Closed-circuit Oxygen Research Articles

Altitude diving on a closed-circuit oxygen rebreather: A case report

Closed-circuit rebreather diving is becoming more common. Rebreathers are complicated, adding to the stress of diving. Also adding to this complexity in the presented case is diving at a high-altitude cold-water reservoir in Colorado. One diver experienced an oxygen-induced seizure at depth. The other diver had a rapid ascent with loss of consciousness. As will be seen in this case, two experienced divers were able to recover from a possible devastating dive. Fortunately, they both returned to their pre-dive baseline health. Dive planning is important, but as in this case, dive execution is paramount. This is a clinical case for an uncommon event that presented to an emergency department.

The transition from day-to-night activity is a risk factor for the development of CNS oxygen toxicity in the diurnal fat sand rat (Psammomys obesus)

ABSTRACTPerformance and safety are impaired in employees engaged in shift work. Combat divers who use closed-circuit oxygen diving apparatus undergo part of their training during the night hours. The greatest risk involved in diving with such apparatus is the development of central nervous system oxygen toxicity (CNS-OT). We investigated whether the switch from day-to-night activity may be a risk factor for the development of CNS-OT using a diurnal animal model, the fat sand rat (Psammomys obesus). Animals were kept on a 12:12 light–dark schedule (6 a.m. to 6 p.m. at 500 lx). The study included two groups: (1) Control group: animals were kept awake and active during the day, between 09:00 and 15:00. (2) Experimental group: animals were kept awake and active during the night, between 21:00 and 03:00, when they were exposed to dim light in order to simulate the conditions prevalent during combat diver training. This continued for a period of 3 weeks, 5 days a week. On completion of this phase, 6-sulphatoxymelatonin (6-SMT) levels in urine were determined over a period of 24 h. Animals were then exposed to hyperbaric oxygen (HBO). To investigate the effect of acute melatonin administration, melatonin (50 mg/kg) or its vehicle was administered to the animals in both groups 20 min prior to HBO exposure. After the exposure, the activity of superoxide dismutase, catalase and glutathione peroxidase was measured, as were the levels of neuronal nitric oxide synthase (nNOS) and overall nitrotyrosylation in the cortex and hippocampus. Latency to CNS-OT was significantly reduced after the transition from day-to-night activity. This was associated with alterations in the level of melatonin metabolites secreted in the urine. Acute melatonin administration had no effect on latency to CNS-OT in either of the groups. Nevertheless, the activity of superoxide dismutase and catalase, as well as nitrotyrosine and nNOS levels, were altered in the hippocampus following melatonin administration. On the basis of these results, we suggest that a switch from diurnal to nocturnal activity may represent an additional risk factor for the development of CNS-OT. Utilizing a diurnal animal model may contribute to our understanding of the heightened risk of developing CNS-OT when diving with closed-circuit oxygen apparatus at night.

Recovery from central nervous system oxygen toxicity in the rat at oxygen pressures between 100 and 300 kPa

No symptoms related to central nervous system (CNS) oxygen toxicity have been reported when diving with oxygen rebreathers at depths shallower than 3 msw. We hypothesised that recovery from CNS oxygen toxicity will take place when the PO(2) is less than 130 kPa. We exposed rats to a high PO(2) (mainly 608 kPa) to produce CNS oxygen toxicity. The latency to the first electrical discharge (FED) preceding convulsions was determined as the animal's control latency. Thereafter, the rat was exposed to the same PO(2) for 60% of its latency, then to a lower PO(2) for 15 min (sufficient time for full recovery in normoxia), and finally to the high PO(2) again until appearance of the FED. If recovery from CNS oxygen toxicity takes place during the interim period, the latency for the final exposure to the high oxygen pressure should not be shorter than the control. The latencies to CNS oxygen toxicity for exposure to the high oxygen pressure after a 15-min interim period at 21, 101, 132, 203, 304, 405, and 456 kPa were 110, 110, 125, 94, 85, 54 and 38% of the control value, respectively. Only after the last two interim pressures were the latencies significantly shorter than control values. The remaining latencies were not significantly different from 100%. Recovery from CNS oxygen toxicity in the rat takes place at a PO(2) anywhere between 21 and 304 kPa. The present findings support our previous suggestion that recovery from CNS oxygen toxicity in humans will take place at a PO(2) below 130 kPa. If our findings are corroborated by further human studies, this will justify including recovery in the algorithm for CNS oxygen toxicity in closed-circuit oxygen divers.

