2003 OPEN FORUM Abstracts
VENTILATOR INDUCED LUNG INJURY MAY BE AMPLIFIED
BY A PRIOR INSULT.
Dana Simonson BA, Alexander Adams RRT, Eric Korbach MD, David Dries MD, John Marini MD. Regions Hospital /Healthpartners, University of Minnesota, St. Paul, MN.
Background: Ventilator induced lung injury (VILI) is a risk of unknown incidence or prevalence. Injury induced by elevated airway pressures alone will develop in large mammals over 1-6 hours. Frank physical disruption of lung tissue and/or inflammatory signaling may cause the injury, yet the role of pre-existing "priming" factors has not been examined. Using a porcine model, we examined the role of thoracotomy to place pleural pressure wafers as a priming factor for VILI.
Methods: Animals were deeply anesthetized in an approved protocol for generating VILI over a 6 hour period: PCV set to achieve 35 cmH20 Ptp , I:E=1:2, f=10, PEEP = 3 cmH20. Routine instrumentation included a continuous indwelling ABG analysis system. Pleural pressure-sensing wafers were positioned via right thoracotomy in 5 of the animals with subsequent chest wall closure.
RESULTS: VILI developed more rapidly and, by 6 hours, to a greater severity in animals with the pre-protocol thoracotomy (n=5) compared to VILI only (n=17) (figure - P/F ratio over time-±SEM, bullet = p<.05). A measure of lung injury, WW/DW, for the thoracotomy-primed animals was significantly greater than those without prior surgery (9.53±0.39 vs. 7.15±.38 (p<.001).
CONCLUSION: We conclude that the thoracotomy amplified injury development by initiating an inflammatory process and/or the chest wall invasion exposed the lungs to injurious pressure differences not realized in a closed chest.