Compromised mesenteric blood flow causes significant metabolic and histologic changes. These local changes could not be detected by arterial or mixed venous lactate concentrations, pH, and PCO2 determinations. Under closed-system conditions, mesenteric CO2 accumulation causes an impairment of the CO2-HCO3- buffer, resulting in an unchanged cHCO3-. With impaired mesenteric perfusion, only intramucosal PCO2 alterations occur and an intramucosal pH calculation based on systemic cHCO3-changes is not necessarily correct. Therefore, the only parameter of importance is the intraluminal measurement of intramucosal PCO2 that can reflect isolated mesenteric changes. Thus, we recommended abolishing the terms "intramucosal pH measurement" and "gastric tonometry" and propose using the definition "intramucosal PCO2 measurement."
Long-stored packed red blood cells (PRBCs) have a large potassium load. In patients with end-stage renal failure, the transfusion of such PRBCs may cause a critical increase in plasma potassium levels. Washing PRBCs with an autotransfusion device allows for a marked decrease in potassium load, thus preventing hyperkalemia.
Gastric tonometry has been introduced for the early detection of impaired splanchnic perfusion by determination of the intramucosal PCO2. However, due to methodological problems, i.e., instability of CO2 in water, to assess the exact intramucosal PCO2 with the nasogastric tonometer is unreliable. The present in vitro and in vivo study examines a new fiberoptic PCO2 sensor for the continuous determination of the intramucosal PCO2 and compares these data with that of conventional tonometry. In an in vitro experiment the fiberoptic PCO2 sensor was used to determine the PCO2 of water and humidified air with predefined CO2 values. In both media, predefined CO2 values (35, 42, 49 mm Hg) could be assessed exactly after 9 min of equilibration with a maximum deviation less than 3.5%. In contrast, the values obtained by conventional tonometry showed larger differences. In in vivo experiments on six pigs PCO2 differences were induced by ventilatory changes to validate the fiberoptic PCO2 sensor. Under anesthesia a laparotomy was performed, the ileum punctured, and the fiberoptic PCO2 sensor introduced into the ileal lumen. Arterial PCO2 (PaCO2), mesenteric venous PCO2 (PmvCO2), and intramucosal PCO2, (PiCO2) were determined during normoventilation, hypoventilation, and hyperventilation. During hypoventilation the PiCO2 increased from 53.8 +/- 2.0 mm Hg (PaCO2 = 39.8 +/- 1.4 mm Hg, PmvCO2 = 48.7 +/- 2.7 mm Hg) to 66.5 +/- 4.9 mm Hg (PaCO2 = 52.7 +/- 3.1 mm Hg, PmvCO2 = 62.4 +/- 5.7 mm Hg). With hyperventilation the PiCO2 decreased to 46.8 +/- 2.5 mm Hg (PaCO2 = 29.8 +/- 1.8 mm Hg, PmvCO2 = 41.8 +/- 2.7 mm Hg). The coefficient of correlation (r2) between PiCO2 and PaCO2 was 0.82, and between PiCO2 and PmvCO2 0.94. The fiberoptic PCO2 sensor can determine PiCO2 in a precise and reliable manner, and can continuously record fast intraluminar changes of CO2 in the ileum that were caused by ventilatory changes. The fiberoptic PCO2 sensor is the only method that reliably monitors PiCO2 in the gastrointestinal tract. By the direct measurement of PCO2 the methodological problems associated with the conventional nasogastric tonometry are abolished.
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