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Background The narcotic effect of hyperbaric nitrogen is most pronounced in air-breathing divers because it impairs diver’s cognitive and behavioral performance, and limits the depth of dive profiles. We aimed to investigate the cognitive effects of simulated (500 kPa) air environments in recreational SCUBA divers, revealed by auditory event-related potentials (AERPs). Methods A total of 18 healthy volunteer recreational air SCUBA divers participated in the study. AERPs were recorded in pre-dive, deep-dive, and post-dive sessions. Results False-positive score variables were found with significantly higher differences and longer reaction times of hits during deep-dive and post-dive than pre-dive sessions. Also, P3 amplitudes were significantly reduced and peak latencies were prolonged during both deep-dive and post-dive compared with pre-dive sessions. Conclusion We observed that nitrogen narcosis at 500 kPa pressure in the dry hyperbaric chamber has a mild-to-moderate negative effect on the cognitive performance of recreational air SCUBA divers, which threatened the safety of diving. Although relatively decreased, this effect also continued in the post-dive sessions. These negative effects are especially important for divers engaged in open-sea diving. Our results show crucial implications for the kinds of control measures that can help to prevent nitrogen narcosis and diving accidents at depths up to 40 msw.

Divers commonly breathe air, containing nitrogen. Nitrogen under hyperbaric conditions is a narcotic gas. In dives beyond a notional threshold of 30 m depth (405 kPa) this can cause cognitive impairment, culminating in accidents due to poor decision making. Helium is known to have no narcotic effect. This study explored potential approaches to developing an electroencephalogram (EEG) functional connectivity metric to measure narcosis produced by nitrogen at hyperbaric pressures. Twelve human participants (five female) breathed air and heliox (in random order) at 284 and 608 kPa while recording 32-channel EEG and psychometric function. The degree of spatial functional connectivity, estimated using mutual information, was summarized with global efficiency. Air-breathing at 608 kPa (experienced as mild narcosis) caused a 35% increase in global efficiency compared to surface air-breathing (mean increase = 0.17, 95% CI [0.09-0.25], p = 0.001). Air-breathing at 284 kPa trended in a similar direction. Functional connectivity was modestly associated with psychometric impairment (mixed-effects model r

(Wilmshurst P, Clamp M. Impaired consciousness when scuba diving associated with vasovagal syncope. Diving and Hyperbaric Medicine. 2020 December 20;50(4):421–423. doi: 10.28920/dhm50.4.421-423. PMID: 33325026.) Introduction: Drowning is likely to result from impairment of consciousness when scuba diving. Causes include toxic effects of breathing gas, including nitrogen narcosis and oxygen toxicity, and arterial gas embolism. Methods: Review of the medical records of scuba divers who had impaired consciousness underwater that could not be attributed to toxic effects of breathing gas or arterial gas embolism. Results: Four scuba divers had episodes of impaired consciousness when at shallow depths (8−18 m) underwater. The descriptions of the episodes were very similar. Three had histories of recurrent episodes of vasovagal syncope on land. Conclusions: Absence of other causes for their impaired consciousness underwater leads to the conclusion that the probable cause was vasovagal syncope.

Introduction: Cold water imposes many risks to the diver. These risks include decompression illness, physical and cognitive impairment, and hypothermia. Cognitive impairment can be estimated using a critical flicker fusion frequency (CFFF) test, but this method has only been used in a few studies conducted in an open water environment. We studied the effect of the cold and a helium-containing mixed breathing gas on the cognition of closed circuit rebreather (CCR) divers. Materials and Methods: Twenty-three divers performed an identical dive with controlled trimix gas with a CCR device in an ice-covered quarry. They assessed their thermal comfort at four time points during the dive. In addition, their skin temperature was measured at 5-min intervals throughout the dive. The divers performed the CFFF test before the dive, at target depth, and after the dive. Results: A statistically significant increase of 111.7% in CFFF values was recorded during the dive compared to the pre-dive values (p < 0.0001). The values returned to the baseline after surfacing. There was a significant drop in the divers’ skin temperature of 0.48°C every 10 min during the dive (p < 0.001). The divers’ subjectively assessed thermal comfort also decreased during the dive (p = 0.01). Conclusion: Our findings showed that neither extreme cold water nor helium-containing mixed breathing gas had any influence on the general CFFF profile described in the previous studies from warmer water and where divers used other breathing gases. We hypothesize that cold-water diving and helium-containing breathing gases do not in these diving conditions cause clinically relevant cerebral impairment. Therefore, we conclude that CCR diving in these conditions is safe from the perspective of alertness and cognitive performance.

Background Physiological changes are induced by immersion, swimming and using diving equipment. Divers must be fit to dive. Using medication may impact the capacity to adapt to hyperbaric conditions. The aim of this systematic review is to assess the interaction of diving/hyperbaric conditions and medication and to provide basic heuristics to support decision making regarding fitness to dive in medicated divers. Methods This was a systematic review of human and animal studies of medications in the hyperbaric environment. Studies were subdivided into those describing a medication/hyperbaric environment interaction and those concerned with prevention of diving disorders. Studies without a relation to diving with compressed air, and those concerning oxygen toxicity, hyperbaric oxygen therapy or the treatment of decompression sickness were excluded. Results Forty-four studies matched the inclusion criteria. Animal studies revealed that diazepam and valproate gave limited protection against the onset of the high-pressure neurological syndrome. Lithium had a protective effect against nitrogen-narcosis and losartan reduced cardiac changes in repetitive diving. Human studies showed no beneficial or dangerous pressure-related interactions. In prevention of diving disorders, pseudoephedrine reduced otic barotrauma, vitamins C and E reduced endothelial dysfunction after bounce diving and hepatic oxidative stress in saturation diving. Discussion and conclusions Animal studies revealed that psycho-pharmaceuticals can limit the onset of neurologic symptoms and cardiovascular protective drugs might add a potential protective effect against decompression sickness. No evidence of significant risks due to changes in pharmacologic mechanisms were revealed and most medication is not a contraindication to diving. For improving decision making in prescribing medicine for recreational and occupational divers and to enhance safety by increasing our understanding of pharmacology in hyperbaric conditions, future research should focus on controlled human studies.

