Cardiac output was measured in 55 patients by the direct Fick method and an automatized thermodilution method. The results showed a good correlation (correlation factor r = 0.87, regression equation y = 0.91 x + 0.59). For the thermodilution method ice-cold normal saline solution as indicator substance was injected into the right atrium. The temperature-time-curve was measured by a thermistor located in the pulmonary artery. The area of indicator dilution was determined by electronic integration, the calculated cardiac output appeared as 1/min in digital display.

When a high frequency alternating current is passed through the thorax by means of tape-electrodes, the electrical impedance Z is changing synchronously with the cardiac cycle. The relation between the first derivative dZ/dt and the stroke volume is the basis for the application of impedance cardiography (IK) Determinations of cardiac output (CO) at rest during ergometer exercise using this noninvasive technique were compared with CO values obtained by the thermal dilution method. In 57 subjects simultaneous determinations using both methods were performed at resting conditions. The correlation coefficient was r = 0.63. In addition, in 48 of the subjects CO was measured with both methods during supine ergometer exercise. Comparison of the exercise values resulted in a correlation coefficient of r = 0.63. In all 48 cases there was a concordant change of the IK and thermodilution CO values. It is concluded that relative changes of CO are reliably detected by IK. The absolute values can be utilized only approximately.

Haemodynamic tests were performed at rest and during exercise in 41 patients with arterial hypertension and early impairment of left-ventricular function, before and after administration of a single dose of 0.6 mg beta-methyl-digoxin. After clinical, ECG and coronary-angiographic studies, the patients were assigned to two groups. Group I: 17 patients with transmural infarcts in the chronic stage or with angina. Cardiac output was within normal limits at rest and on exercise and was not significantly altered by administration of beta-methyl-digoxin. There was no significant fall during exercise of the abnormally elevated pulmonary "wedge" pressure or of other pressures in the lesser circulation after digitalis. Group II: 24 patients without signs of coronary heart disease. They, too, had a normal cardiac output at rest and on exercise, not significantly changed by digitalisation with beta-methyl-digoxin. But pulmonary "wedge" pressure and right-atrial mean pressure were significantly reduced during exercise. Before beta-methyl-digoxin the mean "wedge" pressure rose on exercise to an average of 27.3 +/- 5.4 mm Hg, but after beta-methyl-digoxin to only 21.7 +/- 5.1 mm Hg (P less than 0.001). The mean right atrial pressure changed similar. These results indicate that acute digitalisation at the stated dosage in general has an effect on abnormal myocardial function only if there is no additional coronary heart disease.

Twenty-eight patients with hypertensive cardiovascular disease (HCD) and incipient myocardial dysfunction underwent hemodynamic studies at rest and during exercise before and 30 minutes after administration of 0.6 mg beta-methyl-digoxin intravenously. Measurements were made during right heart catheterization with a balloon-tipped catheter. The hemodynamic changes after administration of digitalis did not demonstrate a consistent and uniform improvement of cardiac performance in all patients with HCD and myocardial dysfunction. When separating 11 patients with pervious myocardial infarctions or documented coronary artery disease (CAD) (= Group I) from the remaining 17 subjects without clinical and/or angiographic signs of CAD (= Group II), there were significant differences in the hemodynamic response to digitalis: In Group I, pulmonary artery wedge pressure (PAWP) after digitalis decreased only slightly and insignificantly from 8.7 to 7.4 mm Hg at rest and from 27.6 to 26.4 mm Hg during steady state exercise. Cardiac output (CO) remained essentially unchanged with a tendency to decrease after digitalis: 5.9 vs. 5.8 L/min at rest and 11.5 vs 11.1 L/min during exercise. At rest, even patients of Group II showed only minor decrease of PAWP from 8.8 to 7.2 mm Hg; during exercise these patients demonstrated marked improvement of cardiac performance with a significant decrease of PAWP after digitalis from 27.8 to 22.3 mm Hg (p less than 0.01). With one exception, there was a more or less pronounced reduction of PAWP after the drug was given. No significant change of CO after digitalis was measured in this group: 6.2 vs. 5.9 L/min at rest and 13.4 vs. 13.5 L/min during exercise. The different hemodynamic patterns of responders and non-responders to the glycoside will be discussed.

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