2003 OPEN FORUM Abstracts
A VERTICAL PLEURAL PRESSURE GRADIENT DEVELOPS IN EXPERIMENTAL VENTILATOR
INDUCED LUNG INJURY.
Alexander Adams RRT, FAARC, Dana Simonson BA, Eric Korbach MD, John Marini MD, David Dries MD. Regions Hospital /Healthpartners, Univ. of Minnesota, St. Paul, MN.
Background: The tendency for lung injury to develop in the dependent lung regions is, presumably, due to the increasing weight of overlying lung that is accumulating fluid and debris. In a porcine VILI model, we measured ventral and dorsal pleural pressures over the course of injury in an attempt to monitor the development of a vertical pleural pressure gradient.
Methods: Supine animals (n = 5) were deeply anesthetized in an approved protocol for generating VILI. After initial instrumentation, pleural pressure-sensing wafers were positioned via right thoracotomy in ventral and dorsal midthoracic pleural spaces. Pressure controlled ventilation set to attain Ptp of 35 cm H2O, I:E=1:2, f=10/min, FIO2 = 0.6 and PEEP = 3 cmH2O was applied for 6 hours.
RESULTS: Oxygenation deteriorated from 1-6 hours (mean P/F ratio ± SEM; hour 1 = 543±39, 2 = 352±108, 3 = 265±83, 4 = 201±68, 5 = 137±36, 6 = 93±12 mmHg) as a vertical pressure gradient developed (mean Ppl±SEM, cross - p<.09, # - p<.05 - see figure). The measure of lung weight gain by WW/DW indicated the development of VILI (mean WW/DW = 9.53 ± 0.86 compared with control = 6.5). Ex vivo, lung injury appeared to be predominantly dorsal - the region of increased pleural pressure.
CONCLUSION: In a porcine lung injury model, VILI development coincided with an increase in dorsal pleural pressure that caused a widened vertical pressure gradient. An increasing pressure gradient could explain generation and propagation of VILI from dorsal lung regions.