Dysbarism is a general term which includes the signs and symptoms that can manifest when the body is subject to an increase or a decrease in the atmospheric pressure which occurs either at a rate or duration exceeding the capacity of the body to adapt safely. In the following review, we take dysbarisms into account for our analysis. Starting from the underlying physical laws, we will deal with the pathologies that can develop in the most frequently affected areas of the body, as the atmospheric pressure varies when acclimatization fails. Manifestations of dysbarism range from itching and minor pain to neurological symptoms, cardiac collapse, and death. Overall, four clinical pictures can occur: decompression illness, barotrauma, inert gas narcosis, and oxygen toxicity. We will then review the clinical manifestations and illustrate some hints of therapy. We will first introduce the two forms of decompression sickness. In the next part, we will review the barotrauma, compression, and decompression. The last three parts will be dedicated to gas embolism, inert gas narcosis, and oxygen toxicity. Such an approach is critical for the effective treatment of patients in a hostile environment, or treatment in the emergency room after exposure to extreme physical or environmental factors.

The scope of extreme-environment diving defined within this work encompasses diving modes outside of the generally accepted no-decompression, open-circuit, compressed-air diving limits on selfcontained underwater breathing apparatus (scuba) in temperate or warmer waters. Extreme-environment diving is scientifically and politically interesting. The scientific diving operational safety and medical framework is the cornerstone from which diving takes place in the scientific community. From this effective baseline, as evidenced by decades of very low DCS incidence rates, the question of whether compressed air is the best breathing medium under pressure was addressed with findings indicating that in certain depth ranges a higher fraction of oxygen (while not exceeding a PC 2 of 1.6 ATA) and a lower fraction of nitrogen result in extended bottom times and a more efficient decompression. Extremeenvironment diving under ice presents a set of physiological. equipment, training and operational challenges beyond regular diving that have also been met through almost 50 years of experience as an underwater research tool. Diving modes such as mixed-gas, surface-supplied diving with helmets may mitigate risk factors that the diver incurs as a result of depth, inert gas narcosis or gas consumption. A close approximation of inert gas loading and decompression status monitoring is a function met by dive computers, a necessity in particular when the diver ventures outside of the single-dive profile into the realm of multi-level, multi-day repetitive diving or decompression diving. The monitoring of decompression status in extreme environments is now done exclusively through the use of dive computers and evaluations of the performance of regulators under ice have determined the characteristics of the next generation of life-support equipment for extreme-environment diving for science. These polar, deep and contaminated water environments require risk assessment that analyzes hazards such as cold stress, hydration, overheating, narcosis, equipment performance and decompression sickness. Scientific diving is a valuable research tool that has become an integral methodology in the pursuit of scientific questions in extreme environments of polar regions, in contaminated waters, and at depth.

Divers try to limit risks associated with their sport, for instance by breathing enriched air nitrox (EANx) instead of air. This double blinded, randomized trial was designed to see if the use of EANx could effectively improve cognitive performance while diving., info:eu-repo/semantics/published

We report a rare case of syndrome of inappropriate antidiuretic hormone secretion (SIADH) associated with amyotrophic lateral sclerosis (ALS). A 69-year-old man was admitted to our hospital with sustained hyponatremia. Hyposmolality with elevated urinary osmolality and sodium excretion was observed, which indicated SIADH. The treatment for SIADH was challenging; the patient developed carbon dioxide narcosis, which led to the diagnosis of ALS. After the initiation of noninvasive positive-pressure ventilation, the patient's serum sodium concentration normalized and became stable. Thus, ALS should be recognized as a possible cause of SIADH in the clinical setting.

Introduction Gas narcosis impairs divers when diving deeper. Pupillometry is sensitive to alcohol intoxication and it has been used in anaesthesia to assess nitrous oxide narcosis. It is a potential novel method to quantify narcosis in diving. The aim of this study was to evaluate pupillometry for objective measurement of narcosis during exposure to hyperbaric air or nitrous oxide. Method Pupil size in 16 subjects was recorded directly at surface pressure and during air breathing at 608 kPa (equivalent to 50 metres' seawater depth) in a hyperbaric chamber. Another 12 subjects were exposed to nitrous oxide at end-tidal percentages of 20, 30 and 40% in random order at surface pressure. Pupil size and pupil light reflex were recorded at baseline and at each level of nitrous oxide exposure. Results Pupil size did not significantly change during exposure to hyperbaric air or nitrous oxide. The pupil light reflex, evaluated using percentage constriction and minimum diameter after exposure to a light stimulus, was affected significantly only during the highest nitrous oxide exposure - an end-tidal level of 40%. Conclusion Pupillometry is insensitive to the narcotic effect of air at 608 kPa in the dry hyperbaric environment and to the effects of low dose nitrous oxide. Pupillometry is not suitable as a monitoring method for gas narcosis in diving.

Although many factors contributing to inert gas narcosis onset and severity have been put forward, the available evidence is not particularly strong. Using objective criteria, we have assessed brain impairment associated with narcosis under various environmental diving conditions. 40 volunteers performed a no-decompression dive (33 m for 20 min) either in a dry chamber, a pool or open sea. They were assessed by critical flicker fusion frequency before the dive, upon arriving at depth, 5 min before ascent, on surfacing and 30 min post-dive. Compared to the pre-dive value, the mean value of each measurement was significantly different. An increase of flicker fusion to 105.00±0.69% when arriving at depth is followed by a decrease to 94.05±0.65%. This impairment persists when surfacing and 30 min post-dive, decreasing further to 96.36±0.73% and 96.24±0.73%, respectively. Intragroup comparison failed to demonstrate any statistical difference. When objectively measured narcosis may not be influenced by external factors other than pressure and gas. This might be of importance for training to avoid any over- or underestimation of the severity of narcosis based only on subjective symptoms.

