Bench-to-bedside review: the effects of hyperoxia during critical illness

Abstract

Oxygen administration is uniformly used in emergency and intensive care medicine and has life-saving potential in critical conditions. However, excessive oxygenation also has deleterious properties in various pathophysiological processes and consequently both clinical and translational studies investigating hyperoxia during critical illness have gained increasing interest. Reactive oxygen species are notorious by-products of hyperoxia and play a pivotal role in cell signaling pathways. The effects are diverse, but when the homeostatic balance is disturbed, reactive oxygen species typically conserve a vicious cycle of tissue injury, characterized by cell damage, cell death, and inflammation. The most prominent symptoms in the abundantly exposed lungs include tracheobronchitis, pulmonary edema, and respiratory failure. In addition, absorptive atelectasis results as a physiological phenomenon with increasing levels of inspiratory oxygen. Hyperoxia-induced vasoconstriction can be beneficial during vasodilatory shock, but hemodynamic changes may also impose risk when organ perfusion is impaired. In this context, oxygen may be recognized as a multifaceted agent, a modifiable risk factor, and a feasible target for intervention. Although most clinical outcomes are still under extensive investigation, careful titration of oxygen supply is warranted in order to secure adequate tissue oxygenation while preventing hyperoxic harm.

Automated Weaning from Mechanical Ventilation after Off-Pump Coronary Artery Bypass Grafting

“…The negative impact of hyperoxia has been studied for many years, and now it is known that excessive oxygen supply may lead to the absorption atelectases and lung damage (17–19). In addition, hyperoxia has been associated with poor outcomes in ICU patients, particularly after cardiac arrest and stroke (18).…”

The Ongoing Challenge of Acute Mesenteric Ischemia

“…Dobutamine, low-dose dopamine, or milrinone improve cardiac function while causing minimal impairment of intestinal blood flow [10]. Supraphysiological parameters for the improvement of cardiovascular function are not an established concept [11]. Volume overload can lead to abdominal compartment syndrome; therefore, the intra-abdominal pressure should be clinically monitored and if a compartment syndrome is suspected, it should be confirmed by measurement of the intravesical pressure.…”

The impact of hyperoxia on outcomes after cardiac surgery: a systematic review and narrative synthesis

“…Given that there is no universally accepted definition of hyperoxia, 19 we did not pre-specify thresholds for hyperoxic or normoxic F I O 2 or PaO 2 targets, but instead relied on the individual study definitions. 1,17 The primary outcome examined was postoperative organ dysfunction defined by: 1) postoperative increases in myocardial enzymes (creatine kinase [CK] and/or troponin), 2) acute kidney injury (AKI), and 3) neurologic dysfunction. The definition of AKI and neurologic dysfunction was in accordance with the individual study report definitions.…”

“…16 This detrimental constellation of events is known as ischemia-reperfusion injury and is believed to be exacerbated by hyperoxic conditions. 4,17 There are compelling arguments both for and against the use of hyperoxia in cardiac surgery. The aim of this systematic review is to identify, critically appraise, and synthesize the highest quality evidence to inform clinical practice and identify unanswered questions for future trials.…”