Hyperoxemia in Mechanically Ventilated,Critically Ill Subjects: Incidence and Related Factors

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.

Keywords

oxygenation hyperoxemia mechanical ventilation oxygen toxicity acute lung injury critical care

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