In medicine, it refers to excess oxygen in the lungs or other body tissues, which can be caused by breathing air or oxygen at pressures greater than normal atmospheric pressure. This kind of hyperoxia can lead to oxygen toxicity, caused from the harmful effects of breathing molecular oxygen at elevated partial pressures. Hyperoxia is the opposite of hypoxia; hyperoxia refers to a state in which oxygen supply is excessive, and hypoxia refers to a state in which oxygen supply is insufficient.
In the environment, it refers to excess oxygen in a body of water or other habitat.
Signs and symptomsEdit
Associated with hyperoxia is an increased level of reactive oxygen species (ROS), which are chemically reactive molecules containing oxygen. These oxygen containing molecules can damage lipids, proteins, and nucleic acids, and react with surrounding biological tissues. The human body has naturally occurring antioxidants to combat reactive molecules, but the protective antioxidant defenses can become depleted by abundant reactive oxygen species, resulting in oxidation of the tissues and organs.
The symptoms produced from breathing high concentrations of oxygen for extended periods have been studied in a variety of animals, such as frogs, turtles, pigeons, mice, rats, guinea pigs, cats, dogs and monkeys. The majority of these studies reported the occurrence of irritation, congestion and edema of the lungs, and even death following prolonged exposures.
The supplementation of oxygen can lead to oxygen toxicity, also known as oxygen toxicity syndrome, oxygen intoxication, and oxygen poisoning. There are two main types of oxygen toxicity: central nervous system toxicity (CNS), and pulmonary and ocular toxicity.
Temporary exposure to high partial pressures of oxygen at greater than atmospheric pressure can lead to central nervous system toxicity (CNS). An early but serious sign of CNS oxygen toxicity is a grand-mal seizure, also known as a generalized tonic-clonic seizure. This type of seizure consists of a loss of consciousness and violent muscle contractions. Signs and symptoms of oxygen toxicity are usually prevalent, but there are no standard warning signs that a seizure is about to ensue. The convulsion caused by oxygen toxicity does not lead to hypoxia, a side effect common to most seizures, because the body has an excess amount of oxygen when the convulsion begins. The seizures can lead to drowning, however, if the convulsion is suffered by a diver still in the water.
Prolonged exposure to higher oxygen levels at atmospheric pressure can lead to pulmonary and ocular toxicity. Symptoms of oxygen toxicity may include disorientation, respiratory problems, or myopia. Prolonged exposure to higher than normal partial pressures of oxygen can result in oxidative damage to cell membranes. Signs of pulmonary (lung) oxygen toxicity begin with slight irritation in the trachea. A mild cough usually ensues, followed by greater irritation and a worse cough until breathing becomes quite painful and the cough becomes uncontrollable. If supplementation of oxygen is continued, the individual will notice tightness in the chest, difficulty breathing, shortness of breath, and if exposure is continued, fatality due to lack of oxygen.
Oxygen supplied at greater than atmospheric pressure has been known to damage plants, animals, and aerobic bacteria such as Escherichia coli. The damaging effects vary depending on the specimen used, its age, physiological state, and diet.
The supplementation of oxygen has been a common procedure of prehospital treatment for many years. Guidelines include cautions about chronic obstructive pulmonary disease (COPD). These guidelines stress the use of 28% oxygen masks and caution the dangers of hyperoxia. Long-term use of supplemental oxygen improves survival in patients with COPD, but can lead to lung injury.
An additional cause of hyperoxia is related to underwater diving with breathing apparatus. Underwater divers breath a mixture of gasses which must include oxygen, and the partial pressure of any given gas mixture will increase with depth. A mixture known as nitrox is used to reduce the risk of decompression sickness by substituting oxygen for part of the nitrogen content. Breathing nitrox can lead to hyperoxia due to the high partial pressure of oxygen if used too deep or for too long. Protocols for the safe use of raised oxygen partial pressure in diving are well established and used routinely by recreational scuba divers, military combat divers and professional saturation divers alike. The highest risk of hyperoxia is in hyperbaric oxygen therapy, where it is a high probability side effect of the treatment for more serious conditions, and is considered an acceptable risk as it can be managed effectively without apparent long term effects.
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Oxygen supplementation is used to treat tissue hypoxia and to relieve arterial hypoxemia. High concentrations of oxygen are often given to patients with chronic obstructive pulmonary disease (COPD) or acute lung injury (ALI). Supplementing oxygen is known to cause tissue damage, with toxicity increasing with the increase of oxygen concentrations and exposure pressures. Unfortunately, the supplementation of oxygen is necessary if an individual is not able to obtain sufficient oxygen through respiration and perfusion. To decrease the chances of hyperoxia, the therapist should use the lowest concentration of oxygen required by an individual. At this time, there are no known alternatives to oxygen supplementation.
- Mach, William J.; Thimmesch, Amanda R.; Pierce, J. Thomas; Pierce, Janet D. (2011). "Consequences of Hyperoxia and the Toxicity of Oxygen in the Lung". Nursing Research and Practice. 2011: 1–7. doi:10.1155/2011/260482. PMC 3169834. PMID 21994818.
- COMROE, JULIUS H. (7 July 1945). "OXYGEN TOXICITY". Journal of the American Medical Association. 128 (10): 710. doi:10.1001/jama.1945.02860270012004.
- Sawatzky, David. "Oxygen Toxicity Signs and Symptoms". www.diverite.com/. Retrieved 12 November 2014.
- New, A (1 February 2006). "Oxygen: kill or cure? Prehospital hyperoxia in the COPD patient". Emergency Medicine Journal. 23 (2): 144–146. doi:10.1136/emj.2005.027458. PMC 2564043. PMID 16439751.
- Lang, Michael A., ed. (2001). DAN nitrox workshop proceedings. Durham, NC: Divers Alert Network. Retrieved 25 January 2017.
- Bitterman, N (2004). "CNS oxygen toxicity". Undersea and Hyperbaric Medicine. 31 (1): 63–72. PMID 15233161. Retrieved 25 January 2017.
- Jenkinson, SG (November 1993). "Oxygen toxicity". New Horizons (Baltimore, Md.). 1 (4): 504–11. PMID 8087571.