Effects of acute digitalization on the pulmonary blood volume in patients with heart disease.

Abstract

Basic hemodynamic data and the pulmonary blood volume (PBV) were determined in 23 patients before and after intravenous administration of acetyl strophanthidin during right and left heart catheterization. These patients were divided into two groups depending upon whether or not digitalization produced a significant fall in left ventricular end-diastolic pressure (LV D ). Group I consisted of 11 patients who manifested a significant decrease in LV D , while in group II no change was noted after digitalization. In both groups, a significant rise in LV stroke volume, stroke work, and maximal rate of rise of LV systolic pressure (dp/dt) was recorded. In group I, a significant decrease in the pulmonary vascular distending pressure (P d ) was accompanied by a decrease in PBV. In contrast, no change in P d or PBV was noted in the patients in group II. Changes in pulmonary vascular resistance (PVR) were inconsistent. It is concluded that: (1) in patients of group I the concordant decrease in P d and PBV represented a passive effect on the pulmonary vascular bed mediated by improved LV performance and decrease in LV D ; (2) in patients of group II, despite evidence of significant positive inotropic effects on the left ventricle, the failure of LV D to fall prevented a decrease in P d and PBV; (3) no evidence of active vasomotor effects of acetyl strophanthidin in the lung could be demonstrated. Changes in PVR were capricious and not apparently useful in assessment of the presence or absence of pulmonary vasomotor effects induced by digitalis. The results of this study differ from the findings of other investigators in cardiac patients and experimental animals. Some of the differences may be attributed to different experimental methods and to species variation in vascular reactivity. Also, the findings in this report contrast with those previously reported for isoproterenol and aminophylline, agents that produce both positive inotropic effects on the heart and active vasomotion in the pulmonary circulation.