Effects of hyperoxia on biomarkers of oxidative stress in closed-circuit oxygen military divers

Oxygen toxicity is a problem in diving which can have fatal consequences in the water. When divers use closed-circuit oxygen rebreathing apparatus they are taking only oxygen 100% and this hyperoxic exposure increases the generation of reactive oxygen species (ROS) in biological tissues. The objective of the present study is to evaluate the effects of hyperoxia on biomarkers of oxidative stress in closed-circuit oxygen military divers. Fifteen professional divers of Spanish Navy Diving Centre participated in a training program which consisted of one-hour immersion at seven metres of depth breathing oxygen 100% with closed-circuit oxygen rebreathing apparatus. The training went on two or three times per week for the first six weeks and once a week for the last six weeks. Serum total antioxidant status (TAS), levels of glutathione peroxidase (GPx), nitrates (NO3(-)) and urinary concentrations of 15-isoprostane F2t were measured. The results show that TAS decreased significantly after 6 weeks (mean 1.38 versus 1.23 mmol/l), with a slight increase at the end (mean 1.31 mmol/l). GPx and F2-isoprostanes were significantly lower after 6 and 12 weeks and NO3(-) was significantly lower after 6 weeks and remained unchanged until the end. In summary, professional divers who use closed-circuit apparatus and therefore breathe oxygen 100%, do not suffer an important oxidative hyperoxia-induced stress, probably due an adaptive process after hyperoxia. The age and good physical form of the subjects studied could probably enhance the adaptive process to hyperoxia.

Performance Characteristics of the Second-Generation Remote Emergency Medical Oxygen Closed-Circuit Rebreather

Closed-circuit oxygen rebreathers may provide high concentrations of oxygen at extremely low flow rates appropriate for field use with limited oxygen supplies. The performance of the preproduction, second-generation remote emergency medical oxygen (REMO(2)) system developed for Divers Alert Network was evaluated. The unidirectional circuit was made up of a solid, prepackaged CO(2) scrubber canister (984 +/- 14 [SD] g scrubber mass), standard 22-mm-inside-diameter anesthesia circuit hoses, 5-L breathing bag, 5-cm H(2)O positive end-expiratory pressure valve, and oronasal mask. Oxygen flow, inspired oxygen, expired CO(2), peak inspired and expired mask pressures, time to reach scrubber canister saturation or "breakthrough" (postscrubber CO(2) concentration reaching 3.8 mm Hg), and subject tolerance were measured under standard laboratory conditions. Six trials were completed using healthy volunteers (94.7 +/- 19.6 kg). Five of the 6 completed trials did not reach breakthrough at the planned trial limit of 8 hours. Mean average oxygen flow rate was 1.00 +/- 0.17 L x min(-1). Mean peak inspired and expired mask pressures were -5.0 +/- 1.9 and 6.5 +/- 1.9 cm H(2)O, respectively. Subjects generally reported good tolerance to circuit breathing. The second-generation REMO(2) was well tolerated by healthy subjects during 8-hour laboratory evaluation trials. The device provided high mean inspired oxygen fractions at low mean oxygen flow rates, relatively modest mean maximal inspired and expired pressures, and excellent scrubber canister duration. Further evaluation of field performance with a patient population is warranted.

The Use of Closed-Circuit Oxygen in the Himalayas

Two days before the first ascent of Mt. Everest in 1953, Tom Bourdillon and Charles Evans climbed to within 90 m of the summit at unprecedented speeds. By breathing pure oxygen from a closed circuit, the pair were able to obtain an enormous physiological advantage. Unfortunately, due to a malfunction in Evans's circuit, the pair abandoned their attempt on the South Summit. For many who used the circuit in the 1930s and 1950s, the device proved too heavy, uncomfortable, and tiring for mountaineering. These factors, together with the wider ethical concerns of using supplemental oxygen at altitude, have meant that closed-circuit oxygen has been ignored for more than 50 years. In this article the authors will attempt to describe the history of this discarded circuit and the experience of those who utilized it.

Modeling pulmonary and CNS O(2) toxicity and estimation of parameters for humans.

