The investigators have developed a non-steady state, five compartment pulmonary model of gas kinetics that incorporates interactions between O2 and CO2 in the lung, blood, and tissues. New methodology has been developed that includes both O2 uptake per breath (uses a new humidity sensor) and esophageal Doppler measure of cardiac output (QT). The computer model has formulated the following hypotheses: 1) Acute decreases in cardiac output (QT) by patient position change will transiently decrease pulmonary O2 consumption (VO2), but the decrease in CO2 elimination (VCO2) is sustained because tissue CO2 stores are a hundred fold greater than O2. 2) Positive end-expiratory pressure decreases VO2 and VCO2 due to decreases in QT and alveolar ventilation (VA) and appearance of high VA/Q. 3) Pulmonary shunting decreases VCO2, because redistribution of VA to the rest of the lung contributes only to CO2 and not O2 exchange. 4) Changes in global tissue metabolic activity can monitor anesthetic depth, and changes in regional body function can be measured by pulmonary gas exchange. 5) These and other cardiovascular, pulmonary, and metabolic pathophysiology cause specific and unique changes in non-steady state O2 and CO2 kinetics by mechanisms elucidated by the computer model. Determining the mechanisms underlying acute pathophysiology will advance the understanding of O2 and CO2 kinetics during non-steady state, and allow the non-invasive diagnosis of critical events during clinical anesthesia.
