Prostacyclin for the Treatment of Pulmonary Hypertension in the Adult Respiratory Distress Syndrome

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Abstract
Nine patients who had developed pulmonary artery hypertension during the adult respiratory distress syndrome (ARDS) were treated with an infusion of prostacyclin (PGI2) (12.5-35.0 ng .cntdot. kg-1 min-1). Whether PGI2 might decrease the pulmonary capillary pressure (PCP) obtained by analysis of the pulmonary artery occlusion pressure decay curve and improve systematic oxygen delivery was examined. Gas exchange alterations induced by PGI2 were analyzed by using the multiple inert gas elimination technique. PGI2 reduced the pulmonary artery pressure from 35.6 to 28.8 mmHg (P < 0.001) and the PCP from 22.9 to 19.7 mmHg (P < 0.01) without changing the contribution of the pulmonary venous resistance to the total pulmonary vascular resistance. The cardiac index increased from 4.2 to 5.7 1 .cntdot. min-1 .cntdot. m-2 (P < 0.001) due to both increased stroke volume and heart rate. Despite a marked deterioration of ventilation-perfusion (.ovrhdot.VA/.ovrhdot.Q) matching with increased true intrapulmonary shunt flow from 28.6% to 38.6% (P < 0.01) of the cardiac output, the Pao2 was unchanged due to increased mixed venous oxygen content indicated by an augmented mixed venous Po2 (from 37.0 to 41.9 mmHg, P < 0.01). This caused a 35% (P < 0.001) increase of the systemic oxygen delivery rate. Thus, short-term infusions of PGI2 reduced PAP and PCP without deleterious effects on arterial oxygenation inpatients with ARDS. Hence, PGI2 may be useful to lower pulmonary vascular pressures in patients with ARDS.