Oxygen therapy

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Oxygen therapy
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A person wearing a simple face mask
Clinical data
Other namessupplemental oxygen, enriched air
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Drug classmedical gas
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Chemical and physical data

Oxygen therapy, also known as supplemental oxygen, is the use of oxygen as medical treatment.[1] Acute indications for therapy include hypoxemia (low blood oxygen levels), carbon monoxide toxicity and cluster headache. It may also be prophylactically given to maintain blood oxygen levels during the induction of anesthesia.[2] Oxygen therapy is often useful in chronic hypoxemia caused by conditions such as severe COPD or cystic fibrosis.[3][1] Oxygen can be delivered via nasal cannula or face mask, or via high pressure conditions such as in endotracheal intubation or hyperbaric chamber.[4][5] It can also be given through bypassing the airway, such as in ECMO therapy.

Oxygen is required for normal cellular metabolism.[6] However, excessively high concentrations can result in oxygen toxicity, leading to lung damage and respiratory failure.[2][7] Higher oxygen concentrations can also increase the risk of airway fires, particularly while smoking.[1] Oxygen therapy can also dry out the nasal mucosa without humidification.[1] In most conditions an oxygen saturation of 94–96% is adequate, while in those at risk of carbon dioxide retention saturations of 88–92% are preferred.[1][8] In cases of carbon monoxide toxicity or cardiac arrest, saturations should be as high as possible.[1][8] While air is typically 21% oxygen by volume, oxygen therapy can increase O2 content of air up to 100%.[7]

The medical use of oxygen first became common around 1917, and is the most common hospital treatment in the developed world.[1][9][10][11] It is currently on the World Health Organization's List of Essential Medicines.[11] Home oxygen can be provided either by oxygen tanks or oxygen concentrator.[1]

Medical uses

Oxygen piping and regulator with flow meter, for oxygen therapy, mounted in an ambulance

Oxygen is widely used by hospitals, EMS, and first-aid providers in a variety of conditions and settings. A few indications frequently requiring high-flow oxygen include resuscitation, major trauma, anaphylaxis, major bleeding, shock, active convulsions, and hypothermia.[12][13]

Acute conditions

In context of acute hypoxemia, oxygen therapy should be titrated to a target level based on pulse oximetry (94–96% in most patients, or 88–92% in people with COPD).[12][8] This can be performed by increasing oxygen delivery, described as FIO2(fraction of inspired oxygen). In 2018, the British Medical Journal recommended that oxygen therapy be stopped for saturations greater than 96% and not started for saturations above 90 to 93%.[14] This may be due to an association between excessive oxygenation in the acutely ill and increased mortality.[8] Exceptions to these recommendations include carbon monoxide poisoning, cluster headaches, sickle cell crisis, and pneumothorax.[14]

Oxygen therapy has also been used as emergency treatment for decompression sickness for years.[15] Recompression in a hyperbaric chamber with 100% oxygen is the standard treatment for decompression illness.[15][16][17] The success of recompression therapy is greatest if given within four hours after resurfacing, with earlier treatment associated with a decreased number of recompression treatments required for resolution.[18] It has been suggested in literature that heliox may be a better alternative to oxygen therapy.[19]

In the context of stroke, oxygen therapy may be beneficial as long as hyperoxic environments are avoided.[20]

People receiving outpatient oxygen therapy for hypoxemia following acute illness or hospitalization should be re-assessed by a physician prior to prescription renewal to gauge the necessity of ongoing oxygen therapy.[21] If the initial hypoxemia has resolved, additional treatment may be an unnecessary use of resources.[21]

Chronic conditions

Common conditions which may require a baseline of supplementary oxygen include chronic obstructive pulmonary disease (COPD), chronic bronchitis, and emphysema. Patients may also require additional oxygen during acute exacerbations. Oxygen may also be prescribed for breathlessness, end-stage cardiac failure, respiratory failure, advanced cancer, or neurodegenerative disease in spite of relatively normal blood oxygen levels. Physiologically, it may be indicated in people with arterial oxygen partial pressure PaO
≤ 55mmHg (7.3kPa) or arterial oxygen saturation SaO
≤ 88%.[22][23][24]

Careful titration of oxygen therapy should be considered in patients with chronic conditions predisposing them to carbon dioxide retention (e.g., COPD, emphysema). In these instances, oxygen therapy may decrease respiratory drive, leading to accumulation of carbon dioxide (hypercapnia), acidemia, and increased mortality secondary to respiratory failure.[25] Improved outcomes have been observed with titrated oxygen treatment largely due to gradual improvement of the ventilation/perfusion ratio.[26] The risks associated with loss of respiratory drive are far outweighed by the risks of withholding emergency oxygen, so emergency administration of oxygen is never contraindicated. Transfer from the field to definitive care with titrated oxygen typically occurs long before significant reductions to the respiratory drive are observed.


