Effects of hydralazine on cardiopulmonary function in canine low-pressure pulmonary edema

The authors investigated the acute cardiopulmonary effects of hydralazine in canine low-pressure pulmonary edema. Ninety minutes after oleic acid, right to left shunt (Qs/Qt) had increased from 16-46.7%, and arterial O2 tension decreased from 444-194 mmHg. In the presence of oleic acid pulmonary edema, hydralazine infusion increased cardiac output (CO) and stroke volume (SV) from 3.65-4.9 mmHg . 1 (-1) . min (P less than 0.001) and from 26-31 ml (P less than 0.005), respectively. These changes occurred despite reduced preload as mean pulmonary capillary wedge pressure (PCWP) decreased from 6.6-4.1 mmHg (P less than 0.005). These changes are most likely explained by a reduction in resistive afterload because hydralazine reduced systemic vascular resistance (SVR) from 29.1-20.8 mmHg . 1(-1) . min. Despite improved CO, Qs/Qt remained constant and arterial O2 tension increased (P less than 0.005) with hydralazine. Because Qs/Qt remained constant with hydralazine, the improvement in arterial O2 tension is explained most likely by the increased mixed venous oxygen tension secondary to the increase in CO. To the extent that canine oleic acid edema resembles low-pressure pulmonary edema in patients, hydralazine is a potential agent to reduce PCWP, increase CO and arterial O2 tension.