RESUMEN
The influence of positive end expiratory pressure (PEEP) on the fluid filtration rate (FFR) in the pulmonary circulation has been the subject of considerable investigation but data are conflicting. We studied twenty-nine isolated rabbit lung preparations, FFR was sensed by a force transducer. Autologous blood was used to prime the perfusion circuit. Hydrostatic oedema was achieved by increasing the left atrial pressure to 16 mmHg. In order to bring about increased membrane permeability oleic acid was injected through the pulmonary artery. Increasing and decreasing levels of PEEP at 0, 5, 10 and 15 cm H2O were each used for ten minutes in each of three experimental models. The FFR, pH, mean pulmonary arterial pressure (MPAP), mean left atrial pressure (MLAP), PaO2, PaCO2 and oncotic pressure were measured in each experiment. There was a significant correlation between PEEP and FFR (+0.94) in non-oedema lungs. With no PEEP the FFR was 0 g/min and with 15 cm of PEEP it increased to 0.07 g/min, on removing the PEEP the FFR returned to 0 g/min. In the hydrostatic lung oedema model the correlation was also significant but negative (r = -0.94). With no PEEP the FFR was 0.33 g/min, with PEEP of 15 cm H2O it decreased to 0.08 g/min. No correlation between PEEP and FFR was found in the oleic acid preparation. In the normal lung PEEP increases capillary hydrostatic pressure and total lung vascular area and decreases interstitial pressure. It is by these mechanisms that PEEP causes an increase in FFR. In the hydrostatic oedema model PEEP decreases FFR by increasing the interstitial pressure and by decreasing the total lung vascular area. In the oleic acid preparation the coefficient of filtration is so large that small changes in pressure or vascular area do not modify the FFR. We suggest that PEEP may be beneficial by decreasing FFR in hydrostatic lung oedema, but it may increase the FFR in the normal lung, while having no effect in oleic acid lung injury.