Diving narcosis results from the complex interaction of gases, activities, and environmental conditions. We hypothesized that these interactions could be separated into their component parts. Where previous studies have tested single cognitive tasks sequentially, we varied inspired partial pressures of CO2, N2, and O2 in immersed, exercising subjects while assessing multitasking performance with the Multi-Attribute Task Battery II (MATB-II) flight simulator. Cognitive performance was tested under 20 conditions of gas partial pressure and exercise in 42 male subjects meeting U.S. Navy age and fitness profiles. Inspired nitrogen (N2) and oxygen (O2) partial pressures were 0, 4.5, and 5.6 ATA and 0.21, 1.0, and 1.22 ATA, respectively, at rest and during 100-W immersed exercise with and without 0.075-ATA CO2. Linear regression modeled the association of gas partial pressure with task performance while controlling for exercise, hypercapnic ventilatory response, dive training, video game frequency, and age. Subjects served as their own controls. Impairment of memory, attention, and planning, but not motor tasks, was associated with N2 partial pressures >4.5 ATA. Sea level O2 at 0.925 ATA partially rescued motor and memory reaction time impaired by 0.075-ATA CO2; however, at hyperbaric pressures an unexpectedly strong interaction between CO2, N2, and exercise caused incapacitating narcosis with amnesia, which was augmented by O2. Perception of narcosis was not correlated with actual scores. The relative contributions of factors associated with diving narcosis will be useful to predict the effects of gas mixtures and exercise conditions on the cognitive performance of divers. The O2 effects are consistent with O2 narcosis or enhanced O2 toxicity.

Gases that are not metabolized by the organism are thus chemically inactive under normal conditions. Such gases include the "noble gases" of the Periodic Table as well as hydrogen and nitrogen. At increasing pressure, nitrogen induces narcosis at 4 absolute atmospheres (ATAs) and more in humans and at 11 ATA and more in rats. Electrophysiological and neuropharmacological studies suggest that the striatum is a target of nitrogen narcosis. Glutamate and dopamine release from the striatum in rats are decreased by exposure to nitrogen at a pressure of 31 ATA (75% of the anesthetic threshold). Striatal dopamine levels decrease during exposure to compressed argon, an inert gas more narcotic than nitrogen, or to nitrous oxide, an anesthetic gas. Inversely, striatal dopamine levels increase during exposure to compressed helium, an inert gas with a very low narcotic potency. Exposure to nitrogen at high pressure does not change N-methyl-d-aspartate (NMDA) glutamate receptor activities in Substantia Nigra compacta and striatum but enhances gama amino butyric acidA (GABAA) receptor activities in Substantia Nigra compacta. The decrease in striatal dopamine levels in response to hyperbaric nitrogen exposure is suppressed by recurrent exposure to nitrogen narcosis, and dopamine levels increase after four or five exposures. This change, the lack of improvement of motor disturbances, the desensitization of GABAA receptors on dopamine cells during recurrent exposures and the long-lasting decrease of glutamate coupled with the higher sensitivity of NMDA receptors, suggest a nitrogen toxicity induced by repetitive exposures to narcosis. These differential changes in different neurotransmitter receptors would support the binding protein theory. © 2016 American Physiological Society. Compr Physiol 6:1579-1590, 2016.

Breathing hyperbaric air or gas mixtures, for example during diving or when working underwater is known to alter the electrophysiological behavior of neuronal cells, which may lead to restricted cognition. During the last few decades, only very few studies into hyperbaric effects have been published, especially for the most relevant pressure range of up to 10 bar. We designed a pressurized measuring chamber to record pressure effects on the electrical activity of neuronal networks formed by primary cells of the frontal cortex of NMRI mice. Electrical activity was recorded with multi-electrode arrays (MEAs) of glass neuro chips while subjected to a step-by-step pressure increase from atmospheric pressure (1 bar) to 2 and 4 bar, followed by a decompression to 1 bar, in order to record recovery effects. The effects of pressure on the total spike rates (TSRs), which were averaged from at least 45 chips, were detected in two cell culture media with different compositions. In a DMEM medium with 6% horse serum, the TSR was increased by 19% after a pressure increase to 2 bar and remained stable at 4 bar. In NMEM medium with 2% B27, the TSR was not altered by a pressure increase to 2 bar but increased by 9% at 4 bar. After decompression to 1 bar, the activities decreased to 76% and 101% of their respective control levels in the two media. MEA recordings from neuronal networks in miniaturized hyperbaric measuring chambers provide new access for exploring the neuronal effects of hyperbaric breathing gases.

Human beings are exposed to compressed air or a nitrogen-oxygen mixture, they will produce signs and symptoms of nitrogen narcosis such as amnesia or even loss of memory, which may be disappeared once back to the normobaric environment. This study was designed to investigate the effect of nitrogen narcosis induced by repetitive hyperbaric nitrogen-oxygen mixture exposure on long-term cognitive function in newborn mice and the underlying mechanisms. The electroencephalogram frequency was decreased while the amplitude was increased in a pressure-dependent manner during 0.6, 1.2, 1.8 MPa (million pascal) nitrogen-oxygen mixture exposures in adult mice. Nitrogen narcosis in postnatal days 7-9 mice but not in adult mice induced by repetitive hyperbaric exposure prolonged the latency to find the platform and decreased the number of platform-site crossovers during Morris water maze tests, and reduced the time in the center during the open field tests. An increase in the expression of cleaved caspase-3 in the hippocampus and cortex were observed immediately on the first day after hyperbaric exposure, and this lasted for seven days. Additionally, nitrogen narcosis induced loss of the dendritic spines but not of the neurons, which may mainly account for the cognitive dysfunction. Nitrogen narcosis induced long-term cognitive and emotional dysfunction in the postnatal mice but not in the adult mice, which may result from neuronal apoptosis and especially reduction of dendritic spines of neurons.

It was hypothesized that normoxic 30% nitrous oxide (N2O) would suppress and hyperthermia would increase exercise ventilation during short duration, high intensity exercise. Thirteen males (24.2±0.8y; mean±SE), of normal physique (BMI, 23.8±1.0kgm(-2)), performed 4 separate 30s Wingate tests on a cycle ergometer. Exercise ventilation and its components, as well as mean skin and esophageal temperature (TES), were assessed in 2 way experimental design with factors of Thermal State (Normothermia or Hyperthermia) and Gas Type (Air or 30% Normomoxic N2O). In the 2 hyperthermic tests TES was elevated to ∼38.5°C in a 40°C bath. The main results indicated a significant interaction (F=7.14, P=0.02) between Gas Type and Thermal state for the exercise-induced increase in ventilation (ΔV˙E). During both the normothermia and hyperthermia conditions with AIR breathing, the exercise ΔV˙E was ∼80Lmin(-1) and it was significantly decreased to 73.1±24.1Lmin(-1) in the normothermia condition with N2O breathing relative to that of 92.0±25.0Lmin(-1) in the hyperthermia condition with N2O breathing. In conclusion, normoxic N2O breathing suppressed high intensity exercise ventilation during normothermia relative to that during hyperthermia on account of decreases in the tidal volume and this led CO2 retention.

