VENOUS HYPERCARBIA ASSOCIATED WITH SEVERE SEPSIS AND SYSTEMIC HYPOPERFUSION

We studied 37 patients with severe sepsis and systemic hypoperfusion to assess changes in Pv̄CO2. Before fluid administration, the cardiac index (CI) was 2.64 ± 0.14 L/min·m2. The Pv̄CO2 was 38 ± 1 torr and mixed venous pH was 7.32 ± 0.02. The venous-arterial CO2 tension gradient (P[v̄-a]CO2) was 6 ± 1 torr. After fluid administration, the CI increased to 3.45 ± 0.14 L/min·m2 (p < .001) and the P(v̄-a)CO2 decreased to 5 ± 1 torr. The correlation between the change in CI and the change in P(v̄-a)CO2 was r = .42, p < .01). P(v̄-a)CO2 was elevated in 19 (51%) patients before fluid administration (P[v̄-a]CO2 > 6 torr) (hypercarbic group). The P(v̄-a)CO2 gradient in this group was 9 ± 1 compared with 4 ± 1 torr in 18 patients with a normal (P(v̄-a)CO2 gradient (p < .001) (normocarbic group). Pv̄CO2 was 41 ± 2 torr in the hypercarbic group compared with 35 ± 2 torr in the normocarbic group (p < .05). No difference was noted in PaCO2. Venous arterial pH and HCO3- gradients were of greater magnitude in the hypercarbic group, -0.05 ± 0.003 and 2.4 ± 0.3 mEq/L compared to -0.02 ± 0.004 (p < .001) and 1.1 ± 0.2 mEq/L (p < .001), respectively. CI in the hypercarbic group was 2.3 ± 0.2 compared to 3.0 ± 0.2 L/min·m2 in the normocarbic group (p < .05). Fluid administration resulted in a decrease in P(v̄-a)CO2 from 9 ± 1 to 5.9 ± 0.8 torr in the hyperbaric group (p < .01). This was associated with a significant increase in CI from 2.3 ± 0.2 to 3.4 ± 0.2 L/min·m2 (p < .001). The correlation between the change in CI and the change in P(v̄-a)CO2 was r = .46, p < .01. These data suggest that venous hypercarbia contributes to the acid-base disturbances associated with sepsis and circulatory failure. Furthermore, the development of venous hypercarbia is related to decreases in systemic blood flow.