The power expression for cumulative oxygen toxicity and the exponential recovery were successfully applied to various features of oxygen toxicity. From the basic equation, we derived expressions for a protocol in which PO(2) changes with time. The parameters of the power equation were solved by using nonlinear regression for the reduction in vital capacity (DeltaVC) in humans: %DeltaVC = 0.0082 x t(2)(PO(2)/101.3)(4.57), where t is the time in hours and PO(2) is expressed in kPa. The recovery of lung volume is DeltaVC(t) = DeltaVC(e) x e(-(-0.42 + 0.00379PO(2))t), where DeltaVC(t) is the value at time t of the recovery, DeltaVC(e) is the value at the end of the hyperoxic exposure, and PO(2) is the prerecovery oxygen pressure. Data from different experiments on central nervous system (CNS) oxygen toxicity in humans in the hyperbaric chamber (n = 661) were analyzed along with data from actual closed-circuit oxygen diving (n = 2,039) by using a maximum likelihood method. The parameters of the model were solved for the combined data, yielding the power equation for active diving: K = t(2) (PO(2)/101.3)(6.8), where t is in minutes. It is suggested that the risk of CNS oxygen toxicity in diving can be derived from the calculated parameter of the normal distribution: Z = [ln(t) - 9.63 +3.38 x ln(PO(2)/101.3)]/2.02. The recovery time constant for CNS oxygen toxicity was calculated from the value obtained for the rat, taking into account the effect of body mass, and yielded the recovery equation: K(t) = K(e) x e(-0.079t), where K(t) and K(e) are the values of K at time t of the recovery process and at the end of the hyperbaric oxygen exposure, respectively, and t is in minutes.

Latency to CNS oxygen toxicity in rats as a function of PCO(2) and PO(2).

Central nervous system (CNS) oxygen toxicity can occur as convulsions and loss of consciousness, without any premonitory symptoms. We have made a quantitative study of the effect of inspired carbon dioxide on sensitivity to oxygen toxicity in the rat. Rats were exposed to four oxygen pressures (PO(2); 456, 507, 608 and 709 kPa) and an inspired partial pressure of carbon dioxide (PCO(2)) in the range 0-12 kPa until the appearance of the electroencephalograph first electrical discharge (FED) that precedes the clinical convulsions. Exposures were conducted at a thermoneutral temperature of 27 degrees C. Latency to the FED decreased linearly with the increase in PCO(2) at all four PO(2) values studied. This decrease, which is probably related to the cerebral vasodilatory effect of carbon dioxide, reached a minimal value that remained constant on further elevation of PCO(2). The slopes (absolute value) and intercepts of latency to the FED as a function of carbon dioxide decreased with the increase in PO(2). This log-linear relationship made possible the derivation of equations that describe latency to the FED as a function of both PO(2) and PCO(2) in the PCO(2) - dependent range: Latency (min) = e((5.19-0.0040)(P)(O(2)))-e((2.77-0.0034)(P)(O(2))) x PCO(2) (kPa), and in the PCO(2)-independent range: Latency(min) = e((2.44-0. 0009)(P)(O(2))). A PCO(2) as low as 1 kPa significantly reduced the latency to the FED. It is suggested that in closed-circuit oxygen diving, any accumulation of carbon dioxide should be avoided in order to minimize the risk of CNS oxygen toxicity.

Thermal status of wet-suited divers using closed circuit O2 apparatus in sea water of 17-18.5 degrees C.

A wet suit may not provide adequate thermal protection when diving in moderately cold water (17-18 degrees C), and any resultant mild hypothermia may impair performance during prolonged diving. We studied heat exchange during a dive to a depth of 5 m in sea water (17-18.5 degrees C) in divers wearing a full wet suit and using closed-circuit oxygen breathing apparatus. Eight fin swimmers dived for 3.1 h and six underwater scooter (UWS) divers propelled themselves through the water for 3.7 h. The measurements taken throughout the dive were the oxygen pressure in the cylinder and skin and rectal temperatures (Tre). Each subject also completed a cold score questionnaire. The Tre decreased continuously in all subjects. Oxygen consumption in the fin divers (1.40 l.min-1) was higher than that of the UWS divers (1.05 l.min-1). The mean total insulation was 0.087 degree C.m2.W-1 in both groups. Mean body insulation was 37% of the total insulation (suit insulation was 63%). The reduction in Tre over the 1st hour was related to subcutaneous fat thickness. There was a correlation between cold score and Tre at the end of 1 h, but not after that. A full wet suit does not appear to provide adequate thermal protection when diving in moderately cold water.

An automatic, closed-circuit oxygen consumption apparatus for small animals.

An apparatus suitable for the continuous measurement of oxygen consumption of rats and mice is described. The system uses a motorized syringe dispenser to deliver fixed volumes of oxygen to a closed animal chamber. The dispenser is controlled by a micro-differential pressure switch to maintain chamber pressure slightly above ambient. The rate of oxygen consumption is determined by timing the interval between successive operations of the dispenser. The system has proved suitable for a range of experimental conditions and treatments.