The Impact of Arterial Oxygen Tension on Venous Oxygen Saturation in Circulatory Failure

Abstract

Central and mixed venous oxygen saturations have been used to guide resuscitation in circulatory failure, but the impact of arterial oxygen tension on venous oxygen saturation has not been thoroughly evaluated. This observational study investigated the impact of arterial oxygen tension on venous oxygen saturation in circulatory failure. Twenty critically ill patients with circulatory failure requiring mechanical ventilation and a pulmonary artery catheter in an intensive care unit in a tertiary hospital in Western Australia were recruited. Samples of arterial blood, central venous blood, and mixed venous blood were simultaneously and slowly drawn from the arterial, central venous, and pulmonary artery catheter, respectively, at baseline and after the patient was ventilated with 100% inspired oxygen for 5 min. The blood samples were redrawn after a significant change in cardiac index (>or =10%) from the baseline, occurring within 24 h of study enrollment while the patient was ventilated with the same baseline inspired oxygen concentration, was detected. An increase in inspired oxygen concentration significantly increased the arterial oxygen tension from 12.5 to 38.4 kPa (93.8-288 mmHg) (mean difference, 25.9 kPa; 95% confidence interval [CI], 7.5-31.9 kPa; P < 0.001) and the venous oxygen saturation from 69.9% to 76.5% (mean difference, 6.6%; 95% CI, 5.3% - 7.9%; P < 0.001). The effect of arterial oxygen tension on venous oxygen saturation was more significant than the effect associated with changes in cardiac index (mean difference, 2.8%; 95% CI, -0.2% to 5.8%; P = 0.063). In conclusion, arterial oxygen tension has a significant effect on venous oxygen saturation, and this effect is more significant and consistent than the effect associated with changes in cardiac index.

Effect of hyperoxia and vascular occlusion on tissue oxygenation measured by near infra‐red spectroscopy (InSpectra™): a volunteer study

“…Our previous work has suggested that central or mixed venous oxygen saturation becomes an unreliable indicator of cardiac output when the arterial oxygen tension is high [7, 8]. In this study, although high inspired oxygen concentrations did increase S t O 2 , its effect on S t O 2 was relatively small and reached a plateau between 30% and 40% inspired oxygen.…”

“…We have assumed that arterial oxygen tension would be very high by using 70% inspired oxygen because all our participants were healthy individuals. However, it is possible that S t O 2 may increase more significantly when 100% inspired oxygen is used [7, 8].…”

“…Resuscitation guided by these additional targets requires invasive vascular access and frequent blood measurements, limiting its applicability. Evidence also suggests that a high inspired oxygen concentration and arterial oxygen tension can have a substantial effect on brain, myocardial and central or mixed venous oxygen saturations [5, 6], thus potentially limiting the validity of using the latter parameters for haemodynamic targets in patients who receive a high concentration of oxygen during resuscitation [7, 8].…”

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

“…Ho et al have previously shown that in humans with shock, high levels of PaO 2 can increase SvO 2 levels (8). From their data, however, it was not possible to determine whether the increase in SvO 2 was indeed reflecting a better oxygen supply/demand relationship or whether the SvO 2 represented a false marker of the adequacy of such a relationship.…”

“…Venous oxygen saturation is part of the current guidelines for early resuscitation during sepsis (7). Nevertheless, SvO 2 can respond differently to changes in DO 2 if the changes are obtained through changes in different component of the DO 2 equation (8), even when these changes lead to similar VO 2 values. In this paper, we developed a mathematical model to investigate whether the type of DO 2 optimization, specifically increases in the arterial partial pressure of oxygen versus increases in cardiac output, would have different effects on SvO 2 .…”