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• W2042493309 abstract "When oxygen therapy is warranted, the minimum effective dose generally should be given. Hypoxemic patients who have normal baseline ABG may be treated initially with an intermediate to high FiO2 in the range of 35% to 100%, depending on the severity of the respiratory distress. The majority of patients with exacerbations of COPD who are not in extremis may be given an initial FiO2 of 28%, especially if their previous response to oxygen is known.13,31,32 When treating patients who have chronic severe hypercapnia (eg, those requiring chronic home oxygen), the initial FiO2 should be 24% even though renal compensation of the respiratory acidosis has occurred.29 Further mild elevation of the PaCO2, due mainly to the V/Q mismatch that oxygen therapy induces, may be sufficient to precipitate unacceptable hypercapnia. Patients with exacerbations of COPD who are obviously in extremis, with severe hypoxemia and acidosis, should start with an FiO2 of 24% unless they are being mechanically ventilated.9,12,29 The severity of the hypoxemia and acidosis is more predictive for the development of CO2 narcosis and respiratory failure than is the degree of hypercapnia in these patients.13,20,21 The FiO2 can be increased to 28% and incrementally higher if low FiO2 is tolerated. The use of a high FiO2 is subject to the following guidelines for prevention of clinically significant oxygen toxicity: 100% oxygen at atmospheric pressure is safe if given for less than six hours; 52,66 70% oxygen is probably safe for 24 hours;54,55,58,66,67 and after this time, 45% should be the approximate upper limit to the FiO2.67–69,71,82 The alternatives to increasing the FiO2 to achieve a better PaO2 in an intubated patient who is being ventilated, include increasing the tidal volume, application of optimal positive end expiratory pressure (PEEP), good bronchial toilet, and physiotherapy. The alternative to PEEP in an extubated patient is continuous positive airway pressure (CPAP).83,84 The obvious question arising from the free radical theory of oxygen toxicity is whether exogenous antioxidants can modify the manifestations of oxygen damage. Vitamin E administered to premature infants, who are normally deficient in vitamin E, has been reported to reduce the incidence of retrolental fibroplasia after oxygen therapy.85,86 Experimental infusion of superoxide dismutase may be of some benefit in modifying hyperoxic pulmonary damage.87 It is interesting to speculate that the secret of aging may lie in the gradual oxidation of our body tissues, and that endogenous antioxidants preserve us for our average three score and ten years. When oxygen therapy is warranted, the minimum effective dose generally should be given. Hypoxemic patients who have normal baseline ABG may be treated initially with an intermediate to high FiO2 in the range of 35% to 100%, depending on the severity of the respiratory distress. The majority of patients with exacerbations of COPD who are not in extremis may be given an initial FiO2 of 28%, especially if their previous response to oxygen is known.13,31,32 When treating patients who have chronic severe hypercapnia (eg, those requiring chronic home oxygen), the initial FiO2 should be 24% even though renal compensation of the respiratory acidosis has occurred.29 Further mild elevation of the PaCO2, due mainly to the V/Q mismatch that oxygen therapy induces, may be sufficient to precipitate unacceptable hypercapnia. Patients with exacerbations of COPD who are obviously in extremis, with severe hypoxemia and acidosis, should start with an FiO2 of 24% unless they are being mechanically ventilated.9,12,29 The severity of the hypoxemia and acidosis is more predictive for the development of CO2 narcosis and respiratory failure than is the degree of hypercapnia in these patients.13,20,21 The FiO2 can be increased to 28% and incrementally higher if low FiO2 is tolerated. The use of a high FiO2 is subject to the following guidelines for prevention of clinically significant oxygen toxicity: 100% oxygen at atmospheric pressure is safe if given for less than six hours; 52,66 70% oxygen is probably safe for 24 hours;54,55,58,66,67 and after this time, 45% should be the approximate upper limit to the FiO2.67–69,71,82 The alternatives to increasing the FiO2 to achieve a better PaO2 in an intubated patient who is being ventilated, include increasing the tidal volume, application of optimal positive end expiratory pressure (PEEP), good bronchial toilet, and physiotherapy. The alternative to PEEP in an extubated patient is continuous positive airway pressure (CPAP).83,84 The obvious question arising from the free radical theory of oxygen toxicity is whether exogenous antioxidants can modify the manifestations of oxygen damage. Vitamin E administered to premature infants, who are normally deficient in vitamin E, has been reported to reduce the incidence of retrolental fibroplasia after oxygen therapy.85,86 Experimental infusion of superoxide dismutase may be of some benefit in modifying hyperoxic pulmonary damage.87 It is interesting to speculate that the secret of aging may lie in the gradual oxidation of our body tissues, and that endogenous antioxidants preserve us for our average three score and ten years." @default.
• W2042493309 created "2016-06-24" @default.
• W2042493309 creator A5029634377 @default.
• W2042493309 date "1983-05-01" @default.
• W2042493309 modified "2023-09-27" @default.
• W2042493309 title "Oxygen therapy and oxygen toxicity" @default.
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• W2042493309 doi "https://doi.org/10.1016/s0196-0644(83)80520-4" @default.
• W2042493309 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/6414343" @default.
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