Our objective was to study molecular processes that might be responsible for inert gas narcosis and high-pressure nervous syndrome. The classical molecular dynamics trajectories (200 ns) of dioleoylphosphatidylcholine (DOPC) bilayers simulated by the Berger force field were evaluated for water and the atomic distribution of noble gases around DOPC molecules in the pressure range of 1-1000 bar and at a temperature of 310 K. Xenon and argon have been tested as model gases for general anaesthetics, and neon has been investigated for distortions that are potentially responsible for neurological tremors in hyperbaric conditions. The analysis of stacked radial pair distribution functions of DOPC headgroup atoms revealed the explicit solvation potential of the gas molecules, which correlates with their dimensions. The orientational dynamics of water molecules at the biomolecular interface should be considered as an influential factor, while excessive solvation effects appearing in the lumen of membrane-embedded ion channels could be a possible cause of inert gas narcosis. All the noble gases tested exhibit similar order parameter patterns for both DOPC acyl chains, which are opposite of the patterns found for the order parameter curve at high hydrostatic pressures in intact bilayers. This finding supports the 'critical volume' hypothesis of anaesthesia pressure reversal. The irregular lipid headgroup-water boundary observed in DOPC bilayers saturated with neon in the pressure range of 1-100 bar could be associated with the possible manifestation of neurological tremors at the atomic scale. The non-immobiliser neon also demonstrated the highest momentum impact on the normal component of the DOPC diffusion coefficient representing the monolayer undulation rate, which indicates that enhanced diffusivity rather than atomic size is the key factor.

The diver's nervous system is extremely sensitive to high ambient pressure, which is the sum of atmospheric and hydrostatic pressure. Neurological complications associated with diving are a difficult diagnostic and therapeutic challenge. They occur in both commercial and recreational diving and are connected with increasing interest in the sport of diving. Hence it is very important to know the possible complications associated with this kind of sport. Complications of the nervous system may result from decompression sickness, pulmonary barotrauma associated with cerebral arterial air embolism (AGE), otic and sinus barotrauma, high pressure neurological syndrome (HPNS) and undesirable effect of gases used for breathing. The purpose of this review is to discuss the range of neurological symptoms that can occur during diving accidents and also the role of patent foramen ovale (PFO) and internal carotid artery (ICA) dissection in pathogenesis of stroke in divers.

BACKGROUND Nitrogen (N2) in air causes cognitive impairment from gas narcosis when breathed at increased ambient pressures. This impairment might be reduced by using enriched air nitrox (EANx) mixtures, which have a higher oxygen and lower N2 content compared to air. This study aimed to investigate if divers differed in memory ability and self-assessment when breathing air and EANx30. METHODS The effect of depth (shallow vs. deep) and breathing gas (air vs. EANx30) on memory ability and subjective ratings of impairment was compared in 20 divers. RESULTS Memory performance was significantly worse in deep water (Air: M = 22.1%, SD = 21.7%; EANx30: M = 22.1%, SD = 17.2%) compared to shallow water (Air: M = 29.2%, SD = 18.3%; EANx30: M = 33.3%, SD = 18.2%), but this impairment did not differ significantly between air and EANx30. Subjective ratings of impairment increased significantly from shallow water (Air: M = 5.2, SD = 5.9; EANx30: M = 3.0, SD = 4.4) to deep water (Air: M = 36.8, SD = 25.3; EANx30: M = 24.8, SD = 16.1) when breathing both air and EANx30. However, ratings were significantly lower when breathing EANx30 compared to air when in the deep water. DISCUSSION It was concluded EANx30 does not reduce narcotic impairment over air. Additionally, divers were able to make a correct global self-assessment they were impaired by narcosis, but were unable to make a finer assessment, leading them to erroneously believe that EANx30 was less narcotic than air.

This paper provides a brief overview of the shift from studies describing the personality profiles of divers to studies exploring associations between personality variables and diving performance in terms of behavioural outcomes. The personality associations that were investigated include performance during training, panic proneness, diving injuries, susceptibility to inert gas narcosis, and the behaviour of tourist divers. The paper concludes with a number of suggested directions for further research on personality and diving that may provide tangible benefits in terms of both enhanced safety and improved performance underwater.

Recreational scuba diving is no longer reserved for young healthy individuals, and as a result, medical drug consumption is on the rise in the diving population. Due to the possible potentiation of nitrogen narcosis by psychotropic drugs, the latter are hence discouraged and are subject to contraindications for practice. However, there are no available experimental data to support this theoretical assumption. The objective of this study is to investigate whether psychotropic drug users are more at risk of severe narcosis. An online survey was sent to the licensed divers from the East of France registered with the French Underwater Federation. Divers were surveyed regarding their consumption of psychotropic drugs, the occurrence of nitrogen narcosis as well as their respective diver’s curriculum vitae.1 608 divers responded to the survey of which 15.2% confirmed having used psychotropic drugs and 7.8% since they became divers. Overall, 40.0% and 5.5% experienced severe and critical narcosis. In multivariate analysis, neither severe nor critical narcosis was associated with psychotropic drug use (OR 0.97 [0.59–1.57] and 0.76 [0.29–2.00], respectively).In conclusion, despite the recommendations, a significant proportion of divers use psychotropic drugs but do not seem to be more prone to severe narcosis.

