Tissue surface pH monitoring during reduced blood flow: Metabolic implications and sources of error.

Abstract

To evaluate tissue surface pH as an indicator of the acid base status of arterial blood during periods of reduced blood flow, we examined the relationship between tissue surface pH, arterial pH, arterial lactic acid levels, and base deficit in fifteen spontaneously breathing anesthetized cats. Blood flow was reduced by hemorrhage to 50% of control blood pressure values (Fig. 3) or by infusing norepinephrine (10 mcg/kg/min intravenously) for one hour (Fig. 2). During these procedures, tissue surface pH was inversely related to arterial base deficit (r = - 0.665, p less than 0.02) and lactic acid (r = 0.822, p less than 0.001) but not related to blood pH (Fig. 4). The errors resulting from measuring tissue surface pH continuously for 2 1/2 to 8 hours were examined by comparing the in vivo recalibration drift of the electrodes. The pH and reference electrodes drifted less than 0.1 pH units during this time. However, when examined in separate experiments for recalibration drift in vitro, we observed up to 0.67 pH units drift after 24 hours of reference electrode contamination with blood, but only 0.02 pH units drift in the pH electrode after this period. Since tissue surface pH is linearly correlated with the blood concentration of lactic acid or the base deficit during periods of acute blood flow reduction, tissue surface pH monitoring may be helpful for following the severity of the resulting anaerobic metabolism in neonates at risk for reduced peripheral perfusion or hypoxia. However, improvements in the reference electrode will be necessary to make long term tissue surface pH monitoring reliable if there is a reasonable risk of contamination of the reference electrode with blood.