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

Abstract

BACKGROUND: Excessive supplemental oxygen causes injurious hyperoxemia. Before establishing the best P aO 2 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 aO 2 > 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. , and decompensated heart failure (odds ratio 1.9, 95% CI 1.1 to 3.5). CONCLUSIONS: During mechanical ventilation of critically ill subjects, P aO 2 increased, and F IO 2 decreased. One in 4 subjects were hyperoxemic at T2, and hyperoxemia persisted until T3.

Hyperoxemia and excess oxygen use in early acute respiratory distress syndrome: insights from the LUNG SAFE study

“…Consequently, clinicians are faced with the task of titrating the amount of oxygen delivered to avoid both hypoxemia and hyperoxemia. Prior studies show that clinicians appear to use higher FIO 2 than is necessary in the critically ill [3]. While the reasons are unclear, potential explanations include concerns over the need to avoid tissue hypoxia, [4,5] a desire to provide a "buffer" should a clinical deterioration occur, or because the consequences of hyperoxia are considered less severe than hypoxia.…”

“…While oxygen therapy can reverse tissue hypoxia, little evidence exists regarding the optimal use of oxygen in patients with ARDS. Critically ill patients frequently receive higher inspired oxygen concentrations than necessary [3], perhaps due to concerns regarding tissue hypoxia [4,5]. Hyperoxemia and the resultant tissue hyperoxia may worsen systemic organ injury in the critically ill. Arterial hyperoxemia has been associated with increased mortality in some older [6][7][8] but not more recent [9,10] studies of patients with acute brain injury.…”

Oxygen supplementation for critically ill patients—A protocol for a systematic review

“…1,[44][45][46][47] Thus, current practice of supplemental oxygen administration is usually more liberal and may result in hyperoxaemia. [17][18][19][20]23,48,49 Recently, two metaanalyses of observational studies and a randomised clinical trial found an association between hyperoxaemia and mortality. 50,51,56 With the outlined systematic review, we aim to evaluate the benefits and harms of supplemental oxygen administration in critically ill patients.…”

“…1,45 Current practice of oxygen administration is usually liberal and may result in hyperoxaemia. [17][18][19][20]23,48,49 A systematic review of randomised trials in patients with acute myocardial infarction suggests a harmful effect of oxygen administration, but due to lack of power this was not conclusive. 32 Recently two meta-analyses of observational studies found an association between hyperoxaemia and mortality in critically ill patients.…”

Synergistic Effect of Hyperoxia and Biotrauma On Ventilator-Induced Lung Injury

“…However, recently, more detailed factors for development of VILI have emerged: loading of alveolocapillary membrane, duration of exposure to MV, intensity of the exposure (tidal volume; Vt), end-expiratory pulmonary volume, magnitude of the available "baby lung" heterogeneity (which includes atelectasis, consolidation and edema) and hyperoxia. Endotoxin, vascular pressures and fluid/ transfusions are additional factors leading to VILI [2,3]. High Vt and high plateau pressure (Plat) can give excessive distension, or "stretch," of the aerated lungs, thus resulting in volutrauma and barotrauma.…”