How do pulmonary arterial pulse wave velocity and impedance differ between normal subjects and those with pulmonary hypertension?
The elasticity of the pulmonary arterial tree is a key determinant of the energy required for pulsatile pulmonary blood flow, with increased stiffness and energy dissipation observed in pulmonary hypertension.
The 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 cm -5 and 1.68 m/sec in the normals; 46 dyne sec cm -5 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.
Milnor et al. (1969) studied this question.