The Effect of Nitroprusside on Pulmonary Edema, Oxygen Exchange, and Blood Flow in Hydrochloric Acid Aspiration

Open Access
Publisher Website
Google Scholar
Abstract
In canine pulmonary capillary leak induced by intravenous oleic acid, reducing pulmonary wedge pressure (Ppw) reduces pulmonary edema, venous admixture (Qva/Qt), and cardiac output (Qt). The authors tested the possibility that in another canine model of pulmonary capillary leak, that induced by endobronchial instillation of hydrochloric acid, nitroprusside would reduce Ppw and edema without reducing Qt or oxygen delivery (QO2). In 18 dogs, the authors measured extravascular lung water (EVLW) by thermal-dye dilution and the hemodynamic and gas exchange variables before and at intervals (1, 1.5, 3, and 5 h) after .1 N HCl bronchial infusion. By 1 h, HCl increased EVLW from 175 to 250 ml and Qva/Qt from 11 to 21%. Immediately after the 1-h measurements, the dogs were divided into three equal groups: six controls (C) were maintained with a Ppw of 12 mmHg, while plasmapheresis (P) or nitroprusside (NP) reduced Ppw to 5 mmHg for the next 4 h. EVLW continued to increase to 548 ml in C, but did not increase further in P and NP. Weights of lungs excised at 5 h confirmed that P and NP reduced edema by 50% in 4 h. In C, Qva/Qt increased, but there was no reduction in Qt or QO2. In contrast, plasmapheresis reduced Qva/Qt, Qt, and QO2. With nitroprusside, Qt and QO2 were maintained despite reduced Ppw at 1.5 and 3 h, and Qva/Qt did not decrease as in Group P. We conclude that plasmapheresis-induced reduction in Ppw reduces the pulmonary capillary leak and venous admixture following acid aspiration, but this has the potentially adverse effect of reducing cardiac output and oxygen delivery. Nitroprusside decreases Ppw and edema by a similar amount, but maintains Qt and QO2.