Ventilatory response to low levels of CO 2

Abstract

Ventilation and P A CO 2 were measured in six subjects after 10–12 min of breathing 1–2% CO 2 during hyperoxia and hypoxia. These inspired CO 2 concentrations were achieved in two ways: by enriching the inspirate with CO 2 and by having the subjects breathe through dead spaces of 100–400 cm 3. Breathing through dead space gave the same results as CO 2 enrichment of the inspirate when the effect of the dead spaces on mean inspired CO 2 was allowed for. During hyperoxia all subjects demonstrated isocapnic hyperpnea in response to mean inspired CO 2 concentrations of 1% ; ventilation increased without change in P A CO 2 . When mean inspired CO 2 concentration approximated 1.5% two subjects showed isocapnic hyperpnea, and one subject demonstrated isocapnic hyperpnea in response to mean inspired CO 2 concentrations of 2%. The increase in P A CO 2 observed in each subject in response to 2% CO 2 in O 2 correlated negatively with the slope of that subject's rebreathing CO 2 response curve. Hypoxia ( P A O 2 = 45–50 mm Hg ) depressed the response to 1% CO 2 in that, while hypoxic, no subject showed isocapnic hyperpnea in response to 1% CO 2. The isocapnic hyperpnea we observed was chiefly due to increased tidal volume, and was therefore not analogous to the isocapnic hyperpnea observed by others in dogs in response to increases of CO 2 in lung gas. When low levels of CO 2 produced an increase in P A CO 2 the associated change in ventilation (ΔV̇ E/ΔP A CO 2 )was much less than that observed while rebreathing 7% CO 2. Isocapnic hyperpnea in response to low levels of CO 2 is common among normal individuals, and is depressed by hypoxia; the stimulus responsible for this response is unknown.