Tlie differential pressure method of Womersley and McDonald was used to measure instantaneous blood flow in the main pulmonary artery in ten human subjects. Three subjects had normal pulmonary arterial pressures and flows, seven had mitral stenosis and pulmonary hypertension. The spectrum of input impedance versus frequency was similar to that previously reported for the dog and rabbit, with the modulus decreasing from relatively high values at zero frequency to a minimum between 2 and 5 cycles/sec. Characteristic impedance and phase velocity were lower in the normal subjects than in those with pulmonary hypertension (averages, 23 dyne sec crrr r ' and 1.68 m/sec in the normals; 46 dyne sec c n r ' and 4.77 m/sec in the hypertensives). Hydraulic energy dissipated per unit time by pulsations in the pulmonary bed was usually higher in the hypertensive than in the normal cases, because of the greater stiffness of the pulmonary arteries in the subjects with pulmonary hypertension. The elasticity of the pulmonary arterial tree appears to be as important as the state of the arterioles and capillaries in determining the energy required for pulsatile pulmonary blood flow. ADDITIONAL KEY WORDS differential pressure hydraulic energy vascular elasticity pulmonary hypertension mitral stenosis blood flow

To determine the systemic input impedance, pulsatile pressure and flow were measured in the ascending aorta in 16 human subjects who were undergoing diagnostic cardiac catheterization. Blood flow was measured with a catheter-tip electromagnetic velocity meter, and pressure with an external transducer connected with the fluid-filled lumen of the catheter. Five subjects were found to have no evidence of cardiovascular disease (group A, mean age 32 +/- 2 years, mean aortic pressure 97 +/- 4 mm Hg). Seven had clinical and angiographic signs of coronary arterial disease, and mean pressures less than 100 mm Hg (group B, mean age 48 +/- 2 years). Four subjects had signs of coronary disease and mean pressures greater than 100 mm Hg (group C, mean age 48 +/- 3 years). The frequency spectra of impedance were qualitatively similar in all three groups and resembled those previously observed in the canine aorta. Characteristic impedance was lower in the normal subjects (group A, average 53 dyn sec cm-5) than in the subjects with coronary artery disease (groups B and C, average 129 dyn sec cm-5). Among the subjects with coronary disease, characteristic impedance was higher in the hypertensive subjects (group C, average 202 dyn sec cm-5) than in those with lower mean pressures (group B, average 95 dyn sec cm-5). External left ventricular work per unit time (hydraulic power) averaged 1715 milliwatts (mW) in group A, 1120 mW in group B, and 2372 mW in group C. Cardiac outputs were within normal limits in all subjects, but tended to be lower in group B than in group C. These results suggest that the subjects of group C were better able to meet the increased energy demands imposed by an abnormally high aortic input impedance. Further investigation is needed to learn whether the high impedances in subjects with coronary disease represent an increase with age and transmural pressure alone, or whether some additional factor is involved. The data on relatively normal subjects permit a tentative definition of the normal limits for aortic input impedance in man: 26-80 dyn sec cm-5.

Pulmonary vascular input impedance and hydraulic power were measured at various heart rates in 29 anesthetized and 5 unanesthetized dogs. Hydraulic power at the pulmonary veno-atrial junction was measured in 5 dogs. The pulmonary vascular impedance spectrum in the unanesthetized dogs did not differ significantly from that in the anesthetized dogs. Average pulmonary arterial power in the anesthetized dogs was 157 milliwatts (mw), of which 108 mw was associated with mean pressure and flow, and 49 mw with the pulsations around these means. Seventy-eight per cent of this input power was dissipated in passage through the pulmonary bed. Kinetic energy accounted for 1% of the total input power.Because of a steep fall in impedance between zero and 3 cycles/sec, and a rate-dependent change in the harmonic structure of flow pulsations, there was an inverse relationship between heart rate and the input power for a given mean flow, up to 180 beats/ min. Pulmonary vascular dimensions and elasticity, which determine impedance, thus embody a mechanism whereby tachycardia can increase pulmonary blood flow by as much as 35% with an increase in pulmonary arterial input power of less than 5%, without the intervention of vasomotor activity.