Abstract
Abstract : The goal of our study for the first year was to investigate whether the changes in sublingual PCO2 reflect changes in tissue blood flow during hemorrhage and hemorrhagic shock. Hemorrhagic shock was induced by a modification of Wigger's method in male domestic pigs weighting 35 to 40 kg. Sublingual PCO2 increased from 60 to 129 mmHg in parallel with average decreases in cardiac output to 44% and mean arterial pressure to 47%, decreases in EtCO2 from 35 to 28 mmHg together with increases in arterial blood lactate concentrations from 0.7 to 7.8 mmol/l over the two-hour interval of shock. Utilizing colored microspheres for measurements, sublingual blood flow decreased to 34%, liver flow to 56%, and renal flow to 47%. After reinfusion of shed blood, sublingual PCO2 was restored to approximately baseline values together with arterial pressure, cardiac output and EtCO2, but there was delayed reversal of lactic acidosis. Increases in sublingual PCO2, is accomplished by proportionate decreases in sublingual and vital organ blood flows. Our study supports the rationale for non-invasive measurements of sublingual PCO2 for diagnosis and quantitation of the severity of hemorrhagic shock. The goal of our task for the second year was to investigate the possibility that buccal PCO2 provided an additional option as a site of measurement that would facilitate longer term non-invasive monitoring of tissue perfusion. Two groups of pentobarbital anesthetized Sprague-Dawley male rats were bled 40 percent of their estimated blood volume over an interval of 30 minutes. The animals were randomly assigned to measurement of either sublingual or buccal PCO2 with an optical PCO2 sensor. A linear regression analysis between P(BU)CO2 and P(SL)CO2 yielded r=0.94. Buccal PCO2 measurement provides values correlated highly with those of sublingual measurement for the diagnosis and evaluation of the severity of circulatory failure and facilitates continuous recording.
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