Hypoxia signatures in closed-circuit rebreather divers.

INTRODUCTION: Faults or errors during use of closed-circuit rebreathers (CCRs) can cause hypoxia. Military aviators face a similar risk of hypoxia and undergo awareness training to determine their 'hypoxia signature', a personalised, reproducible set of symptoms. We aimed to establish a hypoxia signature among divers, and to investigate their ability to detect hypoxia and self-rescue while cognitively overloaded. METHODS: Eight CCR divers and 12 scuba divers underwent an initial unblinded hypoxia exposure followed by three trials; a second hypoxic trial and two normoxic trials in randomised order. Hypoxia was induced by breathing on a CCR with no oxygen supply. Subjects pedalled on a cycle ergometer while playing a neurocognitive computer game to simulate real world task loading. Subjects identified hypoxia symptoms by pointing to a board listing common hypoxia symptoms, and were instructed to perform a 'bailout' procedure to mimic self-rescue if they perceived hypoxia. Divers were prompted to bailout if peripheral oxygen saturation fell to 75%, or after six minutes during normoxic trials. Subsequently we interviewed subjects to determine their ability to distinguish hypoxia from normoxia. RESULTS: Ninety-five percent of subjects (19/20) showed agreement between unblinded and blinded hypoxia symptoms. Subjects correctly identified the gas mixture in 85% of the trials. During unblinded hypoxia, only 25% (5/20) of subjects performed unprompted bailout. Fifty-five percent of subjects (11/20) correctly performed the bailout but only when prompted, while 15% (3/20) were unable to bailout despite prompting. During blinded hypoxia 45% of subjects (9/20) performed the bailout unprompted while 15% (3/20) remained unable to bailout despite prompting. CONCLUSIONS: Although our data support a normobaric hypoxia signature among both CCR and scuba divers under experimental conditions, most subjects were unable to recognise hypoxia in real time and perform a self-rescue unprompted, although this improved in the second hypoxia trial. These results do not support hypoxia exposure training for CCR divers.

Plasma gelsolin modulates the production and fate of IL-1ß-containing microparticles following high-pressure exposure and decompression.

Plasma gelsolin (pGSN) levels fall in association with diverse inflammatory conditions. We hypothesized that pGSN would decrease due to the stresses imposed by high pressure and subsequent decompression, and repletion would ameliorate injuries in a murine decompression sickness (DCS) model. Research subjects were found to exhibit a modest decrease in pGSN level while at high pressure and a profound decrease after decompression. Changes occurred concurrent with elevations of circulating microparticles (MPs) carrying interleukin (IL)-1ß. Mice exhibited a comparable decrease in pGSN after decompression along with elevations of MPs carrying IL-1ß. Infusion of recombinant human (rhu)-pGSN into mice before or after pressure exposure abrogated these changes and prevented capillary leak in brain and skeletal muscle. Human and murine MPs generated under high pressure exhibited surface filamentous actin (F-actin) to which pGSN binds, leading to particle lysis. In addition, human neutrophils exposed to high air pressure exhibit an increase in surface F-actin that is diminished by rhu-pGSN resulting in inhibition of MP production. Administration of rhu-pGSN may have benefit as prophylaxis or treatment for DCS.NEW & NOTEWORTHY Inflammatory microparticles released in response to high pressure and decompression express surface filamentous actin. Infusion of recombinant human plasma gelsolin lyses these particles in decompressed mice and ameliorates particle-associated vascular damage. Human neutrophils also respond to high pressure with an increase in surface filamentous actin and microparticle production, and these events are inhibited by plasma gelsolin. Gelsolin infusion may have benefit as prophylaxis or treatment for decompression sickness.

Safety proposals for freediving time limits should consider the metabolic-rate dependence of oxygen stores depletion.

INTRODUCTION: There is no required training for breath-hold diving, making dissemination of safety protocols difficult. A recommended breath-hold dive time limit of 60 s was proposed for amateur divers. However, this does not consider the metabolic-rate dependence of oxygen stores depletion. We aimed to measure the effect of apnoea time and metabolic rate on arterial and tissue oxygenation. METHODS: Fifty healthy participants (23 (SD 3) y, 22 women) completed four periods of apnoea for 60 s (or to tolerable limit) during rest and cycle ergometry at 20, 40, and 60 W. Apnoea was initiated after hyperventilation to achieve PETCO2 of approximately 25 mmHg. Pulse oximetry, frontal lobe oxygenation, and pulmonary gas exchange were measured throughout. We defined hypoxia as SpO2 < 88%. RESULTS: Static and exercise (20, 40, 60 W) breath-hold break times were 57 (SD 7), 50 (11), 48 (11), and 46 (11) s (F [2.432, 119.2] = 32.0, P < 0.01). The rise in PETCO2 from initiation to breaking of apnoea was dependent on metabolic rate (time × metabolic rate interaction; F [3,147] = 38.6, P < 0.0001). The same was true for the fall in SpO2 (F [3,147] = 2.9, P = 0.03). SpO2 fell to < 88% on 14 occasions in eight participants, all of whom were asymptomatic. CONCLUSIONS: Independent of the added complexities of a fall in ambient pressure on ascent, the effect of apnoea time on hypoxia depends on the metabolic rate and is highly variable among individuals. Therefore, we contend that a universally recommended time limit for breath-hold diving or swimming is not useful to guarantee safety.

Microparticle and interleukin-1ß production with human simulated compressed air diving.

