• Rafael Fernandez, Gisela Gili, and Josefina Lopez-Aguilar.
• Intensive Care Unit, Hospital S. Joan de Deu - Fundacio Althaia, CIBERES, Universitat Internacional de Catalunya, c/ Dr Joan Soler 1, 08242, Manresa, Spain. rfernandezf@althaia.cat
• Intensive Care Med. 2013 Apr 1;39(4):711-6.

PurposeAlthough low doses of oxygen (FiO2 <0.50) are considered nontoxic, recent studies have shown that even lower doses increase pulmonary inflammatory mediators. We aimed to evaluate the acute effects of reducing FiO2 on pulmonary inflammation in mechanically ventilated patients without respiratory failure.MethodsThis study was a prospective, single-center crossover study in a medical/surgical intensive care unit at a university hospital. Hemodynamically stable patients under mechanical ventilation for >24 h without severe respiratory failure (PaO2/FiO2 >250). A basal FiO2 of 0.40 was reduced to 0.21 provided SpO2 remained higher than 90 %. Patients who could not tolerate the reduction in FiO2 to 0.21 were excluded.ResultsWe screened 40 patients, but only 28 (70 %) tolerated FiO2 0.21. We measured common clinical variables and inflammatory mediators in plasma and in exhaled breath condensate (EBC) at the end of three 4-h periods: (1) basal (FiO2 0.40), (2) after FiO2 reduction to 0.21, and (3) after returning FiO2 0.40. We used one-way ANOVA for repeated measurements with FiO2 as the grouping variable. Median values of inflammatory mediators in EBC showed nonsignificant changes among the three periods: NO2 + NO3 17.1, 14.1 and 11.0 μmol/L (p = 0.2), and 8-isoprostane 4.4, 8.2 and 5.3 pg/ml (p = 0.6) for the three periods, respectively. Plasma levels also showed nonsignificant changes during the period of the study: NO2 + NO3 12.6, 16.3 and 15.0 μmol/L (p = 0.9), TNFα 13.5, 18.0 and 14.5 pg/ml (p = 0.8), IL-4 12.9, 18.7 and 23.9 pg/ml (p = 0.1), IL-6 50.9, 35.1 and 28.3 pg/ml (p = 0.6), and IL-10 15.2, 22.2 and 22.2 pg/ml (p = 0.7) for the three periods, respectively.ConclusionFiO2 0.40 in mechanically ventilated patients without severe respiratory failure did not increase systemic or pulmonary inflammation.

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