In 10 anesthetized, paralyzed, supine dogs, arterial blood gases and CO2 production (V̇CO2) were measured after 10-min runs of high-frequency ventilation (HFV) at three levels of mean airway pressure (P̄aw) (0, 5, and 10 cmH2O). HFV was delivered at frequencies (f) of 3, 6, and 9 Hz with a ventilator that generated known tidal volumes (VT) independent of respiratory system impedance. At each f, VT was adjusted at P̄aw of 0 cmH2O to obtain a eucapnia. As P̄aw was increased to 5 and 10 cmH2O, arterial PCO2 (Pa(CO2)) increased and arterial PO2 (Pa(O2)) decreased monotonically and significantly. The effect of P̄aw on Pa(CO2) and Pa(O2) was the same at 3, 6, and 9 Hz. Alveolar ventilation (V̇A), calculated from V̇CO2 and Pa(CO2), significantly decreased by 22.7 ± 2.6 and 40.1 ± 2.6% after P̄aw was increased to 5 and 10 cmH2O, respectively. By taking into account the changes in anatomic dead space (VD) with lung volume, V̇A at different levels of P̄aw fits the gas transport relationship for HFV derived previously: V̇A = 0.13 (VT/VD)1.2VTf (J. Appl. Physiol. 60: 1025-1030, 1986). We conclude that increasing P̄aw and lung volume significantly decreases gas transport during HFV and that this effect is due to the concomitant increase of the volume of conducting airways.
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