Effects of arterial oxygen tension and cardiac output on venous saturation: a mathematical modeling approach

Abstract

OBJECTIVES:Hemodynamic support is aimed at providing adequate O2 delivery to the tissues; most interventions target O2 delivery increase. Mixed venous O2 saturation is a frequently used parameter to evaluate the adequacy of O2 delivery.METHODS:We describe a mathematical model to compare the effects of increasing O2 delivery on venous oxygen saturation through increases in the inspired O2 fraction versus increases in cardiac output. The model was created based on the lungs, which were divided into shunted and non-shunted areas, and on seven peripheral compartments, each with normal values of perfusion, optimal oxygen consumption, and critical O2 extraction rate. O2 delivery was increased by changing the inspired fraction of oxygen from 0.21 to 1.0 in steps of 0.1 under conditions of low (2.0 L.min-1) or normal (6.5 L.min-1) cardiac output. The same O2 delivery values were also obtained by maintaining a fixed O2 inspired fraction value of 0.21 while changing cardiac output.RESULTS:Venous oxygen saturation was higher when produced through increases in inspired O2 fraction versus increases in cardiac output, even at the same O2 delivery and consumption values. Specifically, at high inspired O2 fractions, the measured O2 saturation values failed to detect conditions of low oxygen supply.CONCLUSIONS:The mode of O2 delivery optimization, specifically increases in the fraction of inspired oxygen versus increases in cardiac output, can compromise the capability of the “venous O2 saturation” parameter to measure the adequacy of oxygen supply. Consequently, venous saturation at high inspired O2 fractions should be interpreted with caution.

Changes in tissue oxygen tension, venous saturation, and Fick‐based assessments of cardiac output during hyperoxia

“…It is possible that the magnitude of this phenomenon (here calculated as 4.9% points in SvO 2 per 100 mm Hg change in PaO 2 ) would be less prominent in the setting of diminished oxygen delivery (whether globally or regionally). As suggested previously by mathematical modeling, tissue hypoxia may cause excess dissolved oxygen to more rapidly diffuse to the mitochondrion, diminishing the magnitude of change in tPO 2 and therefore SvO 2 during hyperoxemia. Nonetheless, given these findings, SvO 2 cannot be viewed as a pure marker of the adequacy of DO 2 , but rather must be interpreted in the context of PaO 2 .…”

Brazilian recommendations of mechanical ventilation 2013. Part 2

“…Suggestion - Avoid systemic systemic vasodilators in refractory hypoxemia (they inhibit hypoxic vasoconstriction). ( 141 )…”

Clinical Predictors of a Low Central Venous Oxygen Saturation after Major Surgery: A Prospective Prevalence Study

“…Indeed, our recent work on patients with circulatory failure requiring vasopressors showed that PaO 2 could increase ScvO 2 and mixed venous oxygen saturation in a very substantial fashion (up to 10% in some patients)-more than the effect associated with changes in cardiac output 31 . Mathematical modelling also supports the fact that ScvO 2 could be affected by PaO 2 in a substantial fashion 32 . This novel concept is important because any increases in ScvO 2 due to an increase in PaO 2 would confound its associations with the cardiac output status of patients, rendering a 'good' ScvO 2 uninterpretable as a marker of adequate cardiac output or oxygen delivery 33 .…”