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Objective: The current study tested whether undersea divers are able to accurately judge their level of memory impairment from inert gas narcosis. Background: Inert gas narcosis causes a number of cognitive impairments, including a decrement in memory ability. Undersea divers may be unable to accurately judge their level of impairment, affecting safety and work performance. Method: In two underwater field experiments, performance decrements on tests of memory at 33 to 42 m were compared with self-ratings of impairment and resolution. The effect of depth (shallow [1-11 m] vs. deep [33-42 m]) was measured on free-recall (Experiment 1; n = 41) and cued-recall (Experiment 2; n = 39) performance, a visual-analogue self-assessment rating of narcotic impairment, and the accuracy of judgements-of-learning (JOLs). Results: Both free- and cued-recall were significantly reduced in deep, compared to shallow, conditions. This decrement was accompanied by an increase in self-assessed impairment. In contrast, resolution (based on JOLs) remained unaffected by depth. The dissociation of memory accuracy and resolution, coupled with a shift in a self-assessment of impairment, indicated that divers were able to accurately judge their decrease in memory performance at depth. Conclusion: These findings suggest that impaired self-assessment and resolution may not actually be a symptom of narcosis in the depth range of 33 to 42 m underwater and that the divers in this study were better equipped to manage narcosis than prior literature suggested. The results are discussed in relation to implications for diver safety and work performance.

Background: This paper considers the relationship between measures of personality and mood states, and susceptibility to inert gas narcosis. It briefly reviews the topics of inert gas narcosis affecting personality, and personality affecting the susceptibility to inert gas narcosis. There appears to be is a theoretical argument for a possible relationship between measures of personality, mood states, and susceptibility to narcosis. Practically, such a relationship may speak to issues in selection, training and preparation, risk assessments, and even accident investigation in the diving and/or hyperbaric environment. Materials and methods: Twenty one divers completed measures of personality and mood states, and were then compressed to 709 kPa (equivalent to 60 msw) in a dry compression chamber, where they completed a task measuring speed of information processing, and a scale measuring subjective narcosis. Results and Conclusions: The main finding was the absence of any significant correlations between measures of personality traits and mood, and susceptibility to inert gas narcosis. Although the study found no evidence of any major relationship, it is presented as a case study to highlight some of the issues and pitfalls involved in such research. The lessons learned — including the careful defining and describing of concepts, and choosing of samples and measurements — are used to discuss some of the methodological and conceptual issues and future directions for researchers to consider.

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Inert gas narcosis (IGN) impairs cognitive performance and some divers are more susceptible to IGN than others. We compared the sensitivity of two reaction time tests to detect changes in performance at pressure and compared these results with critical flicker fusion frequency (CFF) changes at the same ambient pressures.The study assessed simple reaction time (RT), mean time correct of the discrimination reaction time (MTC) and CFF in 30 professional divers breathing air at 101 kPa and 608 kPa in a hyperbaric chamber.RT and MTC increased at 608 kPa by 5.1 ± 9.4% (P = 0.04) and 7.3 ± 12.3% (P = 0.01) respectively. RT decreased to pre-compression level after decompression and MTC decreased to a level lower than pre-compression (P0.001) values. CFF increased by 2.5 ± 2.8% (P0.001) at 608 kPa. CFF decreased to pre-compression level after decompression. An increase in CFF was inversely correlated with a decrease in RT (r = 0.38, P = 0.04) and in MTC (r = 0.43, P = 0.02) at 608 kPa.Response speeds of the same subjects were impaired in both reaction time tasks at 608 kPa, whereas CFF increased at depth. An association between changes in response times and changes in CFF suggests that divers susceptible to IGN may also be susceptible to the effects of elevated oxygen partial pressure. If this holds true, the future selection of professional divers could be improved by the use of simple cognitive tests.

Contribution of skin thermal sensors under inert gas narcosis to the raising hypothermia is not known. Such information is vital for understanding the impact of narcosis on behavioural thermoregulation, diver safety and judgment of thermal (dis)comfort in the hyperbaric environment. So this study aimed at establishing the effects of normoxic concentration of 30% nitrous oxide (N(2)O) on thermo-tactile threshold sensation by studying 16 subjects [eight females and eight males; eight sensitive (S) and eight non-sensitive (NS) to N(2)O]. Their mean (SD) age was 22.1 (1.8) years, weight 72.8 (15.3) kg, height 1.75 (0.10) m and body mass index 23.8 (3.8) kg m(-2). Quantitative thermo-tactile sensory testing was performed on forearm, upper arm and thigh under two experimental conditions: breathing air (air trial) and breathing normoxic mixture of 30% N(2)O (N(2)O trial) in the mixed sequence. Difference in thermo-tactile sensitivity thresholds between two groups of subjects in two experimental conditions was analysed by 3-way mixed-model analysis of covariance. There were no statistically significant differences in thermo-tactile thresholds either between the Air and N(2)O trials, or between S and NS groups, or between females and males, or with respect to body mass index. Some clinically insignificant lowering of thermo-tactile thresholds occurred only for warm thermo-tactile thresholds on upper arm and thigh. The results indicated that normoxic mixture of 30% N(2)O had no influence on thermo-tactile sensation in normothermia.

INTRODUCTION: Performance impairments attributed to the effects of nitrogen narcosis have been reported to be significantly larger in studies conducted underwater compared to in hyperbaric chambers. One suggestion is that the larger impairment results from higher levels of anxiety in the underwater environment. The current study aimed to investigate the impact of anxiety and narcosis, in isolation and in combination, on a measure of psychomotor performance. METHODS: The effects of self-reported anxiety (anxious vs. not anxious) and depth (surface vs. underwater) on performance on the digit letter substitution test (DLST) were measured in 125 divers. RESULTS: Change from baseline scores indicated that divers performed significantly worse on the DLST underwater (mean = 3.35; SD = 4.2) compared to the surface (mean = 0.45-0.73; SD = 4.0-4.2). This decrement was increased when divers reported they were also anxious (mean = 7.11; SD = 6.1). There was no difference on DLST performance at the surface between divers reporting they were anxious and those reporting they were not anxious. DISCUSSION: The greater decrement in performance at depth in divers reporting anxiety compared to those not reporting anxiety and the lack of this effect on the surface suggested that anxiety may magnify performance deficits presumed to be caused by narcosis. Language: en

Previous microdialysis studies performed in rats have revealed a decrease of striatal dopamine and glutamate induced by nitrogen narcosis. We sought to establish the hypothetical role of the glutamatergic corticostriatal pathway because of the glutamate deficiency which occurs in the basal ganglia in this hyperbaric syndrome. Retrodialysis with 1 mM of Saclofen and 100 mM of KCl in the prefrontal cortex under normobaric conditions led to an increase in striatal levels of glutamate by 95.2% and no changes in dopamine levels. Under 3 MPa of nitrogen and with the infusion, the rate of striatal glutamate decreased by 51.3%, to a greater extent than under pressurised nitrogen alone (-23.8%). The rate of dopamine decreased, which also occurred under pressurised nitrogen (-36.9 and -31.4%, respectively). In conclusion, the function of the corticostriatal pathway is affected by nitrogen under pressure. This suggests that the nitrogen-induced break point seems to be located at the glutamatergic striatopetal neurons.

