Breath-Hold Diving Injuries - A Primer for Medical Providers.

ABSTRACT: Breath-hold divers, also known as freedivers, are at risk of specific injuries that are unique from those of surface swimmers and compressed air divers. Using peer-reviewed scientific research and expert opinion, we created a guide for medical providers managing breath-hold diving injuries in the field. Hypoxia induced by prolonged apnea and increased oxygen uptake can result in an impaired mental state that can manifest as involuntary movements or full loss of consciousness. Negative pressure barotrauma secondary to airspace collapse can lead to edema and/or hemorrhage. Positive pressure barotrauma secondary to overexpansion of airspaces can result in gas embolism or air entry into tissues and organs. Inert gas loading into tissues from prolonged deep dives or repetitive shallow dives with short surface intervals can lead to decompression sickness. Inert gas narcosis at depth is commonly described as an altered state similar to that experienced by compressed air divers. Asymptomatic cardiac arrhythmias are common during apnea, normally reversing shortly after normal ventilation resumes. The methods of glossopharyngeal breathing (insufflation and exsufflation) can add to the risk of pulmonary overinflation barotrauma or loss of consciousness from decreased cardiac preload. This guide also includes information for medical providers who are tasked with providing medical support at an organized breath-hold diving event with a list of suggested equipment to facilitate diagnosis and treatment outside of the hospital setting.

Combined effects of mild hypothermia and nitrous-oxide-induced narcosis on manual and cognitive performance.

Divers are at enhanced risk of suffering from acute cognitive deterioration because of the low ambient temperatures and the narcotic action of inert gases inspired at high pressures. Yet, the behavioral effects of cold and inert gas narcosis have commonly been assessed in isolation and during short-term provocations. We therefore evaluated the interactive influence of mild hypothermia and narcosis engendered by a subanesthetic dose of nitrous oxide (N2O; a normobaric intervention analog of hyperbaric nitrogen) on cognitive function during prolonged iterative exposure. Fourteen men partook in two ∼12-h sessions (separated by ≥4 days), wherein they performed sequentially three 120-min cold (20°C) water immersions (CWIs), while inhaling, in a single-blinded manner, either normal air or a normoxic gas mixture containing 30% N2O. CWIs were separated by a 120-min rewarming in room-air breathing conditions. Before the first CWI and during each CWI, subjects performed a finger dexterity test, and the Spaceflight Cognitive Assessment Tool for Windows (WinSCAT) test assessing aspects of attention, memory, learning, and visuospatial ability. Rectal and skin temperatures were, on average, reduced by ∼1.2 °C and ∼8 °C, respectively (P < 0.001). Cooling per se impaired (P ≤ 0.01) only short-term memory (∼37%) and learning (∼18%); the impairments were limited to the first CWI. N2O also attenuated (P ≤ 0.02) short-term memory (∼37%) and learning (∼35%), but the reductions occurred in all CWIs. Furthermore, N2O invariably compromised finger dexterity, attention, concentration, working memory, and spatial processing (P < 0.05). The present results demonstrate that inert gas narcosis aggravates, in a persistent manner, basic and higher-order cognitive abilities during protracted cold exposure.

Possible causes of narcosis-like symptoms in freedivers.

During deep-sea freediving, many freedivers describe symptoms fairly similar to what has been related to inert gas narcosis in scuba divers. This manuscript aims to present the potential mechanisms underlying these symptoms. First, known mechanisms of narcosis are summarized while scuba diving. Then, potential underlying mechanisms involving the toxicity of gases (nitrogen, carbon dioxide and oxygen) are presented in freedivers. As the symptoms are felt during ascent, nitrogen is likely not the only gas involved. Since freedivers are frequently exposed to hypercapnic hypoxia toward the end of the dive, it is proposed that carbon dioxide and oxygen gases both play a major role. Finally, a new "hemodynamic hypothesis" based on the diving reflex is proposed in freedivers. The underlying mechanisms are undoubtedly multifactorial and therefore require further research and a new descriptive name. We propose a new term for these types of symptoms: freediving transient cognitive impairment.

EEG functional connectivity is sensitive for nitrogen narcosis at 608 kPa.

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 r2 = 0.60, receiver-operating-characteristic area, 0.67 [0.51-0.84], p = 0.02). Heliox breathing did not cause a significant change in functional connectivity. In conclusion, functional connectivity increased during hyperbaric air-breathing in a dose-dependent manner, but not while heliox-breathing. This suggests sensitivity to nitrogen narcosis specifically.

