Increases in tissue Pco2 during circulatory shock reflect selective decreases in capillary blood flow*

Abstract

Tissue Pco2 reflects metabolic alterations due to circulatory failure during circulatory shock. This study addresses simultaneous changes in gastric and buccal tissue Pco2 with changes in microcirculatory blood flow in a rat model of circulatory shock induced by cecal ligation and puncture. Prospective controlled laboratory study. University-affiliated research laboratory. Male breeder Sprague-Dawley rats. Induction of polymicrobial, abdominal sepsis by cecal ligation and puncture. Tissue Pco2 was continuously measured with the aid of a miniature carbon dioxide electrode. Using orthogonal polarization spectral imaging, recordings of the microcirculation were taken at baseline and hourly intervals until death and compared with sham-operated animals. Gastric and buccal tissue Pco2 values progressively increased in animals after cecal ligation and puncture and terminated in death. Microcirculatory blood flow in vessels >20 microm was well preserved during progression of shock, whereas there was an early and progressive decrease in microcirculatory blood flow in vessels <20 microm, mostly representing capillaries. Tissue Pco2, the tissue Pco2-Paco2 gradient, and blood flow in vessels <20 microm were highly correlated. This contrasted with sham control animals in which no significant hemodynamic, blood gas, lactate, microcirculatory, and tissue Pco2 abnormalities were observed. These observations suggest that microcirculatory failure in capillaries appears as an early defect in close association with anaerobic metabolism during progression of circulatory shock in an animal model of septic peritonitis.