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Influence of positive end‐expiratory pressure on extravascular lung water during the formation of experimental hydrostatic pulmonary oedema
Author(s) -
Wickerts C.J.,
Berg B.,
Blomqvist H.
Publication year - 1992
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1992.tb03473.x
Subject(s) - medicine , positive end expiratory pressure , anesthesia , arterial oxygen tension , pulmonary artery , mechanical ventilation , lung , saline , cardiac output , cardiology , hemodynamics
The influence of positive end‐expiratory pressure (PEEP) on extravascular lung water measured with the double‐indicator dilution technique (EVLW i ) 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 EVLW i had increased by 50%. In one group (n = 5) a PEEP of 10 cmH 2 O (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 EVLW i 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. EVLW i 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 Pao 2 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.