Production of blood-borne microparticles (MPs), 0.1-1 µm diameter vesicles, and interleukin (IL)-1ß in response to high pressure is reported in lab animals and associated with pathological changes. It is unknown whether the responses occur in humans, and whether they are due to exposure to high pressure or to the process of decompression. Blood from research subjects exposed in hyperbaric chambers to air pressure equal to 18 meters of sea water (msw) for 60 minutes or 30 msw for 35 minutes were obtained prior to and during compression and 2 hours post-decompression. MPs and intra-particle IL-1ß elevations occurred while at pressure in both groups. At 18 msw (n = 15) MPs increased by 1.8-fold, and IL-1ß by 7.0-fold (p < 0.05, repeated measures ANOVA on ranks). At 30 msw (n = 16) MPs increased by 2.5-fold, and IL-1ß by 4.6-fold (p < 0.05), and elevations persisted after decompression with MPs elevated by 2.0-fold, and IL-1ß by 6.0-fold (p < 0.05). Whereas neutrophils incubated in ambient air pressure for up to 3 hours ex vivo did not generate MPs, those exposed to air pressure at 180 kPa for 1 hour generated 1.4 ± 0.1 MPs/cell (n = 8, p < 0.05 versus ambient air), and 1.7 ± 0.1 MPs/cell (p < 0.05 versus ambient air) when exposed to 300 kPa for 35 minutes. At both pressures IL-1ß concentration tripled (p < 0.05 versus ambient air) during pressure exposure and increased 6-fold (p < 0.05 versus ambient air) over 2 hours post-decompression. Platelets also generated MPs but at a rate about 1/100 that seen with neutrophils. We conclude that production of MPs containing elevated concentrations of IL-1ß occur in humans during exposure to high gas pressures, more so than as a response to decompression. While these events may pose adverse health threats, their contribution to decompression sickness development requires further study.

Delayed hyperbaric oxygen therapy for severe arterial gas embolism following scuba diving: a case report.

We present the case of a 42-year-old female who was critically ill due to an arterial gas embolism (AGE) she experienced while diving in Maui, Hawaii. She presented with shortness of breath and dizziness shortly after surfacing from a scuba dive and then rapidly lost consciousness. The diver then had a complicated hospital course: persistent hypoxemia (likely secondary to aspiration) requiring intubation; markedly elevated creatine kinase; atrial fibrillation requiring cardioversion; and slow neurologic improvement. She had encountered significant delay in treatment due to lack of availability of local hyperbaric oxygen (HBO2) therapy. Our case illustrates many of the complications that can occur when a patient suffers a severe AGE. These cases may occur even without a history of rapid ascent or risk factors for pulmonary barotrauma, and it is imperative that they be recognized and treated as quickly as possible with HBO2. Unfortunately, our case also highlights the challenges in treating critically ill divers, particularly with the growing shortage of 24/7 hyperbaric chambers able to treat these ICU-level patients.

Sleep deficits in the High Arctic summer in relation to light exposure and behaviour: use of melatonin as a countermeasure.

BACKGROUND: There are conflicting reports regarding seasonal sleep difficulties in polar regions. Herein we report differences in actigraphic sleep measures between two summer trials (collected at Canadian Forces Station Alert, 82.5°N, in 2012 and 2014) and evaluate exogenous melatonin for preventing/treating circadian phase delay due to nocturnal light exposure. METHODS: Subjects wore actigraphs continuously to obtain sleep data. Following seven days of actigraphic recording the subjects filled out questionnaires regarding sleep difficulty and psychosocial parameters and subsequently remained in dim light conditions for 24 hours, during which saliva was collected bihourly to measure melatonin. During Trial 2, individuals who reported difficulty sleeping were prescribed melatonin, and a second saliva collection was conducted to evaluate the effect of melatonin on the circadian system. RESULTS: Trial 1 subjects collectively had late dim light melatonin onsets and difficulty sleeping; however, the Trial 2 subjects had normally timed melatonin rhythms, and obtained a good quantity of high-quality sleep. Nocturnal light exposure was significantly different between the trials, with Trial 1 subjects exposed to significantly more light between 2200 and 0200h. Melatonin treatment during Trial 2 led to an improvement in the subjective sleep difficulty between the pre- and post-treatment surveys; however there were no significant differences in the objective measures of sleep. CONCLUSIONS: The difference in sleep and melatonin rhythms between research participants in June 2012 and June 2014 is attributed to the higher levels of nocturnal light exposure in 2012. The avoidance of nocturnal light is likely to improve sleep during the Arctic summer.

Light treatment improves sleep quality and negative affectiveness in high arctic residents during winter.

The seasonal extremes of photoperiod in the high Arctic place particular strain on the human circadian system, which leads to trouble sleeping and increased feelings of negative affect in the winter months. To qualify for our study, potential participants had to have been at Canadian Forces Station (CFS) Alert (82° 30' 00″ N) for at least 2 weeks. Subjects filled out questionnaires regarding sleep difficulty, psychological well-being and mood and wore Actigraphs to obtain objective sleep data. Saliva was collected at regular intervals on two occasions, 2 weeks apart, to measure melatonin and assess melatonin onset. Individuals with a melatonin rhythm that was in disaccord with their sleep schedule were given individualized daily light treatment interventions based on their pretreatment salivary melatonin profile. The light treatment prescribed to seven of the twelve subjects was effective in improving sleep quality both subjectively, based on questionnaire results, and objectively, based on the actigraphic data. The treatment also caused a significant reduction in negative affect among the participants. Since the treatment is noninvasive and has minimal associated side effects, our results support the use of the light visors at CFS Alert and other northern outposts during the winter for individuals who are experiencing sleep difficulty or low mood.