Combination of O 2 and CO 2 -derived variables to detect tissue hypoxia in the critically ill patient

Early detection and prompt reversion of tissue hypoperfusion are key factors to prevent progression to multiorgan dysfunction and death during shock states (1). Techniques commonly used to monitor tissue perfusion have focused mainly on systemic blood flow and the balance between oxygen demand and supply to the tissues (2,3). Indeed, quantitative resuscitation targeting central venous oxygen saturation (ScvO2) and some macro hemodynamic parameters was related with a significant reduction of mortality in an initial single-center randomized controlled trial including patients with septic shock (4). Subsequent studies on implementation of resuscitation bundles targeting similar hemodynamic goals in septic shock were also apparently beneficial (5,6). Nevertheless, the utility of oxygen-derived parameters was promptly challenged (7), and recent clinical trials failed to demonstrate their clinical benefit (8-10). In fact, ScvO2 is often normal at the ICU admission (11), and attaining macro hemodynamic goals and/or normalization of global oxygen-derived parameters in septic shock do not exclude the occurrence or persistence of tissue hypoxia. In this context, other variables such as carbon dioxide (CO2)-derived parameters could provide very important information about macro and micro hemodynamics, even when oxygen- derived variables resemble corrected. Importantly, variations in CO2 occur faster than changes in lactate levels, which make the CO2-derived parameters an attractive tool to monitor tissue perfusion and potentially, cell oxygenation during the early stages of shock