EFFECTS OF ARTIFICIALLY - INDUCED INTRINSIC POSITIVE END - EXPIRATORY PRESSURE IN MECHANICALLY VENTILATED PATIENTS WITH ACUTE RESPIRATORY FAILURE.

It has been suggested that, in patients with acute respiratory failure (ARF), relative to conventional mechanical ventilation with application of external positive end-expiratory pressure (PEEPe), mechanical ventilation artificially inducing intrinsic PEEP (PEEPi) worsens arterial oxygen tension (PaO2) by causing a less homogeneous distribution of inspired gas, even if tidal volume (Vt), respiratory rate (RR) and total PEEP (PEEPtot) are kept invariant. This hypothesis has been investigated assessing spatial ventilation heterogeneity directly with electrical impedance tomography (EIT), and measuring mechanical and capnographic parameters indirectly related to ventilation unevenness, together with measurements of hemodynamic function and gas exchange. Seventeen patients with ARF without chronic obstructive pulmonary disease were mechanically ventilated in four experimental conditions, with the same RR and Vt. In one condition, PEEPe was zero (ZEEP); in the others, PEEPtot was constant, but obtained by either applying external PEEP (PEEPe) or shortening the duration of expiration to induce PEEPi. PEEPi was produced either by increasing the duration of the inflation (PEEPi no pause, PEEPinp), or by introducing a post-inspiratory pause while keeping the duration of the inflation constant (PEEPi with pause, PEEPiwp). In all conditions, we measured PaO2, respiratory mechanics, cardiac output, physiological dead space (DSphys) and the slope of capnographic phase III, ventral and dorsal ventilated surface, and global inhomogeneity index (GI), an index of spatial heterogeneity of ventilation distribution. A similar PEEPtot of ~7 cmH2O was obtained at PEEPe, PEEPinp and PEEPiwp. With respect to PEEPe, PaO2 decreased significantly at ZEEP and both PEEPi conditions. Cardiac output was similarly depressed at PEEPe, PEEPinp and PEEPiwp than at ZEEP. Regarding respiratory mechanics, static elastance did not change among the conditions, while interrupter and additional resistance were respectively lower and higher at PEEPinp than at the other conditions, in line with what expected from the increase in inflation time. Both DSphys and slope of phase III decreased significantly at PEEPiwp than at the other conditions. Ventral ventilated surface did not vary among the conditions and, with respect to ZEEP, the dorsal one increased similarly in all other conditions, while GI was significantly higher at ZEEP than at the other conditions, but similar between PEEPe, PEEPinp and PEEPiwp. Our results confirm previous findings of a worse PaO2 with artificially-induced PEEPi with respect to ventilation with PEEPe. However, none of the measured cardiorespiratory parameters appear to provide a direct explanation for this difference and results of ventilated surface and GI from EIT seem to argue against the hypothesis of an increased ventilation heterogeneity during ventilation with artificial PEEPi. These findings suggest that other mechanisms may be at play and further research is needed to better elucidate the factors behind poorer PaO2 during this kind of ventilation.