Partial pressure of oxygen, hyperoxemia and hyperoxia in the intensive care or anesthesia setting

Abstract

In clinical studies, the partial pressure of oxygen (PaO2) and oxygen pulse saturation are the main variables used to assess blood oxygenation and define the threshold of hypoxia/hyperoxia and hypoxemia/hyperoxemia. Determination of the optimal oxygenation target has generated a lot of interest in recent years, mainly because of the potential risk of worse outcomes associated with hyperoxia, whereas the risk associated with hypoxia has been already well known. In this short narrative review, we recall some fundamental elements of physiology regarding the meaning of PaO2, the diffusion of oxygen to cells, the definitions of hyperoxemia and hyperoxia and the mechanisms of oxygen toxicity to provide a better understanding of these concepts, to which intensive care clinicians are frequently confronted. PaO2 provides only limited information about oxygen concentration carried by blood and does not allow to determine whether cells are exposed to hyperoxia. This should be considered for the design of future studies that aim to determine optimal oxygenation target and by clinicians for their daily practice.

Keywords: gas law; hemoglobin; hyperbaric oxygenation therapy; hyperoxemia; hyperoxia; intensive care unit; oxidative stress; oxygen toxicity; reactive oxygen species.

Figure 1

O₂ travels from the atmosphere to the mitochondria. (1) The first process involves the diffusion and dissolution of O₂ molecules from the alveolar gas to the blood passing through alveolar capillaries. After crossing the alveolocapillary membrane, O₂ dissolves into the blood according to the gradient of the partial pressure of O₂ in the alveolar gas and the deoxygenated blood and the temperature. (2) O₂ will bind to hemoglobin to be efficiently carried up to the tissue while limiting its toxicity. In normobaric environnement O₂ carried in the dissolved state is very low, consequence of the low solubility of O₂ in water based solution (solubility constant of O₂ in blood is equal to 0.0031 mL of O₂/mmHg/100 mL of blood at 37°C and 1 ATM (1 ATM = 760 mmHg)). (3) In capillaries, dissolved O₂ diffuses to the mitochondria according to the local concentration gradient, lowering the concentration of O₂ (or PO₂) in the capillaries’ blood and leading to the passive release of O₂ by hemoglobin. Therefore, the rate of O₂ release depends on the rate of O₂ consumption. Notably, the consumption rate of O₂ is much faster than its release and diffusion across the cell and mitochondrial membranes. This explains why we need such an O₂ carrier system (hemoglobin) whereas the quantity of O₂ consumed is low compared with the O₂ transported. Created with Servier Medical ART, available at https://smart.servier.com/. 2,3 DPG: 2,3-Diphosphyglycerate; ATM: atmosphere; O₂: oxygen.

Figure 2

Proposed measures to limit exposure to high FIO₂ while ensuring adequate O₂ delivery. The few recommendations proposed are, of course, not exhaustive. Owing to the underlying disease and the patient, their application may be limited. However, it represents dynamic logical thinking at the bedside. Apart from etiological treatment, which is fundamental, the role of the clinician is basically to support adequate O₂ delivery to the whole body while limiting the harmful effects of the different treatments or supports used. Ventilation can be achieved by limiting ventilator-induced injury and exposure to supplemental O₂ as much as possible. Created with Servier Medical ART, available at https://smart.servier.com/. CO₂: Carbon dioxide; D(A-V)O₂: venoarterial difference in O₂; F_IO₂: fraction of inspired O₂; O₂: oxygen; ODC: oxyhemoglobin dissociation curve; SvO₂: venous saturation in O₂.