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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<0.01), and the shunt fraction decreased from 6.0 ± 3.8% to 1.2 ± 0.8% (P<0.001). There were significant differences (P<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.