User:RexxS/Hyperoxia

Oxygen toxicity or oxygen toxicity syndrome (also known as the "Paul Bert effect" or the "Lorrain Smith effect") is severe hyperoxia caused by breathing oxygen at elevated partial pressures.^[1][2][3] These above-normal concentrations of oxygen within the body can cause cell damage in two principal regions: the central nervous system (CNS), and the lungs (pulmonary).^[4] Over time, it can also cause damage to the retina and may be implicated in some retinopathic conditions.^[5][6]

The damage may be caused by long exposure (days) to lower concentrations of oxygen or by shorter exposure (minutes or hours) to high concentrations. Long exposures to partial pressures of oxygen above 0.5 

Prevention of oxygen toxicity is an important precaution whenever oxygen is breathed at greater than normal partial pressures. This has led to use of protocols for avoidance of hyperoxia in such fields as diving, hyperbaric therapy and human spaceflight. Hyperventilation does not lead to hyperoxia, because oxygen toxicity never results from breathing air at atmospheric pressure.

Classification

In humans, there are several types of oxygen toxicity:^[1][3]

• Central nervous system (CNS), characterised by convulsions followed by unconsciousness, occurring under hyperbaric conditions

• Pulmonary, characterised by difficulty in breathing and pain within the chest, occurring when breathing elevated pressures of oxygen for extended periods

• Retinopathic, characterised by alterations to the eye, occurring when breathing elevated pressures of oxygen for extended periods

Signs and symptoms

CNS oxygen toxicity manifests as symptoms such as

Early symptoms of pulmonary oxygen toxicity are breathing difficulty and pain or discomfort within the chest (substernal pain). The lungs show inflammation and swelling (pulmonary edema).^[1][2]. Tests in animals have indicated a similar variation in tolerance as found in CNS toxicity.

Causes

As CNS toxicity is caused by breathing oxygen at elevated ambient pressures, patients undergoing hyperbaric oxygen therapy are at risk of suffering hyperoxic seizures.^[1][12][13] For the same reason, divers breathing air at depths greater than 60 metres (200 ft) face a risk of an oxygen toxicity "hit" (seizure) as do divers breathing a gas mixture enriched with oxygen (nitrox).

The lungs have a very large area in contact with the breathing gas and contain thin membranes, making them particularly susceptible to damage by oxygen. The risk of

A seizure caused by CNS oxygen toxicity is a deadly but entirely avoidable event while diving.^[31] The diver may experience no warning symptoms. The effects are sudden convulsions and unconsciousness, during which victims can lose their regulator and drown.^[1][2] There is an increased risk of CNS oxygen toxicity on deep dives, long dives and dives where oxygen-rich breathing gases are used.^[31] Divers are taught to calculate a maximum operating depth for oxygen-rich breathing gases.^[31][32] Cylinders containing such mixtures must be clearly marked with that depth.^[31][32]

In some diver training courses for these types of diving, divers are taught to plan and monitor what is called the "oxygen clock" of their dives.^[31] This is a notional alarm clock, which "ticks" more quickly at increased ppO₂ and is set to activate at the maximum single exposure limit recommended in the National Oceanic and Atmospheric Administration (NOAA) Diving Manual.^[31][32] For the following partial pressures of oxygen the limit is: 45 minutes at 1.6 bar (160 kPa), 120 minutes at 1.5 bar (150 kPa), 150 minutes at 1.4 bar (140 kPa), 180 minutes at 1.3 bar (130 kPa) and 210 minutes at 1.2 bar (120 kPa), but is impossible to predict with any reliability whether or when CNS symptoms will occur.^{[1][2][33][34]} Many Nitrox-capable dive computers calculate an "oxygen loading" and can track it across multiple dives. The aim is to avoid activating the alarm by reducing the ppO₂ of the breathing gas or the length of time breathing gas of higher ppO₂. As the ppO₂ depends on the fraction of oxygen in the breathing gas and the depth of the dive, the diver obtains more time on the oxygen clock by diving at a shallower depth, by breathing a less oxygen-rich gas or by shortening the duration of exposure to oxygen-rich gases.

BPD is reversible in the early stages by use of "break periods" on lower oxygen pressures, but it may eventually result in irreversible lung injury if allowed to progress to severe damage. Usually several days of exposure without "oxygen breaks" are needed to cause such damage.

Pulmonary oxygen toxicity is an entirely avoidable event while diving. The limited duration and naturally intermittent nature of most diving makes this a relatively rare (and even then, reversible) complication for divers. Guidelines have been established that allow divers to calculate when they are at risk of pulmonary toxicity.^{[1][2][35][36][37][38]}

In low-pressure environments oxygen toxicity may be avoided since the toxicity is caused by high oxygen partial pressure, not merely by high oxygen fraction. This is illustrated by oxygen use in spacesuits (historically, for example, the

Vitamin E and selenium were proposed and later rejected as a potential method of protection against pulmonary oxygen toxicity.^[40][41][42] There is however some experimental evidence in rats that vitamin E and selenium aid in preventing in vivo lipid peroxidation and free radical damage, and therefore prevent retinal changes following repetitive hyperbaric oxygen exposures.^[43]

Management

Treatment of seizures during oxygen therapy consists of removing the patient from oxygen, thereby dropping the partial pressure of oxygen delivered.^[2]

Prognosis

An overview of previous studies by Bitterman in 2004 concluded that following removal of breathing gas that contains high fractions of oxygen, no long-term neurological damage from the seizure remains.^[4][44]

Epidemiology

History

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CNS toxicity was first described by Paul Bert in 1878.

Bitterman et al. in 1986 and 1995 showed that darkness and caffeine will delay the onset of changes to brain electrical activity in rats.^[57][58] In the years since, research on CNS toxicity has centered around methods of prevention and safe extension of tolerance.^[59] These include topics such as circadian rhythm, drugs, age, and gender that have been shown to contribute to CNS oxygen toxicity sensitivity.^{[60][61][62][63]}

Pulmonary oxygen toxicity was first described by Lorrain Smith in 1899 when he noted CNS toxicity and discovered in experiments in mice and birds that 0.42 atm (43 kPa) had no effect but 0.74 atm (75 kPa) of oxygen was a pulmonary irritant.