperbaric bradycardia) was counteracted by dissolved gas only if the gas was added after hydrostatic compression. The effect on BF seemed to be related to the narcotic potency of the gas and the effect was reversible. The gases tested were N2O, N2, Ne, and He, in decreasing order of potency. If N2O was added at a moderately raised ambient pressure prior to hydrostatic compression to 150 atm, there was no difference in the degree of hyperbaric bradycardia, compared to compression without gas. During decompression, however, experiments performed with gas showed a significantly higher gain in BF compared to experiments without gas. Autonomic blockade seemed to eliminate the difference between decompression with and without N2O. The results demonstrate that N2O, N2, and Ne, and to a small extent He, may counteract the retarding effect that increased hydrostatic pressure has on cardiac pacemaker activity. These effects on the cardiac pacemaker are similar both to the effects of increased hydrostatic pressure and of gases at elevated pressures on the central nervous system, but some important differences remain to be explained.