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In shock states, aerobically generated carbon dioxide (CO2) decreases together with oxygen (O2) consumption (VO2). When VO2 becomes dependent on O2 delivery (DO2), CO2 can be produced anaerobically mostly due to bicarbonate buffering of protons produced in excess secondary to the hydrolysis of adenosine triphosphate, so that VCO2 can exceed VO2. It has been estimated that anaerobic ATP compensates approximately 6 % of the accumulated O2 depth [1]. Therefore, a respiratory quotient (RQ) [1 may be interpreted as a sign of anaerobic metabolism, since it may indicate that more CO2 is produced than O2 is consumed (Fig. 1), although both are decreased. According to the Fick equation, VCO2 equals the product of cardiac output by the difference between mixed venous and arterial CO2 contents (Cmv–aCO2) whereas VO2 equals the product of cardiac output by the difference between arterial and mixed venous O2 contents (Ca–mvO2) (Fig. 1). By eliminating the cardiac output value, which is common to the numerator and denominator of the RQ (Fig. 1) and taking PCO2 as a surrogate of CO2 content, an increased ratio between mixed venous–arterial PCO2 difference and Cmv–aCO2 (Pmv–aCO2/Ca–mvO2) was shown to be a good indicator of anerobiosis assessed by hyperlactatemia [2]. However, the relationship between CO2 content and PCO2 is curvilinear rather than linear and is influenced by the degree of metabolic acidosis, the hematocrit and the O2 saturation. In this issue of ICM, Ospina-Tascon et al. [3] demonstrate that a Cmv–aCO2/Ca–mvO2 [1 predicts outcome early in septic shock, similar to increased arterial lactate concentration. Patients with both an increased Cmv–aCO2/Ca–mvO2 and lactate concentration 6 h after the study start had the highest mortality [3]. The authors propose that the Cmv–aCO2/Ca–mvO2 could become a resuscitation target [3]. The authors should be congratulated on having conducted this study and having performed the relatively complex calculations of the CO2 contents. However, before targeting to normalize the Cmv–aCO2/ Ca–mvO2, several issues should be considered.

Venous–arterial CO2 to arterial–venous O2 difference ratio as a resuscitation target in shock states?