The main findings of this study were that (1) the effects of PCV on gas exchange and hemodynamics were not different from those of VCY and (2) PC-IRV failed to improve Pa02 while inducing a decrease in Cl and hence in Do2. Few studies have reported the effects of PCV in ARDS. Abraham and Yoshihara reported an improvement in Pa02 with this mode. This beneficial effect might be ascribed to improvement in alveolar recruitment, gas diffusion, and ventilation of alveolar units with slow time constants, induced by the decelerating flow pattern that occurs in PCV Nevertheless, like other authors, we did not observe any difference in Pa02 between VCV and PCV.
Several previous studies have demonstrated a significant increase in Pa02 when patients with ARDS were switched from VCV with PEEP to PC-IRV Three explanations were proposed for the increased P&02 with PC-IRV:2 (1) the occurrence of PEEPi; (2) an increase in mPaw; and (3) recruitment of alveolar units with slow time constants secondary to the prolonged inspiratory time. In our study, PEEPt was maintained at the same level in the different ventilatory modes, so that the effect of an increase in PEEPt due to the occurrence of PEEPi was offset. In this condition, we did not observe any significant improvement in Pa02 with PC-IRV This suggests that the increase in Pa02 usually reported with PC-IRV was mainly due to an increase in PEEPt secondary to the induction of PEEPi. In fact, in most studies on PC-IRV PEEPi was either not measured*- or not reported. The mPaw is another major determinant of gas exchange in ARDS.* We observed a significant increase in mPaw with PC-IRV Since RR, Vt, and PEEPt were kept constant, this increase in mPaw was only due to the increased inspiratory time. Pulmonary Embolization Despite this increased mPaw, Pa02 did not increase in PC-IRV. Such a surprising result was in accordance with findings of East et al. It is generally accepted that in ARDS a minimal level of PEEP is required to prevent alveolar collapse during exhalation. Now, since parenchymal involvement in ARDS is heterogeneous, the distribution of PEEPi induced by PC-IRV is likely to be uneven because of time constant inequalities between lung units. Thus, the less compliant alveolar units could be still collapsed while a substantial level of PEEPi is measured by the end-expiratory occlusion method. This could explain the lack of improvement in Pa02 despite an increase in mPaw in PC-IRV Alternatively, the failure of PC-IRV to improve Pa02 might be related to its short duration of application (1 h), since some studies suggested that the improvement in Pa02 with PC-IRV may require several hours; however, this time-dependent effect of PC-IRV is a matter of controversy, since it was not detected in a recent study in which PC-IRV was used for 24 h or more.