We developed an automated system which measures responses to hypoxia and hypercapnia both in terms of ventilation and P0.1, and timing components of ventilation in terms of the rate of inspiratory to total respiratory cycle duration (Ti/Ttot). The system is composed of a dual control system of arterial blood gases (Pao2, Paco2), a system that measures ventilation, P0.1, Ti and Te, and a microcomputer.
The system was applied in 13 normal subjects (mean age=35.9 years) and 8 patients with chronic pulmonary emphysema (mean age=67.9 years).
1. In both groups, there were no significant differences of ventilatory and P0.1 responses to hypoxia. Patients had significantly lower ventilatory responses to hypercapnia than normal subjects (0.001<P<0.01), but P0.1 responses were the same.
2. When the hypoxic stimulus was chemically denervated, patients showed significantly greater VE and P0.1 and lower Ti/Ttot than normal subjects (VE, P0.1, Ti/Ttot: 0.02<P<0.05). Hypoxia led to a significant increase of P0.1 and f (P0.1:0.001<P<0.01, f:0.02<P<0.05), but VE and VT were not altered. Hypercapnia evoked different changes in the respiratory cycle: VE and VT increased significantly (VE:0.02<P<0.05, VT:0.01<P<0.02) and f was unchanged.
3. In normal subjects, hyperventilation during hypoxia induced a decrease in the ratio of P0.1 to VT/Ti, probably reflecting effective impedance of the respiratory system, but remained unchanged in patients.
