Hazards of Oxygen Therapy
Oxygen therapy can result in both respiratory and nonrespiratory toxicity. Important factors include patient susceptibility, the FIO2, and duration of therapy.
This complication is primarily seen in patients with COPD who have chronic CO2 retention. These patients develop an altered respiratory drive that becomes at least partly dependent on the mainte-nance of relative hypoxemia. Elevation of arterial oxygen tension to “normal” can therefore cause severe hypoventilation in these patients. Conversely, stable, spontaneously breathing patients with pro-found hypercarbia (PaCO2> 80 mm Hg) who are being supported with supplemental oxygen should not have supplemental oxygen discontinued, even for short intervals. Oxygen therapy can be indirectly hazardous for patients being monitored with pulse oximetry while receiving opioids for pain. Hypoven-tilation as a consequence of opioids may fail to cause worrisome change in oxygen saturation, despite respiratory rates as infrequent as 2 per minute, delaying the diagnosis.
High concentrations of oxygen can cause pulmonary atelectasis in areas of low V/Q ratios. As nitrogen is “washed out” of the lungs, the lowered gas tension in pulmonary capillary blood results in increased uptake of alveolar gas and absorption atelectasis. If the area remains perfused but nonventilated, the resulting intrapulmonary shunt can lead to pro-gressive widening of the alveolar-to-arterial (A–a) gradient.
Prolonged high concentrations of oxygen may dam-age the lungs. Toxicity is dependent both on the par-tial pressure of oxygen in the inspired gas and the duration of exposure. Alveolar rather than arterial oxygen tension is most important in the develop-ment of oxygen toxicity. Although 100% oxygen for up to 10–20 h is generally considered safe, con-centrations greater than 50–60% are undesirable for longer periods as they may lead to pulmonary toxicity.
Molecular oxygen (O2) is unusual in that each atom has unpaired electrons. This gives the mol-ecule the paramagnetic property that allows precise measurements of oxygen concentration. Notably, internal rearrangement of these electrons or their interaction with other atoms (iron) or molecules (xanthine) can produce potentially toxic chemi-cal species. Oxygen toxicity is thought to be due to intracellular generation of highly reactive O2 metabolites (free radicals) such as superoxide and activated hydroxyl ions, singlet O2, and hydrogen peroxide. A high concentration of O2 increases the likelihood of generating toxic species. These metab-olites are cytotoxic because they readily react with cellular DNA, sulfhydryl proteins, and lipids. Two cellular enzymes, superoxide dismutase and cata-lase, protect against toxicity by sequentially convert-ing superoxide first to hydrogen peroxide and then to water. Additional protection may be provided by antioxidants and free radical scavengers; however, clinical evidence supporting the use of these agents in preventing pulmonary toxicity is lacking.
In experimental animals oxygen-mediated injury of the alveolar–capillary membrane produces a syndrome that is pathologically and clinically indistinguishable from ARDS. Tracheobronchitis may also be present initially in some patients. Pul-monary O2 toxicity in newborn infants is manifested as bronchopulmonary dysplasia.
Retinopathy of prematurity (ROP), formerly termed retrolental fibroplasia, is a neovascular reti-nal disorder that develops in 84% of premature sur-vivors born at less than 28 weeks’ gestation. ROP may include disorganized vascular proliferation and fibrosis and may lead to retinal detachment and blindness. ROP resolves in approximately 80% of these cases without visual loss from retinal detachments or scars. ROP was very common in the 1940s–1950s when unmonitored high (0.5 FIO2) oxygen was often administered to premature infants. However, it is now known that hyperoxia and hypoxia are risk factors,but not the primary causes of ROP. Neonates’ risk of ROP increases with low birth weight and com-plexity of comorbidities (eg, sepsis). In contrast to pulmonary toxicity, ROP correlates better with arterial than with alveolar O2 tension. The recom-mended arterial concentrations for premature infants receiving oxygen are 50–80 mm Hg (6.6– 10.6 kPa). If an infant requires arterial O2 satura-tions of 96%–99% for cardiopulmonary reasons, fear about causing or worsening ROP is not a rea-son to withhold the oxygen.
The high inspired O 2 tensions associated with hyper-baric O 2 therapy greatly accelerate O2 toxicity. The risk and expected degree of toxicity are directly related to the pressures used as well as the duration of exposure. Prolonged exposure to O2 partial pres-sures in excess of 0.5 atmospheres can cause pul-monary O2 toxicity. This may present initially with retrosternal burning, cough, and chest tightness and will result in progressive impairment of pul-monary function with continued exposure. Patients exposed to O2 at 2 atmospheres or greater are also at risk for central nervous system toxicity that may be expressed as behavior changes, nausea, vertigo, mus-cular twitching, or convulsions.
Oxygen vigorously supports combustion.
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