RESUMO
OBJECTIVES: To examine the hypothesis that the response to inhaled prostacyclin (PGI2 on oxygenation and pulmonary hemodynamics may be related to different morphologic features that are supposed to be present in acute respiratory distress syndrome (ARDS) originating from pulmonary (primary ARDS [ARDS(PR)]) and from extrapulmonary disease (secondary ARDS [ARDS(SEC)]). DESIGN: Prospective, nonrandomized interventional study. SETTING: Multidisciplinary intensive care unit, secondary care center. PATIENTS: Fifteen consecutive, mechanically ventilated patients with ARDS and severe hypoxemia, defined as PaO2/FIO2 of <150 torr at the time of admission. INTERVENTIONS: After an initial stable period of at least 60 mins, patients received nebulized PGI2 in 15-min steps; the drug was titrated to find the dose with the best improvement of PaO2, starting with 2 ng/kg/min up to an allowed maximum dose of 40 ng/kg/min. MEASUREMENTS AND MAIN RESULTS: Blood gas, gas exchange, and hemodynamic measurements were performed at the following time points: a) baseline; b) during the optimal or maximum dose of PGI2; and c) 1 hr after withdrawal of the drug. Patients underwent a computed tomographic (CT) scan using a basal CT section to compute the mean CT numbers and the density histogram. Patients were considered responders to PGI2 if an increase in PaO2 of > or =7.5 torr or an increase in PaO2/FIO2 ratio of > or =10% occurred. For the group as a whole, mean pulmonary artery pressure decreased from 32 +/- 1 to 29 +/- 1 mm Hg during PGI2 nebulization, whereas pulmonary vascular resistance decreased 1 hr after withdrawal of nebulization from 177 +/- 18 to 153 +/- 16 dyne x sec/cm5; oxygenation did not change significantly. Eight patients responded to PGI2 nebulization on oxygenation (all were in the ARDS(SEC) subgroup), whereas seven did not (all but one were in the ARDS(PR) subgroup). Among the physiologic variables examined to assess any difference between the two ARDS groups at time of PGI2 nebulization, there was a significant difference concerning the mean CT density number, which was -445 +/- 22 Hounsfield Units in the ARDS(SEC) group and -258 +/- 16 Hounsfield Units in the ARDS(PR) group. In patients presenting with an ARDS(PR), PGI2 induced a reduction in PaO2/FIO2 and a reduction in PaO2 from 87 +/- 2 to 79 +/- 2 torr, whereas in patients with an ARDS(SEC) there was an increase in PaO2/FIO2 and in PaO2 from 76 +/- 4 to 84 +/- torr with a decrease in mean pulmonary artery pressure. CONCLUSIONS: Based on the data from this study, the clinical recognition of the two types of the syndrome together with the CT number frequency distribution analysis may be associated with a prediction of the PGI2 nebulization response on oxygenation.
