Acute hemodynamic effects of hydralazine in dogs with chronic mitral regurgitation.

The hemodynamic response to hydralazine administration was evaluated in 6 conscious small dogs with chronic mitral regurgitation. All dogs underwent invasive and noninvasive hemodynamic monitoring before and after hydralazine administration. Cardiac output and pulmonary capillary wedge pressure were measured with a Swan-Ganz thermodilution catheter. Systemic arterial blood pressure (AP) was measured directly by inserting a needle into the femoral artery. Standard M-mode echocardiograms and thoracic radiographs were obtained. Other hemodynamic variables were calculated. Base-line hemodynamic variables were altered severely in all dogs. Hydralazine decreased mean arterial blood pressure from 104 +/- 18 (mean +/- SD) to 78 +/- 12 mm of Hg (P less than 0.005), total systemic resistance index from 2,946 +/- 625 to 1,261 +/- 420 dynes-s-cm-5m2 (P less than 0.005), and pulmonary capillary wedge pressure from 40 +/- 5 to 26 +/- 3 mm of Hg, (P less than 0.005). Cardiac index increased from 2.92 +/- 0.72 to 5.36 +/- 1.67 L/min/m2 of body surface area (P less than 0.005). Mixed venous oxygen tension (PvO2) increased from 28.4 +/- 4.3 to 41.2 +/- 5.2 mm of Hg (P less than 0.001). Pulmonary edema resolved, as determined on thoracic radiographs. Mixed venous oxygen tension correlated well with the cardiac index (r = 0.92; P less than 0.001). It was concluded that hydralazine administration caused a small decrease in end diastolic diameter (4.8 +/- 0.9 to 4.5 +/- 0.8 cm, P less than 0.05) and end systolic diameter (2.6 +/- 0.8 to 2.3 +/- 0.7 cm, P less than 0.05). Fractional shortening and heart rate did not change.(ABSTRACT TRUNCATED AT 250 WORDS)