Pupillometry is not sensitive to gas narcosis in divers breathing hyperbaric air or normobaric nitrous oxide.

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.

Personality and behavioural outcomes in diving: current status and recommendations for future research.

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.

Assessment of the interaction of hyperbaric N2, CO2, and O2 on psychomotor performance in divers.

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.

Neurochemistry of Pressure-Induced Nitrogen and Metabolically Inert Gas Narcosis in the Central Nervous System.

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.

[Diving accidents]. / Tauchunfälle.

Decompression injuries occur on account of the special hyperbaric effects during the emerge phase and require superior therapeutic knowledge. Vitally important is emergency treatment with high concentrated oxygen at an early stage. Sever decompression injuries require oxygenation in a hyperbaric treatment chamber.

A comparison of simple reaction time, visual discrimination and critical flicker fusion frequency in professional divers at elevated pressure.

INTRODUCTION: 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. METHODS: 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. RESULTS: 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 (P < 0.001) values. CFF increased by 2.5 ± 2.8% (P < 0.001) 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. CONCLUSIONS: 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.

Age-related effects of increased ambient pressure on discrimination reaction time: A study in 105 professional divers at 6.0 atm abs.

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.

Neurological complications of underwater diving.

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.

Diving medicine.

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.

Effects of hyperbaric nitrogen-induced narcosis on response-selection processes.

Certain underwater circumstances carry risk of inert gas narcosis. Impairment of sensorimotor information processing due to narcosis, induced by normobaric nitrous oxide or high partial nitrogen pressure, has been broadly evidenced, by a lengthening of the reaction time (RT). However, the locus of this effect remains a matter of debate. We examined whether inert gas narcosis affects the response-selection stage of sensorimotor information processing. We compared an air normobaric condition with a hyperbaric condition in which 10 subjects were subjected to 6 absolute atmospheres of 8.33% O2 Nitrox. In both conditions, subjects performed a between-hand choice-RT task in which we explicitly manipulated the stimulus-response association rule. The effect of this manipulation (which is supposed to affect response-selection processes) was modified by inert gas narcosis. It is concluded, therefore, that response selection processes are among the loci involved in the effect of inert gas narcosis on information processing.

A review of recent neurochemical data on inert gas narcosis.

Nitrogen narcosis occurs in humans at around 0.4 MPa (4 ATA). Hydrogen narcosis occurs between 2.6 and 3.0 MPa. In rats, nitrogen disturbances occur from 1 MPa and a loss of righting reflex around 4 MPa. Neurochemical studies in striatum of rats with nitrogen at 3 MPa (75% of anesthesia threshold) with differential pulse voltammetry have demonstrated a decrease in dopamine (DA) release by neurons originated from the substantia nigra pars compacta (SNc). Such a decrease is found also with compressed argon, which is more narcotic than nitrogen and with the anesthetic gas nitrous oxide. Inversely, compressed helium with its very low narcotic potency induces DA increase. Microdialysis studies in the striatum have indicated that nitrogen also induces a decrease of glutamate concentration. Nitrogen pressure did not modify NMDA glutamate receptor activities in SNc or striatum but enhanced GABAA receptors activities in SNc. Repetitive exposures to nitrogen narcosis suppressed the DA decrease and induced an increase. This fact and the lack of improvement of motor disturbances did not support the hypothesis of a physiological adaptation. The desensitization of the GABAA receptors on DA cells during recurrent exposures and the parallel long-lasting decrease of glutamate coupled to the increase in NMDA receptor sensitivity suggest a nitrogen neurotoxicity or addiction induced by recurrent exposures. The differential changes produced by inert gases indifferent neurotransmitter receptors would support the binding protein theory.

Guiding principles in choosing a therapeutic table for DCI hyperbaric therapy.

