VENOARTERIAL CARBON-DIOXIDE GRADIENT IN HUMAN SEPTIC SHOCK

Recent reports have shown that venous hypercarbia, resulting in a widening of the veno-arterial difference in PCo2 (dPCo2), is related to systemic hypoperfusion in various forms of low-flow state. Although spetic shock usually is a hyperdynamic state, other factors can influence the CO2 production and elimination, and thus dPCo2 in shock. This study examined the dPCo2 and acid-base balance together with cardiac output measurements and oxygen-derived variables in 64 adult patients with documented septic shock. For a total of 191 observations, a significant exoponential relation between dPCo2 and CO was found. At time of first measurement, 15 patients had an increased dPCo2 (above 6 mm Hg) and a higher mixed venous PCo2 (PvCo2) (47.2 +/- 10.0 vs 35.9 +/- 7.3 mm Hg, p < 0.001). These patients had a lower cardiac index (2.9 +/- 1.3 vs 3.8 +/- 2.0 L/min-m2, p < 0.01), a higher oxygen extraction ratio, but a similar Vo2 than patients with normal dPCo2+. The higher dPCo2 could also be related to an impaired CO2 elimination as indicated by a higher PaCo2 and a lower PaO2/FIo2 in these patients. Nonsurvivors had a significantly higher dPCo2 than survivors (5.9 +/- 3.4 vs 4.4 +/- 4.4 +/- 2.3 mm Hg, p < 0.05) in the presence of similar cardiac output. The higher dPCo2 in these patients was probably related to the higher blood lactate levels (7.7 +/- 5.3 mmol/L vs 4.5 +/- 2.8 mmol/L, p < 0.01) and the more severe pulmonary impairment (SaO(z) 90 +/- 8 percent vs 95 +/- 4 percent, p < 0.001). Arteriovenous oxygen content difference (dAVo2) and Vo2 were similar in survivors and nonsurvivors. In conclusion, dPCo2 patients with septic shock is related principally to cardiac output but apparently also to the degree of pulmonary impairment. Although dPco2 is larger in nonsurvivors, its prognostic value is modest.