Effect ofBronchodilators on Lung Mechanics intheAcuteRespiratory Distress Syndrome(ARDS)

Theacuterespiratory distress syndrome (ARDS)isa disorder ofdiffuse lunginjury secondary toa widevariety ofclinical insults (eg, sepsis) andismanifested by impaired oxygenation, pulmonary edema, anddecreased static anddynamic compliance. Morerecently, airflow resistance hasbeenshowntobeincreased inhumans withARDS.We designed a prospective, randomized, placebo-controlled, crossover trial todetermine the presence andreversibility ofincreased airflow resistanceinARDS.We studied eight mechanically ventilated patients withARDS(criteria: PaO2.70mm Hg withFIo2.0.4; diffuse bilateral infiltrates; andpulmonary arterywedge pressure .18mm Hg).Eachwas intubated with a No.8.0orotracheal tube. We measured dynamic compliance (Cdyn), static compliance (Cstat), airflow resistance acrossthelungs (RL), shunt fraction (Qs/Qt on F1o2=1.0), minuteventilation (VE), PaO2/ PAO2,anddeadspace totidal volume ratio (VD/VT). Patients were blindly assigned toreceive either metaproterenol (1mL 0.5%in3mL saline solution) or saline solution (4mL)aerosolized over1Smin6hapartandin randomorder sothat patients served astheir own conThe acuterespiratory distress syndrome (ARDS) is observed inpatients withdiverse etiologies and ismarked byabnormalities oflungmechanics and gas exchange thought secondary todiffuse lung inflammation asshowninhumans'14 andinanimal models.5-11 Reduced lung compliance isahallmark of thesyndrome andhasgenerally beenconsidered the primarylungmechanics abnormality. Previous investigations ofgasexchange andlungmechanics abnormalities inARDShavefocused on parenchymal abnormalities resulting fromatelectasis, alveolar and interstitial edema, andairwaysecretions. Thecontribution ofincreased resistance togasexchange and other lungmechanics abnormalities hasbeen examined indetail onlyrecently.'2"13 Inthesheep endotoxin modelofdiffuse lung injury, alterations inresistance, bothearly andlate, following endotoxin are