Effects of airway anesthesia on ventilatory responses to graded dead spaces and CO₂

Ventilatory response to graded external dead space (0.5, 1.0, 2.0, and 2.5 liters) with hyperoxia and CO₂ steady-state inhalation (3, 5, 7, and 8% CO₂ in O₂) was studied before and after 4% lidocaine aerosol inhalation in nine healthy males. The mean ventilatory response (ΔV̇E/ΔPET(CO₂), where V̇E is minute ventilation and PET(CO₂) is end-tidal PCO₂) to graded dead space before airway anesthesia was 10.2 ± 4.6 (SD) l·min^-1·Torr^-1, which was significantly greater than the steady-state CO₂ response (1.4 ± 0.6 l·min^-1·Torr^-1, P < 0.001). Dead-space loading produced greater oscillation in airway PCO₂ than did CO₂ gas loading. After airway anesthesia, ventilatory response to graded dead space decreased significantly, to 2.1 ± 0.6 l·min^-1·Torr^-1 (P < 0.01) but was still greater than that to CO₂. The response to CO₂ did not significantly differ (1.3 ± 0.5 l·min^-1·Torr^-1). Tidal volume, mean inspiratory flow, respiratory frequency, inspiratory time, and expiratory time during dead-space breathing were also depressed after airway anesthesia, particularly during large dead-space loading. On the other hand, during CO₂ inhalation, these respiratory variables did not significantly differ before and after airway anesthesia. These results suggest that in conscious humans vagal airway receptors play a role in the ventilatory response to graded dead space and control of the breathing pattern during dead-space loading by detecting the oscillation in airway PCO₂. These receptors do not appear to contribute to the ventilatory response to inhaled CO₂.