Hyperoxia is the state of being exposed to high levels of oxygen; it may refer to organisms, cells and tissues that are experiencing excessive oxygenation, or to an abnormally high oxygen concentration in an environment (e.g. a body of water). In medicine, it refers to excessive oxygen in the lungs or other body tissues, and results from raised alveolar oxygen partial pressure ― that is, alveolar oxygen partial pressure greater than that due to breathing air at normal (sea level) atmospheric pressure. This can be caused by breathing air at a pressure above normal or by breathing other gas mixtures with a high oxygen fraction, high ambient pressure or both. The body is tolerant of some deviation from normal inspired oxygen partial pressure, but a sufficiently elevated level of hyperoxia can lead to oxygen toxicity over time, with the mechanism related to the partial pressure, and the severity related to the dose. Hyperoxia is the opposite of hypoxia; hyperoxia refers to a state in which oxygen supply to the tissues is excessive, while hypoxia refers to a state in which oxygen supply is insufficient. Supplementary oxygen administration is widely used in emergency and intensive care medicine and can be life-saving in critical conditions, but too much can be harmful and affects a variety of pathophysiological processes. Reactive oxygen species are known problematic by-products of hyperoxia which have an important role in cell signaling pathways. There are a wide range of effects, but when the homeostatic balance is disturbed, reactive oxygen species tend to cause a cycle of tissue injury, with inflammation, cell damage, and cell death.
Signs and symptoms 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.
Oxygen toxicity
Excessive exposure to oxygen can lead to oxygen toxicity, also known as oxygen toxicity syndrome, oxygen intoxication, and oxygen poisoning. There are two main ways in which oxygen toxicity can occur: exposure to significantly elevated partial pressures of oxygen for a short period of time (acute oxygen toxicity), or exposure to more modest elevations in oxygen partial pressures but for a longer duration (chronic oxygen toxicity). Acute toxicity often presents with central nervous system (CNS) effects, while chronic toxicity often manifests with pulmonary (lung) effects. Early CNS signs of acute oxygen toxicity may vary, though perioral twitching and spasm of small muscles of the hand are common. As exposure is prolonged, additional symptoms may develop such as nausea, tinnitus ("ringing in the ears"), dysphoria (feeling of unease), and seizure. A grand-mal seizure, also known as a generalized tonic-clonic seizure may occur. 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 suggest 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. If oxygen toxicity is experienced while in a body of water, such as in underwater diving, a seizure may lead to drowning. If the inciting agent is removed, there are typically no long-term neurological impacts of oxygen toxicity. Pulmonary damage results from reactive oxygen species altering structures within the lungs, such as damaging the pulmonary epithelium and inactivating the surfactant. Pulmonary symptoms may 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, and shortness of breath. If exposure is continued, a fatality may result due to the lack of oxygen. Hemoptysis (coughing up blood) may also be seen. Pulmonary damage is often reversible over time after inciting agent is removed. Ocular (eye) damage may also occur. In premature infants this may be seen as retinopathy of prematurity and retrolental fibroplasia. Swelling of the retina may also occur, and with prolonged exposure there is increased likelihood of cataract development.
… excerpt ends here. Continue reading the full article.
