Taiga Itagaki1, Yuuki Nakano2, Nao Okuda1, Masayo Izawa1, Mutsuo Onodera1, Hideaki Imanaka3, Masaji Nishimura4. 1. Department of Emergency and Critical Care Medicine, University of Tokushima Graduate School, Tokushima, Japan. 2. University of Tokushima Medical School, Tokushima, Japan. 3. Department of Emergency and Disaster Medicine, Tokushima University Hospital, Tokushima, Japan. 4. Department of Emergency and Critical Care Medicine, University of Tokushima Graduate School, Tokushima, Japan. nmasaji@tokushima-u.ac.jp.
Abstract
BACKGROUND: Excessive supplemental oxygen causes injurious hyperoxemia. Before establishing the best P(aO2) targets for mechanically ventilated patients, it is important to understand the incidence of hyperoxemia and related factors. We investigated oxygenation in mechanically ventilated subjects in our ICU and evaluated factors related to hyperoxemia (P(aO2) > 120 mm Hg) at 48 h after initiation of mechanical ventilation. METHODS: We retrospectively reviewed the medical records of patients admitted to our ICU from January 2010 to May 2013. Inclusion criteria were 15 y of age or older and administration of mechanical ventilation for > 48 h. Patients at risk of imminent death on admission or who had received noninvasive ventilation were excluded. We collected subject demographics, reasons for mechanical ventilation, and during mechanical ventilation, we collected arterial blood gas data and ventilator settings on the first day of intubation (T1), 48 h after initiation of mechanical ventilation (T2), and on the day of extubation (T3). Multivariable logistic regression analysis was performed to clarify independent variables related to hyperoxemia at T2. RESULTS: For the study period, data for 328 subjects were analyzed. P(aO2) statistically significantly increased over time to 90 (interquartile range of 74-109) mm Hg at T1, 105 (89-120) mm Hg at T2, and 103 (91-119) mm Hg at T3 (P < .001), coincident with decreases in F(IO2) of 0.4 (0.3-0.5) at T1, 0.3 (0.3-0.4) at T2, and 0.3 (0.3-0.35) at T3 (P < .001). Hyperoxemia occurred in 15.6% (T1), 25.3% (T2), and 22.4% (T3) of subjects. Multivariable logistic regression analysis revealed that hyperoxemia was independently associated with age of < 40 y (odds ratio 2.6, 95% CI 1.1-6.0), Acute Physiology and Chronic Health Evaluation II scores of ≥ 30 (odds ratio 0.53, 95% CI 0.3-1.0), and decompensated heart failure (odds ratio 1.9, 95% CI 1.1 to 3.5). CONCLUSIONS: During mechanical ventilation of critically ill subjects, P(aO2) increased, and F(IO2) decreased. One in 4 subjects were hyperoxemic at T2, and hyperoxemia persisted until T3.
BACKGROUND: Excessive supplemental oxygen causes injurious hyperoxemia. Before establishing the best P(aO2) targets for mechanically ventilated patients, it is important to understand the incidence of hyperoxemia and related factors. We investigated oxygenation in mechanically ventilated subjects in our ICU and evaluated factors related to hyperoxemia (P(aO2) > 120 mm Hg) at 48 h after initiation of mechanical ventilation. METHODS: We retrospectively reviewed the medical records of patients admitted to our ICU from January 2010 to May 2013. Inclusion criteria were 15 y of age or older and administration of mechanical ventilation for > 48 h. Patients at risk of imminent death on admission or who had received noninvasive ventilation were excluded. We collected subject demographics, reasons for mechanical ventilation, and during mechanical ventilation, we collected arterial blood gas data and ventilator settings on the first day of intubation (T1), 48 h after initiation of mechanical ventilation (T2), and on the day of extubation (T3). Multivariable logistic regression analysis was performed to clarify independent variables related to hyperoxemia at T2. RESULTS: For the study period, data for 328 subjects were analyzed. P(aO2) statistically significantly increased over time to 90 (interquartile range of 74-109) mm Hg at T1, 105 (89-120) mm Hg at T2, and 103 (91-119) mm Hg at T3 (P < .001), coincident with decreases in F(IO2) of 0.4 (0.3-0.5) at T1, 0.3 (0.3-0.4) at T2, and 0.3 (0.3-0.35) at T3 (P < .001). Hyperoxemia occurred in 15.6% (T1), 25.3% (T2), and 22.4% (T3) of subjects. Multivariable logistic regression analysis revealed that hyperoxemia was independently associated with age of < 40 y (odds ratio 2.6, 95% CI 1.1-6.0), Acute Physiology and Chronic Health Evaluation II scores of ≥ 30 (odds ratio 0.53, 95% CI 0.3-1.0), and decompensated heart failure (odds ratio 1.9, 95% CI 1.1 to 3.5). CONCLUSIONS: During mechanical ventilation of critically ill subjects, P(aO2) increased, and F(IO2) decreased. One in 4 subjects were hyperoxemic at T2, and hyperoxemia persisted until T3.
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