• Petros Kopterides, Stefanos Bonovas, Irini Mavrou, Eleni Kostadima, Epaminondas Zakynthinos, and Apostolos Armaganidis.
• 2nd Critical Care Department, Attiko University Hospital, School of Medicine, University of Athens, Athens, Greece. petkop@ath.forthnet.gr
• Shock. 2009 Jun 1;31(6):561-7.

AbstractMonitoring of central venous oxygen saturation (ScvO2) is considered comparable with mixed venous oxygen saturation (SvO2) in the initial resuscitation phase of septic shock. Our aim was to assess their agreement in septic shock in the intensive care unit setting and the effect of a potential difference in a computed parameter, namely, oxygen consumption (VO2). In addition, we sought for a central venous to pulmonary artery (PA) lactate gradient. We enrolled 37 patients with septic shock who were receiving noradrenaline infusions, and their attending physicians had placed a PA catheter for fluid management. Blood samples were drawn in succession from the superior vena cava, right atrium (RA), right ventricle, and PA. Hemodynamic and treatment parameters were monitored, and data were compared by correlation and Bland-Altman analysis. Mixed venous oxygen saturation was lower than ScvO2 (70.2% +/- 11.4% vs. 78.6% +/- 10.2%; P < 0.001), with a bias of -8.45% and 95% limits of agreement ranging from -20.23% to 3.33%. This difference correlated significantly to the noradrenaline infusion rate and the oxygen consumption and extraction ratio. These lower SvO2 values resulted in computed VO2v higher than the VO2cv (P < 0.001), with a bias of 104.97 mL min(-1) and 95% limits of agreement from -4.12 to 214.07 mL min(-1). Finally, lactate concentration was higher in the superior vena cava and RA than in the PA (2.42 +/- 3.15 and 2.35 +/- 3.16 vs. 2.17 +/- 3.19 mM; P < 0.01 for both comparisons). Thus, our data suggest that ScvO2 and SvO2 are not equivalent in intensive care unit patients with septic shock. Additionally, the substitution of ScvO2 for SvO2 in the calculation of VO2 produces unacceptably large errors. Finally, the decrease in lactate between RA and PA may support the hypothesis that the mixing of RA and coronary sinus blood is at least partially responsible for the difference between ScvO2 and SvO2.

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