Impact of arterial oxygen tension on venous oxygen saturation.

Abstract

Impact of Arterial Oxygen Tension on Venous Oxygen Saturation To the Editor We read with great interest the article “Influence of Arterial Dissolved Oxygen Level on Venous Oxygen Saturation: Don’t Forget the Pao2!” published ahead of print in Shock (1). First, we noted that the design of this study was exactly the same as an article we published in Shock in 2008 (2), in which inspired oxygen concentrations were increased to 100% transiently, and differences in central and mixed venous oxygen saturations in relation to changes in arterial oxygen tension were compared. We believe it will be beneficial to the readers of Shock to understand that a similar study had been performed and also similar findings were observed. Second, we agreed with the authors that partial oxygen tension of the central (Pvo2) (or mixed) venous blood has a significant bearing on the central venous (Scvo2) (or mixed venous oxygen) saturation. We believe it is a common misunderstanding that the difference between oxygen delivery and oxygen consumption is the main, if not the only, factor in determining Scvo2 (or mixed venous O2) saturation. Our previous work clearly demonstrated that a substantial increase in Scvo2 (and mixed venous oxygen saturation) due to an increase in arterial oxygen tension was more consistently observed than after a 10% change in cardiac index in critically ill patients with circulatory failure who required inotropic or vasopressor support (2). Furthermore, any increases in Scvo2 (or mixed venous oxygen) saturation due to an increase in arterial oxygen tension would confound its associations with the cardiac output status of the patients, rendering a “good” Scvo2 (or mixed venous oxygen) saturation uninterpretable as a marker of adequate cardiac output or oxygen delivery (3). Our observations and interpretations of the effect of arterial oxygen tension on Scvo2 (or mixed venous oxygen) saturation were also supported by a simulation study using mathematical modeling (4). Taking the results of the current study (1), our previous work (2,3), and the mathematical modeling study (4) together, we can conclude that arterial partial oxygen tension can have a substantial effect on Scvo2 (or mixed venous oxygen) saturation, making the suggestion that an adequate cardiac output or oxygen delivery is ensured when a “good” Scvo2 (or mixed venous oxygen) saturation is obtained invalid and misleading unless hyperoxemia is excluded. Any changes in Scvo2 can only be interpreted as reflecting changes in cardiac output and oxygen delivery if arterial oxygen tension is held constant. Finally, perhaps we all need to remember that it is the venous oxygen tension (Pvo2) that determines the venous oxygen saturation, and not the other way round. Increasing arterial oxygen tension will have a small but significant effect on venous oxygen tension (Pvo2), and the small change in venous oxygen tension (Pvo2) can have a substantial effect on Scvo2 (or mixed venous oxygen) saturation due to the steep part of the oxygen-hemoglobin dissociation curve when hemoglobin is saturated with oxygen between 50% and 90%. Kwok M. Ho, PhD, MPH Benjamin Silbert, MBBS Department of Intensive Care Medicine Royal Perth Hospital University of Western Australia Perth, Western Australia Australia