The venous-arterial PCO2 gradient may increase in certain low-flow states, such as CPR and canine endotoxemia. To determine whether venous hypercarbia also occurs in hemorrhagic shock, we studied 12 anesthetized, mechanically ventilated dogs. We performed laparotomies on the animals, inserting catheters into their renal, superior mesenteric, and external iliac veins. Flow in the corresponding arteries were determined using electromagnetic flow probes. The dogs were randomized into a control group (n = 6), and a hemorrhagic shock group (n = 6) which was bled to a mean arterial pressure of 45 to 50 mm Hg and maintained at this pressure for the 6-h study. The results demonstrated a significant (p less than .05) increase in lactate and venous-arterial PCO2 gradient systemically and in all three regional beds. A significant decrease of venous blood pH accompanied these changes which are consistent with our previous findings in low-flow, canine endotoxemia. We conclude that venous hypercarbia is a nonspecific phenomenon, common to low-flow states. The increased CO2 represents both an increased CO2 production and a decreased removal, secondary to low-flow.