Hyperoxemia in mechanically ventilated, critically ill subjects: incidence and related factors.
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.
Department of Emergency and Critical Care Medicine, University of Tokushima Graduate School, Tokushima, Japan.
Taiga
T
Itagaki
University of Tokushima Medical School, Tokushima, Japan.
Yuuki
Y
Nakano
Department of Emergency and Critical Care Medicine, University of Tokushima Graduate School, Tokushima, Japan.
Nao
N
Okuda
Department of Emergency and Critical Care Medicine, University of Tokushima Graduate School, Tokushima, Japan.
Masayo
M
Izawa
Department of Emergency and Critical Care Medicine, University of Tokushima Graduate School, Tokushima, Japan.
Mutsuo
M
Onodera
Department of Emergency and Disaster Medicine, Tokushima University Hospital, Tokushima, Japan.
Hideaki
H
Imanaka
Department of Emergency and Critical Care Medicine, University of Tokushima Graduate School, Tokushima, Japan. nmasaji@tokushima-u.ac.jp.
Masaji
M
Nishimura
D000368:Aged; D001784:Blood Gas Analysis; D016638:Critical Illness / Q000628:therapy*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D018496:Hyperoxia / Q000097:blood / Q000453:epidemiology* / Q000209:etiology; D015994:Incidence; D007564:Japan / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D010100:Oxygen / Q000097:blood*; D012121:Respiration, Artificial / Q000009:adverse effects*; D012124:Respiratory Care Units; D012189:Retrospective Studies; D018570:Risk Assessment / Q000379:methods*; D012307:Risk Factors
D010100:Oxygen
acute lung injury; critical care; hyperoxemia; mechanical ventilation; oxygen toxicity; oxygenation