PCO2 gradients: a reliable marker of macro- and microcirculatory perfusion

Abstract

The increase in venous to arterial and tissue to arterial PCO₂ differences (Pv-aCO₂ and Pt-aCO₂) is a constant result found in experimental and clinical studies on circulatory failure. The value of these two gradients depends on the tissue perfusion. In patients with cardiovascular failure, an “anaerobic” CO₂ production occurs by buffering H⁺ ions produced in excess; however, this production cannot offset the simultaneous decrease in “aerobic” CO₂ production. The increase in venous and tissue CO₂ can no longer be explained by an increase in CO₂ production but rather by hypoperfusion, with lower CO₂ clearance creating an accumulation of CO₂ in the tissues and the venous system. In septic shock, the pathophysiology could associate high cardiac output after initial resuscitation and tissue perfusion heterogeneity by alteration of the microcirculation. In this situation, aPv-aCO₂ gradient < 6 mmHg (together with a SvO₂ > 70%) represents a therapeutic goal to restore the macrocirculation; however, the persistence of a high Pt-aCO₂ gradient reflects an abnormality in microcirculation with residual tissue hypoperfusion. All these points are well illustrated in the literature by several experimental and clinical studies, confirming that PCO₂ gradients reflect themacro-and microcirculatory perfusion in shock states. As easily measured in blood samples or using less and less invasive monitoring devices, their use should be promoted and popularized for daily clinical practice.