There are certain situations in which oxygen therapy has been shown to negatively impact a person's condition.[27]

Adverse effects

In some instances, oxygen delivery can lead to particular complications in population subsets.

Alternative medicine

Some practitioners of alternative medicine have promoted "oxygen therapy" as a cure for many human ailments including AIDS, Alzheimer's disease and cancer. According to the American Cancer Society, "available scientific evidence does not support claims that putting oxygen-releasing chemicals into a person's body is effective in treating cancer", and some of these treatments can be dangerous.[34]

Physiologic Effects

Oxygen supplementation has a variety of physiologic effects on the human body. Whether or not these effects are adverse to a patient is dependent upon clinical context. Cases in which an excess amount of oxygen is available to organs is known as hyperoxia.[35] While the following effects may observed with noninvasive high-dose oxygen therapy (i.e., not ECMO), delivery of oxygen at higher pressures is associated with exacerbation of the following associated effects.

Absorption atelectasis

It has been theorized that oxygen therapy may promote accelerated development of atelectasis (partial or complete lung collapse), as well as denitrogenation of gas cavities (e.g., pneumothorax, pneumocephalus).[36][37] This concept is based on the idea that oxygen is more quickly absorbed compared to nitrogen within the body, leading oxygen-rich areas that are poorly ventilated to be rapidly absorbed, leading to atelectasis.[36] It is thought that higher fractions of inhaled oxygen is associated with increasing rates of atelectasis in the clinical scenario.[38] In clinically healthy adults, it is believed that absorption atelectasis typically does not have any significant implications when managed properly.[39]

Airway inflammation

In regard to the airway, both tracheobronchitis and mucositis have been observed with high levels of oxygen delivery (typically >40% O2).[40] Within the lungs, these elevated concentrations of oxygen have been associated with increased alveolar toxicity (coined the Lorrain-Smith effect).[35] Mucosal damage is observed to increase with elevated atmospheric pressure and oxygen concentrations, which may result in the development of ARDS and possibly death.[41][42]

Central nervous system effects

Decreased cerebral blood flow and ICP have been reported in hyperoxic conditions, with mixed results regarding impact on cognition.[43][44][45][46] Hyperoxia as also been associated with seizures, cataract formation, and reversible myopia.[47]


Among CO2 retainers, excess exposure to oxygen in context of the Haldane effect causes decreased binding of deoxyhemoglobin to CO2 in the blood.[48] This unloading of CO2 may contribute to the development of acid-base disorders due to the associated increase in PaCO2 (hypercapnea). Patients with underlying lung disease such as COPD may not be able to adequately clear the additional CO2 produced by this effect, worsening their condition.[49] In addition, oxygen therapy has also been shown to decrease respiratory drive, further contributing to possible hypercapnea.[37]

Immunological effects

Hyperoxic environments have been observed to decrease granulocyte rolling and diapedesis in specific circumstances in humans.[50] In regard to anaerobic infections, cases of necrotizing fasciitis have been observed to require fewer debridement operations and have improvement in regard to mortality in patients treated with hyperbaric oxygen therapy.[51] This may stem from oxygen intolerance of otherwise anaerobic microorganisms.

Oxidative Stress

Sustained exposure to oxygen may overwhelm the body's capacity to deal with oxidative stress.[52]  Rates of oxidative stress appears to be influenced by both oxygen concentration and length of exposure, with general toxicity observed to occur within hours in certain hyperoxic conditions.[53]

Reduction in erythropoiesis

Hyperoxia is observed to result in a serum reduction in erythropoietin, resulting in reduced stimulus for erythropoiesis.[54] Hyperoxia at normobaric environments does not appear to be able to halt erythropoiesis completely.[54]

Pulmonary vasodilation

Within the lungs, hypoxia is observed to be a potent pulmonary vasoconstrictor, due to inhibition of an outward potassium current and activation of inward sodium current leading to pulmonary vascular muscular contraction.[55] However, the effects of hyperoxia do not seem to have a particularly strong vasodilatory effect from the few studies that have been performed on patients with pulmonary hypertension.[56][57] As a result, an effect appears to be present but minor.[56][57]

Systemic vasoconstriction

In the systemic vasculature, oxygen serves as a vasoconstrictor, leading to mildly increased blood pressure and decreased cardiac output and heart rate. Hyperbaric conditions do not seem to have a significant impact on these overall physiologic effects.[58][46] Clinically, this may lead to increased left-to-right shunting in certain patient populations, such as those with atrial septal defect. While the mechanism of the vasoconstriction is unknown, one proposed theory is that increased reactive oxygen species from oxygen therapy accelerates the degradation of endothelial nitric oxide, a vasodilator.[59][46] These vasoconstrictive effects are thought to be the underlying mechanism helping to abort cluster headaches.[60]

Dissolved O2 in hyperoxic conditions may make also a significant contribution to total gas transport.