Abstract

The evidence for left and right ventricular inotropic response to ouabain was examined in 20 patients in sinus rhythm. A total of 14 patients had left ventricular pressure overload from aortic stenosis or essential hypertension. Sex patients had ischemic (old myocardial infarct) or idiopathic myocardial disease. The clinical severity of the disease varied from functional class I to IV. Myocardial contractility was estimated according to the Frank-Starling concept, using ventricular stroke work and end-diastolic or filling pressure, and compared to changes in LV dp dt . It was concluded that myocardial contractility increased after ouabain in all patients, but that this positive inotropic effect was not reflected with equal clarity in the classical hemodynamic measurements of CO, ventricular filling pressure, or even stroke work in relation to ventricular end-diastolic pressure. In the class III or IV patients as a group, a positive left ventricular inotropic response to ouabain was reflected in an increase in stroke work and a decrease in LV ed pressure. In the class I or II patients as a group, a positive left ventricular inotropic response was present: stroke work increased at unchanged end-diastolic pressure. Individually, 9 of 12 patients in class III or IV and 3 of the patients in class I or II had a positive inotropic response. A positive inotropic response in the other patients was either not present or was not determinable. No patient had a negative inotroipic response. The hemodynamic pattern of patients in classes III and IV was more abnormal than that of patients in class I or II. As a group, the class III or IV patients had elevated LV ed pressure, and patients in class I or II had normal end-diastolic pressure. Thus the clinical classification correlated well with the control hemodynamic status. After ouabain, there was an increase in LV dp dt in all patients; this increase was out of proportion to the change in HR, BA diast., LV ed, and LVs pressure. This finding confirmed the value of dp dt as a measure of contractility. The right ventricular hemodynamic parameters, in general, were less abnormal than the left. The right ventricle also showed evidence for a positive inotropic effect, but less clearly so than the left ventricle. The HR did not change after ouabain in the patients with normal sinus rhythm in contrast to the decrease observed in 3 patients in atrial fibrillation. It is concluded that ouabain probably always has a positive inotropic action upon the diseased ventricle. However, this action is reflected in the conventional hemodynamic measurements as a function of the clinical and hemodynamic status of the patient.

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