During clinical anesthesia, it is astonishing that CO2 monitoring consists mainly of end-tidal PCO2 to confirm endotracheal intubation and to estimate ventilation, and O2 monitoring consists of a single PO2 measurement to detect a hypoxic gas mixture. Better understanding of how O2 and CO2 kinetics monitoring can define systems pathophysiology will greatly enhance safety in anesthesia by detecting critical events such as abrupt decrease in cardiac output (Q.T) by vena-caval compression during abdominal surgery, occurrence of CO2 pulmonary embolism during laparoscopy, rising tissue O2 consumption (V.O2) during light anesthesia, and onset of anaerobic metabolism (V.CO2 is disproportionately higher than V.O2).~In the previous grant period, discoveries of CO2 kinetics during non-steady state revealed significant gaps in understanding of O2 kinetics. To this end, a 5-compartment lung model of gas kinetics in the body during non-steady state has been developed, that incorporates complex interactions between O2 and CO2 in the lung, blood, and tissues. This computer model was used to formulate the following hypotheses, and will elucidate mechanisms underlying the subsequent measured data in anesthetized patients.~The investigators have already developed two innovative devices that are essential for the V.O2 measurement: A fast response temperature and humidity sensor, and a mixing device (a bymixer) for the measurement of mixed gas fraction, especially designed for anesthesia systems. The investigators have also designed a sophisticated bench system for the validation of both devices, which showed the high accuracy and performance of our measurements.~Hypotheses that will be tested in our overall research theme include:~That pulmonary O2 uptake (V.O2) in anesthetized patients is much lower than the value quoted in the literature.~That inhalation anesthesia influences V.O2 differently than total intravenous anesthesia (TIVA).~That an acute decrease in cardiac output (Q.T) (by patient position change) will transiently decrease V.O2 but the decrease in CO2 elimination (V.CO2) is sustained because tissue CO2 stores are a hundred fold greater than O2 (please see previously approved IRB protocol, HS# 2000-1325).~That positive end-expiratory pressure (PEEP) decreases V.O2 and V.CO2 due to decreases in Q.T and alveolar ventilation (V.A), and appearance of high ventilation-to-perfusion (V.A/Q.) units (please see previously approved IRB protocol, HS# 2000-1325).~That Trendelenburg (head down) position increases V.O2 and V.CO2 due to increase in Q.T.~That V.O2 can help to determine the necessity of blood transfusion.~That the continuous measurement of the respiratory quotient (RQ=V.CO2/V.O2) can detect transition to anaerobic metabolism.~That the continuous measurement of the respiratory RQ can be a good alternative to arterial blood gas sampling.~That the continuous measurement of the respiratory RQ can determine the necessity of nutritional support during long operations.~In this protocol, the investigators will study the clinical implications of these measurements, believing that they are the missing links in anesthesia monitoring. Elucidating the mechanisms underlying this 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 conferring increased safety, especially for the majority of healthy patients who receive only non-invasive monitoring.~A separate section of the study, which compliments the metabolic gas exchange study with the bymixer flow system is the examination of respiratory gas with a portable mass-spectrometer to detect volatile organic compounds during anaerobic metabolism. The experimental anaerobic model is adult patients undergoing a surgery that requires tourniquet. Anaerobic metabolism will be detected by acid base balance blood test, the bymixer flow measurement and the mass spectrometer. Anesthesia will be maintained by total intravenous anesthesia (TIVA) and each patient will have an arterial line. No other intervention would be taken. It is an observational type study.
During clinical anesthesia, it is astonishing that CO2 monitoring consists mainly of end-tidal PCO2 to confirm endotracheal intubation and to estimate ventilation, and O2 monitoring consists of a single PO2 measurement to detect a hypoxic gas mixture. Better understanding of how O2 and CO2 kinetics monitoring can define systems pathophysiology will greatly enhance safety in anesthesia by detecting critical events such as abrupt decrease in cardiac output (Q.T) by vena-caval compression during abdominal surgery, occurrence of CO2 pulmonary embolism during laparoscopy, rising tissue O2 consumption (V.O2) during light anesthesia, and onset of anaerobic metabolism (V.CO2 is disproportionately higher than V.O2).