Intramucosal-arterial PCO₂ gap fails to reflect intestinal dysoxia in hypoxic hypoxia

Abstract

Introduction. An elevation in intramucosal-arterial PCO<SUB>2</SUB> gradient (ΔPCO<SUB>2</SUB>) could be determined either by tissue hypoxia or by reduced blood flow. Our hypothesis was that in hypoxic hypoxia with preserved blood flow, ΔPCO<SUB>2</SUB> should not be altered. Methods. In 17 anesthetized and mechanically ventilated sheep, oxygen delivery was reduced by decreasing flow (ischemic hypoxia, IH) or arterial oxygen saturation (hypoxic hypoxia, HH), or no intervention was made (sham). In the IH group (n = 6), blood flow was lowered by stepwise hemorrhage; in the HH group (n = 6), hydrochloric acid was instilled intratracheally. We measured cardiac output, superior mesenteric blood flow, gases, hemoglobin, and oxygen saturations in arterial blood, mixed venous blood, and mesenteric venous blood, and ileal intramucosal PCO<SUB>2</SUB> by tonometry. Systemic and intestinal oxygen transport and consumption were calculated, as was ΔPCO<SUB>2</SUB>. After basal measurements, measurements were repeated at 30, 60, and 90 minutes. Results. Both progressive bleeding and hydrochloric acid aspiration provoked critical reductions in systemic and intestinal oxygen delivery and consumption. No changes occurred in the sham group. ΔPCO<SUB>2</SUB> increased in the IH group (12 ± 10 [mean ± SD] versus 40 ± 13 mmHg; P < 0.001), but remained unchanged in HH and in the sham group (13 ± 6 versus 10 ± 13 mmHg and 8 ± 5 versus 9 ± 6 mmHg; not significant). Discussion. In this experimental model of hypoxic hypoxia with preserved blood flow, ΔPCO<SUB>2</SUB> was not modified during dependence of oxygen uptake on oxygen transport. These results suggest that ΔPCO<SUB>2</SUB> might be determined primarily by blood flow.