Introduction: During HFOV, lung inflation plays a critical role in decreasing ventilation-perfusion mismatch. While inadequate Paw can increase Vd/Vt by promoting alveolar atelectasis, excessive Paw can increase Vd/Vt by decreasing lung perfusion.

Objective: To evaluate the effect of changing Paw on Vd/Vt during HFOV.

Methods: Five healthy New Zealand rabbits were ventilated with HFOV under ketamine anesthesia. End tidal CO2 (PETCO2) was measured in the trachea using a Beckman CO2 gas analyzer. Each animal was randomly ventilated at Paw of 3, 5, 7 and 9 cm H2O pressure. Blood pressure, PETCO2, arterial and venous blood gases were measured at each Paw. After collecting 2 sets of data at each Paw, the lungs were lavaged with 20cc/kg of normal saline to create lung injury. Following lung injury, measurements were repeated at Paw of 10, 13, 16, 19. Vd/Vt was estimated using the following equation: Vd/Vt(%) = 100*(PaCO2 - PETCO2)/ PaCO2. (PETCO2 = mixed expired CO2). In animals with acute lung injury, we noted that the PvCO2 was significantly higher than PaCO2 and we also calculated a“venous” Vd/Vt using PvCO2. We assessed changes using ANOVA.

Results: Changes in Paw were associated with significant changes in Vd/Vt. (table) In normal animals, changes in Paw were not associated with changes in mean blood pressure, central venous pressure, AaDO2, or arterial pH. In animals with acute lung injury, increases in the Paw were associated with decreased mean blood pressure and lower pH.

Table 1

Conclusions: These data demonstrate the feasibility of Vd/Vt measurements during HFOV. Increases in Paw resulted in increased Vd/Vt without a concomitant change in AaDO2. Vd/Vt measurements may be helpful for evaluating the effect of Paw on lung volume and pulmonary blood flow during HFOV.