Treatment of canine low pressure pulmonary edema. Nitroprusside versus hydralazine

In canine oleic acid pulmonary edema, we investigated acute cardiopulmonary effects of different doses of nitroprusside and compared the results with those obtained after intravenously administered hydralazine. Oleic acid increased (p less than 0.05) intrapulmonary shunt (Qs/Qt), increased (p less than 0.01) systemic vascular resistance (SVR), and reduced (p less than 0.05) cardiac output (CO). In the presence of low-pressure pulmonary edema, low-dose nitroprusside (NP1) reduced (p less than 0.01) mean blood pressure (BP) approximately 8%, but with the exception of a small fall in ventricular filling pressure, other parameters remained constant. Compared with control values, a higher dose of nitroprusside (NP2) reduced mean BP 20%, and despite a fall (p less than 0.01) in pulmonary capillary wedge pressure, CO increased (p less than 0.05) 20%. Corresponding to the increase in flow, mean Qs/Qt increased (p less than 0.05) from 26 to 36% with NP2 and arterial O2 tension fell (186 to 166 mmHg, p less than 0.05). Compared with NP2, intravenously administered hydralazine caused a larger (p less than 0.01) change in CO. Despite increased CO and increased (p less than 0.01) mixed venous O2 tension, there was no deterioration in gas exchange with hydralazine. Mean Qs/Qt remained constant and arterial O2 tension, (PaO2) increased (p less than 0.05) from 174 mmHg to 217 mmHg. The increased CO with NP2 and hydralazine is probably explained by the large reduction in systemic vascular resistance. Because Qs/Qt remained constant with hydralazine, the increase in PaO2 is most likely due to the increase in PvO2, which increased because CO increased.(ABSTRACT TRUNCATED AT 250 WORDS)