DIRECT COMPARISON OF INHALED NITRIC-OXIDE AND AEROSOLIZED PROSTACYCLIN IN ACUTE RESPIRATORY-DISTRESS SYNDROME

Citation
D. Walmrath et al., DIRECT COMPARISON OF INHALED NITRIC-OXIDE AND AEROSOLIZED PROSTACYCLIN IN ACUTE RESPIRATORY-DISTRESS SYNDROME, American journal of respiratory and critical care medicine, 153(3), 1996, pp. 991-996
Citations number
29
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
ISSN journal
1073449X
Volume
153
Issue
3
Year of publication
1996
Pages
991 - 996
Database
ISI
SICI code
1073-449X(1996)153:3<991:DCOINA>2.0.ZU;2-2
Abstract
Inhalation of NO and aerosolization of PCI2 have been suggested to ach ieve selective pulmonary vasodilation and improvement of arterial oxyg enation in patients with ARDS. We directly compared these two modes of transbronchial vasodilator therapy in 16 ARDS patients mechanically v entilated (mean lung injury score [1] 2.75 +/- 0.05). Patients were ra ndomized to receive either first NO and then PGI(2), or vice versa. Ea ch drug was individually titrated to find the maximum improvement of a rterial oxygenation. Gas exchange variables, including data from the m ultiple inert gas elimination technique (MIGET), and hemodynamics unde r application of NO/PGI(2) were compared with pre- and post-challenge values. NO (17.8 +/- 2.7 ppm) increased Pa-O2/FIO2 from 115 +/- 12 to 144 +/- 15 mm Hg (p < 0.01) and reduced the shunt-flow from 33.1 +/- 3 .6 to 26.6 +/- 4.5% (p < 0.05). Aerosolized PGI(2) (7.5 +/- 2.5 ng/kg min) augmented Pa-O2/FIO2 from 114 +/- 12 to 135 +/- 12 mm Hg (p < 0.0 1), and decreased shunt from 33.5 +/- 3.8 to 26.0 +/- 3.9% (p < 0.05). In 10 patients, both NO and PCI2 caused an increase in Pa-O2/FIO2 by at least 10 mm Hg. Two further patients displayed an improvement of ar terial oxygenation in response to either NO or PGI(2). NO decreased me an pulmonary artery pressure from 34.8 +/- 2.2 to 33.0 +/- 1.8 mm Hg, and PGI(2) from 35.0 +/- 2.2 to 31.9 +/- 1.7 mm Hg (p < 0.05). We conc lude that individually titrated doses of inhaled NO and aerosolized PG I(2) effect selective pulmonary vasodilation and redistribute blood-fl ow from shunt-areas to well-ventilated regions with nearly identical e fficacy profiles.