Mind the influence of arterial oxygen tension on central venous oxygen saturation.

We read with great interest the study by Hernandez and colleagues published in Critical Care [1]. The study showed that central venous oxygen saturation (ScvO2) increased significantly in response to emergency intubation, and the authors suggested that the early normalization of ScvO2 after intubation might not be reliable to reflect successful resuscitation. However, they might have ignored the influence of arterial oxygen tension (PaO2) on ScvO2.

It is well known that when arterial oxygen saturation is approaching 100%, the increase in oxygen delivery would be limited in response to the increase of PaO2. However, a very high PaO2 could significantly influence ScvO2 even if arterial oxygen saturation reaches 100%. Pre-oxygenation may result in a very high PaO2 in the emergency intubation, so PaO2 should be taken as a potentially confounding factor. Very high PaO2 (about 288 mmHg) has a more significant and consistent effect on ScvO2 than a relevant change in cardiac index (>10%) [2]. Moreover, a decrease in the whole body oxygen consumption under hyperoxia has been reported in critically ill patients [3], and animal studies also noted that hyperoxia could result in the redistribution of cardiac output [4]. Recently, Legrand and colleagues documented that an increase in PaO2 could increase ScvO2 without increasing oxygen delivery [5].

It is worth paying attention to the impact of PaO2 on ScvO2 in the management of critically ill patients.