title: Accelerated deflation promotes homogeneous airspace liquid distribution in the edematous lung.
abstract: Edematous lungs contain regions with heterogeneous alveolar flooding. Liquid is trapped in flooded alveoli by a pressure barrier-higher liquid pressure at the border than in the center of flooded alveoli-that is proportional to surface tension,TStress is concentrated between aerated and flooded alveoli, to a degree proportional toTMechanical ventilation, by cyclically increasingT, injuriously exacerbates stress concentrations. Overcoming the pressure barrier to redistribute liquid more homogeneously between alveoli should reduce stress concentration prevalence and ventilation injury. In isolated rat lungs, we test whether accelerated deflation can overcome the pressure barrier and catapult liquid out of flooded alveoli. We generate a local edema model with normalTby microinfusing liquid into surface alveoli. We generate a global edema model with highTby establishing hydrostatic edema, which does not alterT, and then gently ventilating the edematous lungs, which increasesTat 15 cmH2O transpulmonary pressure by 52%. Thus ventilation of globally edematous lungs increasesT, which should increase stress concentrations and, with positive feedback, cause escalating ventilation injury. In the local model, when the pressure barrier is moderate, accelerated deflation causes liquid to escape from flooded alveoli and redistribute more equitably. Flooding heterogeneity tends to decrease. In the global model, accelerated deflation causes liquid escape, but-because of elevatedT-the liquid jumps to nearby, aerated alveoli. Flooding heterogeneity is unaltered. In pulmonary edema with normalT, early ventilation with accelerated deflation might reduce the positive feedback mechanism through which ventilation injury increases over time.NEW & NOTEWORTHYWe introduce, in the isolated rat lung, a new model of pulmonary edema with elevated surface tension. We first generate hydrostatic edema and then ventilate gently to increase surface tension. We investigate the mechanical mechanisms through which1) ventilation injures edematous lungs and2) ventilation with accelerated deflation might lessen ventilation injury.
authors.affiliation: Biomedical Engineering, Chemistry and Biological Sciences, Stevens Institute of Technology, Hoboken, New Jersey.
authors.forename: You
authors.initials: Y
authors.lastname: Wu
authors.affiliation: Biomedical Engineering, Chemistry and Biological Sciences, Stevens Institute of Technology, Hoboken, New Jersey.
authors.forename: Tam L
authors.initials: TL
authors.lastname: Nguyen
authors.affiliation: Biomedical Engineering, Chemistry and Biological Sciences, Stevens Institute of Technology, Hoboken, New Jersey cperlman@stevens.edu.
authors.forename: Carrie E
authors.initials: CE
authors.lastname: Perlman
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D008297:Male; D011312:Pressure; D011650:Pulmonary Alveoli / Q000293:injuries / Q000503:physiopathology*; D011654:Pulmonary Edema / Q000503:physiopathology*; D012123:Pulmonary Ventilation / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012119:Respiration; D015656:Respiratory Mechanics / Q000502:physiology; D013500:Surface Tension
keywords: acute respiratory distress syndrome; alveolar mechanics; cardiogenic pulmonary edema; surface tension; ventilation injury