SHOCK, Vol. 42, No. 3, pp. 279Y280, 2014
Letters to the Editor (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%.
Impact of Arterial Oxygen Tension on Venous Oxygen Saturation To the Editor: We read with great interest the article BInfluence 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 Bgood[ 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 Bgood[ 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
Kwok M. Ho, PhD, MPH Benjamin Silbert, MBBS Department of Intensive Care Medicine Royal Perth Hospital University of Western Australia Perth, Western Australia Australia
REFERENCES 1. Legrand M, Valle´e F, Mateo J, Payen D: Influence of arterial dissolved oxygen level on venous oxygen saturation: don_t forget the PaO2! Shock 41: 510Y513, 2014. 2. Ho KM, Harding R, Chamberlain J: The impact of arterial oxygen tension on venous oxygen saturation in circulatory failure. Shock 29:3Y6, 2008. 3. Ho KM, Harding R, Chamberlain J, Bulsara M: A comparison of central and mixed venous oxygen saturation in circulatory failure. J Cardiothorac Vasc Anesth 24:434Y439, 2010. 4. Zampieri FG, Park M, Azevedo LC, Amato MB, Costa EL: Effects of arterial oxygen tension and cardiac output on venous saturation: a mathematical modeling approach. Clinics (Sao Paulo) 67:897Y900, 2012.
Reply: We thank Ho et al. for their constructive comments regarding our article in Shock (1) and for bringing to our attention the results of their previous work (2). We are glad that the results appear consistent across different studies by different authors. Our results also confirm that this physiological response applies to regional circulation, i.e., the cerebral circulation. Indeed, increasing the PaO2 above the reference range is expected to raise the ScvO2 significantly, which is confirmed by our results. To further illustrate the predictable behavior of the ScvO2 using the following formula (estimated delta ScvO2 = Hb 1.34 [SaO2(40%) j SaO2(100%)] + 0.003 [PaO2(40%) j PaO2(100%)] j [PvO2(40%) j PvO2(100%)] / (Hb 1.34 100)), we observed a bias (SD) of only j2.8% (4%) between the estimated and measured variation of ScvO2 between FIO2 of 40% and 100%. We also agree with Ho et al. that the influence of the PaO2 can overwhelm the influence of cardiac output under certain circumstances. This appears to be especially true in the setting of low hemoglobin levels, i.e., when baseline arterial oxygen content is low. However, the participation of the dissolved oxygen content to oxygen delivery is expected to be higher in the setting of high cardiac output (since dissolved oxygen delivery to the tissue will increase under combined factor of arterial dissolved oxygen content and cardiac output). In other 279
Copyright © 2014 by the Shock Society. Unauthorized reproduction of this article is prohibited.
Letters to the Editor (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%.
Impact of Arterial Oxygen Tension on Venous Oxygen Saturation To the Editor: We read with great interest the article BInfluence 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 Bgood[ 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 Bgood[ 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
Kwok M. Ho, PhD, MPH Benjamin Silbert, MBBS Department of Intensive Care Medicine Royal Perth Hospital University of Western Australia Perth, Western Australia Australia
REFERENCES 1. Legrand M, Valle´e F, Mateo J, Payen D: Influence of arterial dissolved oxygen level on venous oxygen saturation: don_t forget the PaO2! Shock 41: 510Y513, 2014. 2. Ho KM, Harding R, Chamberlain J: The impact of arterial oxygen tension on venous oxygen saturation in circulatory failure. Shock 29:3Y6, 2008. 3. Ho KM, Harding R, Chamberlain J, Bulsara M: A comparison of central and mixed venous oxygen saturation in circulatory failure. J Cardiothorac Vasc Anesth 24:434Y439, 2010. 4. Zampieri FG, Park M, Azevedo LC, Amato MB, Costa EL: Effects of arterial oxygen tension and cardiac output on venous saturation: a mathematical modeling approach. Clinics (Sao Paulo) 67:897Y900, 2012.
Reply: We thank Ho et al. for their constructive comments regarding our article in Shock (1) and for bringing to our attention the results of their previous work (2). We are glad that the results appear consistent across different studies by different authors. Our results also confirm that this physiological response applies to regional circulation, i.e., the cerebral circulation. Indeed, increasing the PaO2 above the reference range is expected to raise the ScvO2 significantly, which is confirmed by our results. To further illustrate the predictable behavior of the ScvO2 using the following formula (estimated delta ScvO2 = Hb 1.34 [SaO2(40%) j SaO2(100%)] + 0.003 [PaO2(40%) j PaO2(100%)] j [PvO2(40%) j PvO2(100%)] / (Hb 1.34 100)), we observed a bias (SD) of only j2.8% (4%) between the estimated and measured variation of ScvO2 between FIO2 of 40% and 100%. We also agree with Ho et al. that the influence of the PaO2 can overwhelm the influence of cardiac output under certain circumstances. This appears to be especially true in the setting of low hemoglobin levels, i.e., when baseline arterial oxygen content is low. However, the participation of the dissolved oxygen content to oxygen delivery is expected to be higher in the setting of high cardiac output (since dissolved oxygen delivery to the tissue will increase under combined factor of arterial dissolved oxygen content and cardiac output). In other 279
Copyright © 2014 by the Shock Society. Unauthorized reproduction of this article is prohibited.
