Influence of positive end-expiratory pressure on extravascular lung water during the formation of experimental hydrostatic pulmonary oedema.

The influence of positive end-expiratory pressure (PEEP) on extravascular lung water measured with the double-indicator dilution technique (EVLWi) has been studied during formation of hydrostatic pulmonary oedema in a canine model. The oedema was created by elevating the mean pulmonary artery pressure (PAP) to 30 mmHg (4.0 kPa) by inflation of a left atrial balloon, and a simultaneous intravenous saline infusion of 15 ml.kg-1.h-1. All dogs were ventilated with zero end-expiratory pressure (ZEEP) until the initial EVLWi had increased by 50%. In one group (n = 5) a PEEP of 10 cmH2O (1.0 kPa) was applied and the dogs were studied for a further 4 h and in the other group (n = 5) ZEEP was maintained throughout the study. During the first 2 h after ZEEP/PEEP application EVLWi increased from 13.7 +/- 2.1 to 20.2 +/- 1.2 ml.kg-1 with ZEEP ventilation and from 13.6 +/- 1.2 to 18.6 +/- 1.9 ml.kg-1 with PEEP ventilation. EVLWi remained unchanged during the last 2 h in both groups. The gas exchange improved with PEEP, arterial oxygen tension increased from 30.4 +/- 8.9 kPa to 38.6 +/- 2.5 kPa (P less than 0.01), and the shunt fraction decreased from 6.0 +/- 3.8% to 1.2 +/- 0.8% (P less than 0.001). There were significant differences (P less than 0.01) in both PaO2 and shunt fraction between the ZEEP and PEEP groups throughout the study. In conclusion, positive end-expiratory pressure improves gas exchange but does not protect against increasing extravascular lung water during the creation of hydrostatic pulmonary oedema.