Hyperoxia in intensive care, emergency, and peri-operative medicine: Dr. Jekyll or Mr. Hyde? A 2015 update

Abstract

This review summarizes the (patho)-physiological effects of ventilation with high FiO2 (0.8-1.0), with a special focus on the most recent clinical evidence on its use for the management of circulatory shock and during medical emergencies. Hyperoxia is a cornerstone of the acute management of circulatory shock, a concept which is based on compelling experimental evidence that compensating the imbalance between O2 supply and requirements (i.e., the oxygen dept) is crucial for survival, at least after trauma. On the other hand, "oxygen toxicity" due to the increased formation of reactive oxygen species limits its use, because it may cause serious deleterious side effects, especially in conditions of ischemia/reperfusion. While these effects are particularly pronounced during long-term administration, i.e., beyond 12-24 h, several retrospective studies suggest that even hyperoxemia of shorter duration is also associated with increased mortality and morbidity. In fact, albeit the clinical evidence from prospective studies is surprisingly scarce, a recent meta-analysis suggests that hyperoxia is associated with increased mortality at least in patients after cardiac arrest, stroke, and traumatic brain injury. Most of these data, however, originate from heterogenous, observational studies with inconsistent results, and therefore, there is a need for the results from the large scale, randomized, controlled clinical trials on the use of hyperoxia, which can be anticipated within the next 2-3 years. Consequently, until then, "conservative" O2 therapy, i.e., targeting an arterial hemoglobin O2 saturation of 88-95 % as suggested by the guidelines of the ARDS Network and the Surviving Sepsis Campaign, represents the treatment of choice to avoid exposure to both hypoxemia and excess hyperoxemia.

Fig. 1

Beneficial (green arrows) and deleterious (red arrows) effects of hyperoxia, i.e., breathing pure oxygen, during circulatory shock and/or in medical emergencies. FiO ₂ fraction of inspired oxygen, PO ₂ oxygen partial pressure, µ micro, Hb haemoglobin, SO ₂ oxygen saturation, DO ₂ systemic oxygen transport, HPV hypoxic pulmonary vasoconstriction, MAP mean arterial pressure, SVR systemic vascular resistance, NO: nitric oxide, HIF-1α: hypoxia-inducible factor 1 alpha, NF-κB nuclear transcription factor kappaB, ROS reactive oxygen species, ATP adenosine triphosphate; adapted from Asfar et al. [16] with kind permission from Springer Science and Business Media

Fig. 2

Original recordings of ECG and cerebral blood flow velocity (CBFV) in two volunteers undergoing an HBO exposure-test with pure O₂ breathing at three atmospheres of ambient pressure. In the upper panel, HBO-induced seizures were preceded by tachycardia, agitation, and a subsequent marked increase in CBFV. The lower panel shows a volunteer, in whom seizures could be prevented by removing the O₂ face mask; CBFV consecutively fell to lower levels comparable to those during the asymptomatic period

Fig. 3

Effect of increased oxygen partial pressure on bubble size. After creation of a concentration gradient (1), oxygen starts to diffuse into the bubble, simultaneously nitrogen diffuses out of the bubble (2). Thereby, oxygen molecules are now capable of passing the bubble with concomitant reduction of nitrogen concentration (3). Finally, the bubble size decreases significantly (4). Adapted from Muth et al. [103] with kind permission from Springer Science and Business Media