We have developed a dual control system which controls PaO2 and PaCO2 either simultaneously or independently of each other. Since the endtidal to arterial PO2 ratio (PÅO2/PaO2) remains almost constant for a wide range of PIO2 and endtidal PCO2 (PÅCO2) is assumed to be an adequate measure of alveolar PCO2 (PACO2), PÅO2 and PÅCO2 measured by a mass spectrometer can be used to estimate PaO2 and PaCO2, respectively. When PÅO2 and PÅCO2 signals deviated from the preset levels, the control circuit rotated the nozzles of two gas blenders with the pulse motors so as to change PIO2 and PICO2.
In 23 healthy subjects, the system was applied to control their arterial blood gases at preset levels: normoxia (PaO2 90mmHg and PaCO2 40mmHg), normocapnic hypoxia (PaO2 40mmHg and PaCO2 40mmHg), and normoxic hypercapnia (PaO2 90mmHg and PaCO2 55mmHg).
Arterial blood gases attained by the control system were: 91.1±S.D6.5mmHg for PaO2 and 41.2±3.2mmHg for PaCO2 during normoxia, 40.4±3.9mmHg for PaO2 and 38.9±2.5mmHg for PaCO2 during normocapnic hypoxia, and 98.1±11.5mmHg for PaO2 and 52.8±3.4mmHg for PaCO2 during normoxic hypercapnia. The mean difference between target and attained levels were: 1.1mmHg (1.2% of preset level) for PaO2 and 1.2mmHg (3.0%) for PaCO2 during normoxia, 0.4mmHg (1.0%) for PaO2 and 1.1mmHg (2.8%) for PaCO2 during normocapnic hypoxia, and 8.1mmHg (9.0%) for PaO2 and 2.2mmHg (4.0%) for PaCO2 during normoxic hypercapnia. Coefficients of variation around the mean were 7.1 to 11.7% for PaO2 and 6.4 to 7.8% for PaCO2.
This method is useful in physiology as well as clinical medicine because of its accuracy and noninvasiveness.
