[2] 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.
These oxygen containing molecules can damage lipids, proteins, and nucleic acids, and react with surrounding biological tissues.
[1] 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.
[5] 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.
In all these cases, the maximum concentration is naturally limited by the ambient pressure, but the lower limit is usually more difficult to control, and the immediate consequences of hypoxia are generally more serious that the immediate consequences of hyperoxia, so there is a tendency to provide a larger margin for error for hypoxia, and the user is exposed to hyperoxic conditions for much of the time.
This form of exposure leads to lung airway congestion, pulmonary edema, and atelectasis caused by damage to the linings of the bronchi and alveoli.
The overproduction of ROS can disrupt cellular signaling pathways, lead to mitochondrial dysfunction, and trigger inflammatory responses.
[3] Besides, hyperoxia can result in vasoconstriction, particularly affecting cerebral and coronary circulation, potentially leading to adverse outcomes, including increased mortality in critically ill patients.
[12] Further research is ongoing to better understand the long-term impacts of hyperoxia on various organs and systems, as well as to optimize oxygen therapy protocols to minimize these risks while ensuring effective treatment for hypoxic conditions.
Studies have shown that ORI's ability to detect PaO2 levels greater than 100 mmHg is limited, as indicated by an area under the receiver operating characteristic curve (AUROC) of only 0.567.
[13] Similarly, SpO2 measured via pulse oximetry is useful for monitoring oxygen levels, but its diagnostic utility for hyperoxia is constrained because SpO2 readings are capped at 100%.
Clinical guidelines recommend maintaining arterial oxygen saturation (SpO2) within a target range of 88-95% to prevent both hypoxemia and hyperoxemia.
Emerging evidence suggests that prolonged exposure to high oxygen levels, even when clinically indicated, can lead to cellular injury due to oxidative stress.
Hyperoxia-induced lung injury, neurological effects, and disruptions in systemic circulation have been observed in certain cases, particularly in patients with preexisting conditions.
Recent studies emphasize the importance of individualized oxygen therapy, considering the patient’s specific clinical condition and response to treatment.
Protocols have been developed which impose limits on oxygen partial pressure in the breathing gas which expose the diver to acceptable overall risks, bearing in mind that convulsions and loss of consciousness underwater on scuba equipment often lead to death by drowning.
It also appears to reduce the number of hospitalizations, increase effort capacity, and improve health-related quality of life.
It is frequently observed in populations with conditions like COPD, ARDS, and cardiac arrest, where oxygen therapy is routine.
The occurrence of hyperoxia varies across healthcare systems depending on the rigor of oxygen monitoring and management practices.