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1) Intracardiac flows were investigated by bi-directional pulsed Doppler technique with a combined use of the two-dimensional echocardiography. The flow at sampling sites in the heat and great vessels were correctly identified on the two-dimensional echocardiograms. 2) Soundspectrographic analysis of the flow Doppler signals was useful in obtaining information about flow modes and in differentiating flow signals from those of valves. 3) In healthy subjects, intracardiac flow revealed a laminar mode. As a matter of interest, a flow toward the aorta, which is a cranially turned flow, was found at the center and at the outflow tract of the left ventricle from mid to late diastole. 4) In mitral stenosis, the central stream at the stenotic portion exhibited an almost laminar and rapid flow. A good coincidence in flow mode was observed between clinical cases of mitral stenosis and experimental stenosis. 5) Disturbed flows were observed in the following diseased conditions. The diastolic regurgitant flow in the left ventricular outflow tract and mitral inflow in aortic regurgitation, the regurgitant flow into the left atrium and the diastolic mitral inflow in mitral regurgitation, the ejection flow in hypertrophic cardiomyopathy with outflow tract obstruction, and the tricuspid inflow in atrial septal defect. 6) Mechanisms of intracardiac flow dynamics were also discussed.

The ratio of pulmonary to systemic flow (Qp/Qs) was noninvasively evaluated by duplex Doppler echocardiography in 22 patients with atrial septal defects (ASDs). Right and left ventricular stroke volumes (RSV, LSV) were determined from the recordings of ejection blood flow velocity and diameter at the level of the pulmonary and aortic orifices in each ventricular outflow tract. The ratio RSV/LSV, determined by the duplex Doppler echocardiography, was compared with Qp/Qs by oximetry. The RSV/LSV for 10 normal subjects was 0.99 +/- 0.05 (mean +/- SD), whereas the RSV/LSV for patients with ASD, 2.26 +/- 0.63, was significantly higher than that for normal subjects (p less than .01). In patients with ASD, a fairly good correlation was found between RSV/LSV and Qp/Qs (r = .92, p less than .01; y = 1.11x - 0.30), and this high correlation was found even in patients with complications such as pulmonary hypertension, mitral and tricuspid regurgitation, Eisenmenger complex, and ventricular septal defect. We also found that semilunar valve regurgitation modified the value of RSV/LSV in accordance with the degree of regurgitation. These findings indicate that, with a few limitations, the Doppler index RSV/LSV is clinically useful in the estimation of the magnitude of the shunt flow in patients with ASD and that the limitations could be overcome by additional Doppler examination.

In this study, transmitral flow velocity during the diastolic period was non-invasively measured to assess diastolic behavior of the left ventricle by pulsed Doppler flowmetry combined with electronic beam sector-scanning echocardiography. The velocity pattern was found to have 2 wave components: one appears in the early diastolic rapid filling phase (R wave) and the other in the late diastolic phase. The peak of the early diastolic inflow velocity (peak EFV), the deceleration rate of the R wave (DC), and the peak of the late diastolic inflow velocity (peak LFV) were compared in healthy subjects as the control, patients with hypertension, hypertrophic cardiomyopathy and definite old myocardial infarction. Normal peak EFV and DC, 61.3 +/- 6.7 cm/sec and 355 +/- 67 cm/sec2, respectively, were markedly reduced in patients with hypertension (50.0 +/- 10.0 cm/sec and 265 +/- 75 cm/sec2), hypertrophic cardiomyopathy (48.8 +/- 10.7 cm/sec and 205 +/- 78 cm/sec2), and myocardial infarction (46.1 +/- 12.0 cm/sec and 240 +/- 84 cm/sec2). Among all disease groups the DC was most significantly reduced in the hypertrophic cardiomyopathy groups. Normal peak LFV, 39.9 +/- 11.0 cm/sec, was significantly increased in patients with hypertension (54.3 +/- 10.7 cm/sec) and myocardial infarction (50.0 +/- 11.0 cm/sec), but not in patients with hypertrophic cardiomyopathy (42.0 +/- 8.4 cm/sec). The ratio peak LFV/peak EFV was significantly greater in all disease groups than in the normal group. These findings indicate that impaired early diastolic filling in all disease groups was compensated by enhanced atrial contraction in patients with hypertension and myocardial infarction, and by prolonged rapid filling in patients with hypertrophic cardiomyopathy. Left ventricular wall thickness was better correlated with DC in patients with hypertension (r = -0.76, p less than 0.01) than in patients in the other groups, which indicates that the left ventricular wall thickening is a more important factor in determining diastolic behavior of the ventricle in hypertension than in hypertrophic cardiomyopathy and myocardial infarction. Thus, the pulsed Doppler technique was proved to be useful in assessing ventricular diastolic events non-invasively.