Nervous disorders may occur after an organism is saturated with inert gases, which may alter the lipid bilayer structure, according to their liposolubility coefficient. Increase in the nitrogen partial pressure induces a neurological syndrome called 'nitrogen narcosis'. By contrast, high pressures of helium induce epilepsy, an high-pressure nervous syndrome symptom. On the basis of an analogy with anaesthetic mechanisms, we used TREK-1 knockout mice, earlier described to volatile the anaesthetics resistance. These mice had a higher threshold of resistance to the narcotic effects of nitrogen and to the death after recurrent epileptic seizure induced by high pressure. TREK-1 channels seem to play a key role in modulating the anaesthetic potential of inert gases and in neuroprotection.

Diving-related pulmonary effects are due mostly to increased gas density, immersion-related increase in pulmonary blood volume, and (usually) a higher inspired Po2. Higher gas density produces an increase in airways resistance and work of breathing, and a reduced maximum breathing capacity. An additional mechanical load is due to immersion, which can impose a static transrespiratory pressure load as well as a decrease in pulmonary compliance. The combination of resistive and elastic loads is largely responsible for the reduction in ventilation during underwater exercise. Additionally, there is a density-related increase in dead space/tidal volume ratio (Vd/Vt), possibly due to impairment of intrapulmonary gas phase diffusion and distribution of ventilation. The net result of relative hypoventilation and increased Vd/Vt is hypercapnia. The effect of high inspired Po2and inert gas narcosis on respiratory drive appear to be minimal. Exchange of oxygen by the lung is not impaired, at least up to a gas density of 25 g/l. There are few effects of pressure per se, other than a reduction in the P50 of hemoglobin, probably due to either a conformational change or an effect of inert gas binding.

Exposure to nitrogen-oxygen mixture at high pressure induces narcosis, which can be considered as a first step toward general anaesthesia. Narcotic potencies of inert gases are attributed to their lipid solubility. Nitrogen narcosis induces cognitive and motor disturbances that occur from 0.3 MPa in man and from 1 MPa in rats. Neurochemical studies performed in rats up to 3 MPa have shown that nitrogen pressure decreases striatal dopamine release like argon, another inert gas, or nitrous oxide, an anaesthetic gas. Striatal dopamine release is under glutamatergic and other amino acid neurotransmission regulations. The aim of this work was to study the effects of nitrogen at 3 MPa on striatal amino acid levels and to compare to those of 3 MPa of helium which is not narcotic at this pressure, by using a new technique of microdialysis samples extraction under hyperbaric conditions, in freely moving rats. Amino acids were analysed by HPLC coupled to fluorimetric detection in order to appreciate glutamate, aspartate, glutamine and asparagine levels. Nitrogen-oxygen mixture exposure at 3 MPa decreased glutamate, glutamine and asparagine concentrations. In contrast, with helium-oxygen mixture, glutamate and aspartate levels were increased during the compression phase but not during the stay at maximal pressure. Comparison between nitrogen and helium highlighted the narcotic effects of nitrogen at pressure. As a matter of fact, nitrogen induces a reduction in glutamate and in other amino acids that could partly explain the decrease in striatal dopamine level as well as the motor and cognitive disturbances reported in nitrogen narcosis.

Nitrogen pressure exposure in rats results in decreased dopamine (DA) release at the striatal terminals of the substantia nigra pars compacta (SNc) dopaminergic neurons, demonstrating the narcotic potency of nitrogen. This effect is attributed to decreased excitatory and increased inhibitory inputs to dopaminergic neurons, involving a change in NMDA and GABA(A) receptor function. We investigated whether repetitive exposures to nitrogen modify the excitatory and inhibitory control of the dopaminergic nigro-striatal pathway. We used voltammetry to measure dopamine levels in freely-moving rats, implanted with dopamine-sensitive electrodes in the striatum. NMDA/GABA(A) receptor agonists (NMDA/muscimol) and antagonists (AP7/gabazine) were administered through a guide-cannula into the SNc, and their effects on striatal dopamine levels were measured under normobaric conditions, before and after five repetitive exposures to 1 MPa nitrogen. NMDA-mediated dopamine release was greater following repetitive exposures, AP7-mediated inhibition of glutamatergic input was blocked, suggesting that NMDA receptor sensitivity was increased and glutamate release reduced. Muscimol did not modify dopamine levels following repetitive exposures, whereas the effect of gabazine was greater after exposures than before. This suggested that interneuronal GABA(A) receptors were desensitized, leading to an increased GABAergic input at dopaminergic cells. Thus, repetitive nitrogen exposure induced persistent changes in glutamatergic and GABAergic control of dopaminergic neurons, resulting in decreased activity of the nigrostriatal pathway.

Recreational scuba diving is a popular sport, and people with epilepsy often ask physicians whether they may engage in diving. Scuba diving is not, however, without risk for anyone; apart from the risk of drowning, the main physiological problems, caused by exposure to gases at depth, are decompression illness, oxygen toxicity, and nitrogen narcosis. In the United Kingdom, the Sport Diving Medical Committee advises that, to dive, someone with epilepsy must be seizure free and off medication for at least 5 years. The reasons for this are largely theoretical. We review the available evidence in the medical literature and diving websites. The risk of seizures recurring decreases with increasing time in remission, but the risk is never completely abolished. We suggest that people with epilepsy who wish to engage in diving, and the physicians who certify fitness to dive, should be provided with all the available evidence. Those who have been entirely seizure-free on stable antiepileptic drug therapy for at least 4 years, who are not taking sedative antiepileptic drugs and who are able to understand the risks, should then be able to consider diving to shallow depths, provided both they and their diving buddy have fully understood the risks.

