We have developed a dual control system which controls Pa
O2 and Pa
CO2 either simultaneously or independently of each other. Since the endtidal to arterial P
O2 ratio (P
ÅO2/Pa
O2) remains almost constant for a wide range of P
IO2 and endtidal P
CO2 (P
ÅCO2) is assumed to be an adequate measure of alveolar P
CO2 (P
ACO2), P
ÅO2 and P
ÅCO2 measured by a mass spectrometer can be used to estimate Pa
O2 and Pa
CO2, respectively. When P
ÅO2 and P
ÅCO2 signals deviated from the preset levels, the control circuit rotated the nozzles of two gas blenders with the pulse motors so as to change P
IO2 and P
ICO2.
In 23 healthy subjects, the system was applied to control their arterial blood gases at preset levels: normoxia (Pa
O2 90mmHg and Pa
CO2 40mmHg), normocapnic hypoxia (Pa
O2 40mmHg and Pa
CO2 40mmHg), and normoxic hypercapnia (Pa
O2 90mmHg and Pa
CO2 55mmHg).
Arterial blood gases attained by the control system were: 91.1±S.D6.5mmHg for Pa
O2 and 41.2±3.2mmHg for Pa
CO2 during normoxia, 40.4±3.9mmHg for Pa
O2 and 38.9±2.5mmHg for Pa
CO2 during normocapnic hypoxia, and 98.1±11.5mmHg for Pa
O2 and 52.8±3.4mmHg for Pa
CO2 during normoxic hypercapnia. The mean difference between target and attained levels were: 1.1mmHg (1.2% of preset level) for Pa
O2 and 1.2mmHg (3.0%) for Pa
CO2 during normoxia, 0.4mmHg (1.0%) for Pa
O2 and 1.1mmHg (2.8%) for Pa
CO2 during normocapnic hypoxia, and 8.1mmHg (9.0%) for Pa
O2 and 2.2mmHg (4.0%) for Pa
CO2 during normoxic hypercapnia. Coefficients of variation around the mean were 7.1 to 11.7% for Pa
O2 and 6.4 to 7.8% for Pa
CO2.
This method is useful in physiology as well as clinical medicine because of its accuracy and noninvasiveness.
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