Hyperbaric therapy is the basis of treatment for pervasive development disorders. For this reason, the choice of the right therapeutic table for each case is critical. Above all, the delay in recompression time with respect to the first symptoms and to the severity of the case must be considered. In our experience, the use of low-pressure oxygen tables resolves almost all cases if recompression takes place within a short time. When recompression is possible almost immediately, the mechanical effect of reduction on bubble volume due to pressure is of remarkable importance. In these cases, high-pressure tables can be considered. These tables can also be used in severe spinal-cord decompression sickness. The preferred breathing mixture is still disputed. Heliox seems to be favored because it causes fewer problems during the recompression of divers, and above all, because nitrox can cause narcosis and contributes nitrogen. Saturation treatment should be avoided or at least used only in special cases. In cases of arterial gas embolism cerebral injury, it is recommended to start with an initial 6 ATA recompression only if the time between symptom onset and the beginning of recompression is less than a few hours.

Estimates of N2 narcosis and O2 toxicity during submarine escapes from 600 to 1,000 fsw.

The U.S. Navy recommends submarine escape for depths down to 600 fsw, with deeper escapes entailing the risks of decompression sickness, nitrogen (N2) narcosis and CNS oxygen (O2) toxicity. However, the escape equipment, including the submarine escape and immersion equipment and the escape trunk, could probably function even at 1,000 fsw. Here we report a theoretical analysis of the risks of both N2 narcosis and CNS O2 toxicity for different escape profiles from 600 to 1,000 fsw. The effect of N2 narcosis, calculated as a function of N2 pressure in the brain using Gas Man software, was expressed as equivalent narcosis depth (END), corresponding to the depth at which the same pressure of N2 would be produced in the brain after five minutes of scuba diving with air. The risk of O2-induced convulsions was estimated using the model developed by Arieli et al. Different dwell times (DTs) at maximal pressure in the escape trunk (from 0 to 60 s) and lungs-to-brain circulation times (10 to 30 s) were included in our analysis. When DT in the escape trunk is very short (e.g., 10 s), the risk of either incapacitating N2 narcosis and/or O2-induced convulsions occurring in the trunk is low, even during escapes from 1,000 fsw.

Behavioral temperature regulation in humans during mild narcosis induced by inhalation of 30% nitrous oxide.

In this study, we investigated the influence of mild narcosis on temperature perception, thermal comfort, and behavioral temperature regulation in humans. Twelve subjects (six males and six females) participated in two trials, during which they wore a water-perfused suit (WPS). The temperature of the WPS (TWPS) fluctuated sinusoidally from 27 degrees to 42 degrees C, at a heating and cooling rate of 1.2 degrees C x min(-1). In the first trial, the subjects had no control over TWPS: They determined their thermal comfort zone (TCZ) by providing a subjective response whenever they perceived the temperature changing from a comfortable to an uncomfortable level and vice versa; in addition, they provided subjective ratings of temperature perception and thermal comfort on a 7-point and 4-point scale, respectively, at each 3 degrees C change in TWPS. In the second trial, subjects could change the direction of TWPS whenever it became uncomfortable by depressing a button on a manual control. The protocols were conducted with subjects breathing either room air (AIR), or a normoxic breathing mixture containing 30% N2O. Subjects perceived increasing TWPS as equally warm and the decreasing TWPS as equally cold with AIR or N2O. However, equal changes in TWPS were perceived as significantly less discomforting (P<0.05) during N2O, and the magnitude of the TCZ significantly (P<0.01) increased. Thus, narcosis did not alter thermal sensation, but it significantly changed the perception of comfort. These changes were not reflected in the behavioral response. Subjects produced similar TWPS damped-oscillation patterns in the AIR and N2O trials. We conclude that the narcosis-induced alteration in the perception of thermal comfort does not change the preferred temperature, or the ability to behaviorally maintain thermal comfort.

Bubble trouble: a review of diving physiology and disease.

Exposure to the underwater environment for recreational or occupational purposes is increasing. Approximately 7 million divers are active worldwide and 500,000 more are training every year. Diving related illnesses are consequently an increasingly common clinical problem with over 1000 cases of decompression illness reported annually in the USA alone. Divers are exposed to a number of physiological risks as a result of the hyperbaric underwater environment including: the toxic effects of hyperbaric gases, the respiratory effects of increased gas density, drowning, hypothermia and bubble related pathophysiology. Understanding the nature of this pathophysiology provides insight into physiological systems under stress and as such may inform translational research relevant to clinical medicine. We will review current diving practice, the physics and physiology of the hyperbaric environment, and the pathophysiology and treatment of diving related diseases. We will discuss current developments in diving research and some potential translational research areas.

Epilepsy and recreational scuba diving: an absolute contraindication or can there be exceptions? A call for discussion.

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.