Ratios of central venous-to-arterial carbon dioxide content or tension to arteriovenous oxygen content are better markers of global anaerobic metabolism than lactate in septic shock patients

Background To evaluate the ability of the central venous-to-arterial CO 2 content and tension differences to arteriovenous oxygen content difference ratios (∆ContCO 2 /∆ContO 2 and ∆PCO 2 /∆ContO 2 , respectively), blood lactate concentration, and central venous oxygen saturation (ScvO 2 ) to detect the presence of global anaerobic metabolism through the increase in oxygen consumption (VO 2 ) after an acute increase in oxygen supply (DO 2 ) induced by volume expansion (VO 2 /DO 2 dependence). Methods We prospectively studied 98 critically ill mechanically ventilated patients in whom a fluid challenge was decided due to acute circulatory failure related to septic shock. Before and after volume expansion (500 mL of colloid solution), we measured cardiac index, VO 2 , DO 2 , ∆ContCO 2 /∆ContO 2 and ∆PCO 2 /∆ContO 2 ratios, lactate, and ScvO 2 . Fluid-responders were defined as a ≥15 % increase in cardiac index. Areas under the receiver operating characteristic curves (AUC) were determined for these variables. Results Fifty-one patients were fluid-responders (52 %). DO 2 increased significantly (31 ± 12 %) in these patients. An increase in VO 2 ≥ 15 % (“VO 2 -responders”) concurrently occurred in 57 % of the 51 fluid-responders (45 ± 16 %). Compared with VO 2 -non-responders, VO 2 -responders were characterized by higher lactate levels and higher ∆ContCO 2 /∆ContO 2 and ∆PCO 2 /∆ContO 2 ratios. At baseline, lactate predicted a fluid-induced increase in VO 2 ≥ 15 % with AUC of 0.745. Baseline ∆ContCO 2 /∆ContO 2 and ∆PCO 2 /∆ContO 2 ratios predicted an increase of VO 2 ≥ 15 % with AUCs of 0.965 and 0.962, respectively. Baseline ScvO 2 was not able to predict an increase of VO 2 ≥ 15 % (AUC = 0.624). Conclusions ∆ContCO 2 /∆ContO 2 and ∆PCO 2 /∆ContO 2 ratios are more reliable markers of global anaerobic metabolism than lactate. ScvO 2 failed to predict the presence of global tissue hypoxia.