We investigated 105 professional divers using a computerized visual discrimination trial (Cognitrone) to measure the effects of ambient pressure on reaction times. The possible improvement in performance due to practice was anticipated, and the trials were carried out four times prior to pressurization in a hyperbaric chamber. The effect of increased ambient pressure was measured at 6.0 and 1.9 atm abs, and the potential for residual effects was tested after decompression. The results of our study indicate that repeated testing had a systematic influence on the measured time values. The effects of learning, which were independent of diver age, may have independently influenced response times. Exposure to 6.0 atm abs modified the systematic pattern of learning and was associated with increased reaction times. There were also age-related differences in response times associated with exposure to increased ambient pressures. Younger divers were more susceptible to elevated ambient pressure, evidenced by increased response times at 6 atm abs relative to their older colleagues. One out of every four of the younger divers could be considered susceptible to inert gas narcosis (ION) when an increase of one standard deviation/1SD (19%) or more in discrimination reaction time is used as an indicator. ION susceptibility appears independent of body composition and physical fitness. The slowed response speed experienced at 6.0 atm abs was of short duration and returned to baseline immediately with decompression. Our results suggest that IGN is demonstrated by an impaired learning process and decreased response speed and that some younger divers appear more susceptible.

Exposure to the underwater environment for pleasure or work poses many challenges on the human body including thermal stress, barotraumas, decompression sickness as well as the acute effects of breathing gases under pressure. With the popularity of recreational self-contained underwater breathing apparatus (SCUBA) diving on the increase and deep inland dive sites becoming more accessible, it is important that we understand the effects of breathing pressurised gas at depth can have on the body. One of the common consequences of hyperbaric gas is the narcotic effect of inert gas. Nitrogen (a major component of air) under pressure can impede mental function and physical performance at depths of as little as 10 m underwater. With increased depth, symptoms can worsen to include confusion, disturbed coordination, lack of concentration, hallucinations and unconsciousness. Narcosis has been shown to contribute directly to up to 6% of deaths in divers and is likely to be indirectly associated with other diving incidents at depth. This article explores inert gas narcosis, the effect on divers’ movement and function underwater and the proposed physiological mechanisms. Also discussed are some of the factors that affect the susceptibility of divers to the condition. In conclusion, understanding the cause of this potentially debilitating problem is important to ensure that safe diving practices continue.

The interaction of subjective experiences and objective measures of neuropsychological performance during hyperbaric exposure has received less attention in the literature, in part due to the shortage of available and appropriately standardized measures.This study aimed to describe the psychometric properties of a modified version of the Subjective High Assessment Scale when used in the hyperbaric context, by exploring internal reliability, factor structure, associations with psychological variables and simple cognitive delayed recall, and the effect of task focus on the recall of subjective experience.Seventy qualified divers completed dry hyperbaric chamber dives to 607.95 kPa, and completed ratings of their subjective experiences. Some also completed a delayed recall task and psychological measures prior to their dives.The scale displayed good internal consistency, with four meaningful factors emerging. It showed some significant but small associations with trait anxiety and transient mood states, and a small to moderate correlation with recall performance. There was no significant effect of task focus on self-report of subjective experiences.The modified scale, renamed the Subjective Narcosis Assessment Scale here, has useful psychometric properties, and promising potential for future use.

Previous studies have demonstrated opposite effects of high-pressure helium and nitrogen on extracellular dopamine (DA) levels, which may reflect disturbances on the synthesis, release or metabolic mechanisms. Intrastriatal microdialysis was used to measure the precursor (tyrosine), DA and its metabolites (DOPAC, HVA) levels under nitrogen- or helium- at pressure up to 3 MPa. Under 3 MPa of helium–oxygen breathing mixtures, the extracellular concentration of tyrosine is decreased while the extracellular concentration of DA is increased. On the contrary, nitrogen–oxygen breathing mixture at the same pressure increased extracellular tyrosine concentration and decreased DA release. Under both conditions, an increment of the DOPAC and HVA levels could be noted. Our results suggest that changes in DA release and metabolism during high-pressure helium exposure reflect the effect of the pressure per se, whereas the intrinsic effects of narcotic gases, although sensitive to pressure, would be revealed by hyperbaric nitrogen exposure.

As ambient pressure increases, hydrostatic compression of the central nervous system, combined with increasing levels of inspired Po2, Pco2, and N2partial pressure, has deleterious effects on neuronal function, resulting in O2toxicity, CO2toxicity, N2narcosis, and high-pressure nervous syndrome. The cellular mechanisms responsible for each disorder have been difficult to study by using classic in vitro electrophysiological methods, due to the physical barrier imposed by the sealed pressure chamber and mechanical disturbances during tissue compression. Improved chamber designs and methods have made such experiments feasible in mammalian neurons, especially at ambient pressures 2measurements in slices of rat brain demonstrate how to differentiate the neuronal effects of increased gas pressures from pressure per se. Examples also highlight the use of hyperoxia (≤3 ATA O2) as a model for studying the cellular mechanisms of oxidative stress in the mammalian central nervous system.

Inert gas narcosis is a neurological syndrome appearing when humans or animals are exposed to hyperbaric inert gases (nitrogen, argon) composed by motor and cognitive impairments. Inert gas narcosis induces a decrease of the dopamine release at the striatum level, structure involved in the regulation of the extrapyramidal motricity. We have investigated, in freely moving rats exposed to different narcotic conditions, the relationship between the locomotor and motor activity and the striatal dopamine release, using respectively a computerized device that enables a quantitative analysis of this behavioural disturbance and voltammetry. The use of 3 MPa of nitrogen, 2 MPa of argon and 0.1 MPa of nitrous oxide, revealed after a transient phase of hyperactivity, a lower level of the locomotor and motor activity, in relation with the decrease of the striatal dopamine release. It is concluded that the striatal dopamine decrease could be related to the decrease of the locomotor and motor hyperactivity, but that other(s) neurotransmitter(s) could be primarily involved in the behavioural motor disturbances induced by narcotics. This biphasic effect could be of major importance for future pharmacological investigations, and motor categorization, on the basic mechanisms of inert gas at pressure.

