Tissue hypoxia is a common end product of circulatory shock and a primary target for resuscitation efforts. In this issue Podbregar and Mozina show that thenar tissue O2 saturation (StO2) and mixed venous O2 saturation (SvO2) co-vary in patients in left ventricular failure, but in patients with sepsis StO2 was higher than SvO2. Although StO2 may co-vary with SvO2 they have different determinants such that after shock StO2 may increase well before SvO2 as a result of increased O2 demands to repay O2 debt incurred during hypoperfusion. Thus, the use of StO2 alone to define the endpoint of resuscitation may be misleading.
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