The acute respiratory distress syndrome (ARDS) is a disorder of diffus
e lung injury secondary to a wide variety of clinical insults (eg, sep
sis) and is manifested by impaired oxygenation, pulmonary edema, and d
ecreased static and dynamic compliance. More recently, airflow resista
nce has been shown to be increased in humans with ARDS. We designed a
prospective, randomized, placebo-controlled, crossover trial to determ
ine the presence and reversibility of increased airflow resistance in
ARDS. We studied eight mechanically ventilated patients with ARDS (cri
teria: PaO2 less than or equal to 70 mm Hg with FIO2 less than or equa
l to 0.4; diffuse bilateral infiltrates; and pulmonary artery wedge pr
essure less than or equal to 18 mm Hg). Each was intubated with a No.
8.0 orotracheal tube. We measured dynamic compliance (Cdyn), static co
mpliance (Cstat), airflow resistance across the lungs (RL), shunt frac
tion (Qs/Qt on FIO2=1.0), minute ventilation (VE), PaO2/PAO(2), and de
ad space to tidal volume ratio (VD/VT). Patients were blindly assigned
to receive either metaproterenol (1 mL 0.5% in 3 mL saline solution)
or saline solution (4 mt) aerosolized over 15 min 6 h apart and in ran
dom order so that patients served as their own controls, Metaprotereno
l significantly reduced RL, peak and plateau airway pressure, and incr
eased Cdyn. Metaproterenol tended to increase PaO2/PAO(2), but had no
effect on pulmonary shunt or dead space ventilation. We conclude that
the increase in airflow resistance of ARDS is substantially reversed b
y aerosolized metaproterenol without affecting dead space. These data
suggest that abnormalities of RL are at least partially due to broncho
spasm.-