While PFC ventilation improves oxygenation and lung mechanics through alveolar recruitment, PFC dose dependent Va/Q heterogeneity and diffusion limitation may limit improvement in PLV. To test the hypothesis that PFC dose and PEEP influence physiologic dead space, juvenile healthy rabbits(2.16±.09 SE kg) were studied pre-PLV at 5 & 10 cmH2O PEEP and up to 4 hrs during PLV with 2 (Gr 1), 6 (Gr 2), or 17 (Gr 3) ml/kg of PFC(LiquiVent™ Alliance Pharm Corp). Vt (9 ml/kg), rate (30 br/min), and FIO2 (1) were maintained constant; PEEP was increased from 5 to 10 cmH2O at 10 min PLV for 5 min, then returned to 5 cm H2O.Physiologic (Vdphy/Vt), anatomic(Vdanat/Vt), and alveolar (Vdalv/Vt, Vdalv/Valv) dead space were calculated from arterial and expired (mixed & max) CO2 values. Data shown as mean(SE); *p < 0.05 dose effect at 10 min post PLV as compared to pre PLV. These differences were not significant across the remaining time (PEEP = 5 cm H2O). # p < 0.05 PEEP effect. No dose dependent differences in Vdanat/Vt were found. These data demonstrate a transient dose-dependent increase in physiological dead space during the initiation of PLV due to increased alveolar diffusion dead space. The transient increase in dead space may influence the initial gas exchange response to PLV. We speculate that PEEP and time related attenuation of elevated dead space may be due to enhanced distribution and dose-dependent differences in PFC elimination rates. Table

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