It is unnecessary to describe the horror of surgery prior to the demonstration of ether anaesthesia at Massachusetts General Hospital in 1846. It was clearly a nightmare for patients and must have been little better for the medical personnel involved in so terrifying an undertaking. What is less obvious is that the introduction of anaesthesia accomplished far more than the abolition of intraoperative pain. The solution of the problem of pain enabled the evolution of virtually all of modern surgical therapeutics. Prior to this development, the major characteristic of a technically brilliant surgeon was speed the ability to do a below-the-knee amputation in less than a minute made or unmade reputations. Intra-cavitary surgery; operations in the chest, abdomen or skull were largly unthinkable and when attempted, commonly led to the death of the patient, not because of pain per se, but because the surgeon had no time in which to think and take deliberate action. So practical were the properties of anaesthetics, that their clinical use spread rapidly throughout the medical world without the least understanding of the mechanisms by which the agents worked. The drugs obviously produced unconsciousness and freedom from the perception of noxious stimuli. It was also desirable that they did so as rapidly as possible, and that such effects were completely reversible with few physiological side effects. We would not dispute these requirements today. Within the context of thencurrent chemical knowledge, three agents appeared to fit all or some of this description. Diethyl ether, as used by Morton, became the standard for generations. Nitrous oxide provided all the correct attributes but one sufficient potency to cause unconsciousness and surgical anaesthesia. Chloroform also provided the requisite analgesia and unconsciousness and was used for decades, despite its potentially lethal side effects. The early lack of understanding and, indeed, concern about anaesthetic mechanisms of action should not be too surprising. Very few of the drugs then in use were understood in any detail. Drugs were found largely by trial and error in animals and humans. That they worked and were relatively safe was all that was required. In the context of this pragmatic medical world, Ernest Overton was a fascinating exception. Bom in Cheshire, England, in 1865, Overton was a distant relative of Charles Darwin. His maternal grandfather, Reverend W. Darwin Fox was an entomologist, second cousin and close friend of Darwin. With his family, Overton moved to Switzerland at the age of seventeen and there completed his education. He received

Intoxications resulting from asphyxiate gases, such as nitrogen can cause hypoxia and even death. We present a case of a patient with nitrogen intoxication due to inadvertent industrial exposure. In this case, the patient survived and the outcome was different from those reported in the literature. For patients presenting to the emergency department from a workplace with a history of loss of consciousness after using of self-contained breathing apparatus, possibility of nitrogen or other simple asphyxiate gas intoxication should be considered seriously.

Since the early 1960s all Royal Navy submarines have been fitted with an escape system comprising a single escape tower (SET) and submarine escape immersion suit (SEIS). This system enables escape from a submarine at a depth of 180 metres (1.9 MPa) provided that the submarine compartment is at a pressure of no greater than 1 bar (0.1 MPa). Due to a variety of causes which may include flooding and leakage of high pressure air systems it is highly probable that the submarine compartment will be at a pressure in excess of 1 bar (0.1 MPa) at the time of the escape. To investigate and determine what constitutes a ‘safe’ maximum escape depth from any given compartment pressure (the safe to escape curve), a purpose built chamber complex, the Submarine Escape Simulator (SES) has been constructed at the QinetiQ, formerly the Defence Evaluation and Research Agency (DERA), Alverstoke site.Unlike escapes from a submarine where once released from the submarine the escapee’s ascent can not be halted, within the SES it is possible to halt the ascent phase. This article describes the systems and procedures developed to enable medical support to be provided rapidly to a subject at any stage of the compression decompression profile. The article also provides details of the results to date that have been obtained from this work.

Exposure to the undersea environment has unique effects on normal physiology and can result in unique disorders that require an understanding of the effects of pressure and inert gas supersaturation on organ function and knowledge of the appropriate therapies, which can include recompression in a hyperbaric chamber. The effects of Boyle's law result in changes in volume of gas-containing spaces when exposed to the increased pressure underwater. These effects can cause middle ear and sinus injury and lung barotrauma due to lung overexpansion during ascent from depth. Disorders related to diving have unique presentations, and an understanding of the high-pressure environment is needed to properly diagnose and manage these disorders. Breathing compressed air underwater results in increased dissolved inert gas in tissues and organs. On ascent after a diving exposure, the dissolved gas can achieve a supersaturated state and can form gas bubbles in blood and tissues, with resulting tissue and organ damage. Decompression sickness can involve the musculoskeletal system, skin, inner ear, brain, and spinal cord, with characteristic signs and symptoms. Usual therapy is recompression in a hyperbaric chamber following well-established protocols. Many recreational diving candidates seek medical clearance for diving, and healthcare providers must be knowledgeable of the environmental exposure and its effects on physiologic function to properly assess individuals for fitness to dive. This review provides a basis for understanding the diving environment and its accompanying disorders and provides a basis for assessment of fitness for diving.

BACKGROUND Prior research has indicated that inert gas narcosis (IGN) causes decrements in free recall memory performance and that these result from disruption of either encoding or self-guided search in the retrieval process. In a recent study we provided evidence, using a Levels of Processing approach, for the hypothesis that IGN affects the encoding of new information. The current study sought to replicate these results with an improved methodology. METHODS The effect of ambient pressure (111.5-212.8 kPa/1-11 msw vs. 456-516.8 kPa/35-41 msw) and level of processing (shallow vs. deep) on free recall memory performance was measured in 34 divers in the context of an underwater field experiment. RESULTS Free recall was significantly worse at high ambient pressure compared to low ambient pressure in the deep processing condition (low pressure: M = 5.6; SD = 2.7; high pressure: M = 3.3; SD = 1.4), but not in the shallow processing condition (low pressure: M = 3.9; SD = 1.7; high pressure: M = 3.1; SD = 1.8), indicating IGN impaired memory ability in the deep processing condition. In the shallow water, deep processing improved recall over shallow processing but, significantly, this effect was eliminated in the deep water. DISCUSSION In contrast to our earlier study this supported the hypothesis that IGN affects the self-guided search of information and not encoding. It is suggested that IGN may affect both encoding and self-guided search and further research is recommended.