Capillary red blood cell velocity measurements in human nailfold by videodensitometric method.
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Biomedical subjects
Publications and source records attributed to M Anliker.
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The propagation of sounds and pulse waves within the cardiovascular system is subject to strong dissipative mechanisms. To investigate the effects of blood viscosity on dissipation as well as dispersion of small waves in arteries and veins, a parametric study has been carried out. A linearized analysis of axisymmetric waves in a cylindrical membrane that contains a viscous fluid indicates that there are two families of waves: a family of slow waves and one of fast waves. The faster waves are shown to be more sensitive to variations in the elastic properties of the medium surrounding the blood vessels and at high values of the frequency parameter alpha defined by alpha = radicalrhoomegaR(2) (0)/mu the blood viscosity attenuates them more strongly over a length than the slow waves. At low values of alpha, the effects of viscosity on attenuation are reversed; that is, the family of slow waves is much more attenuated than the family of fast waves. For the slow waves the radial displacement component generally exceeds the axial component except at very low frequencies. Conversely the axial displacements are much larger than the radial displacement for the faster waves. The presence of external constraints, however, can modify these results. In the case of the slow waves the phase angle between pressure and radial wall displacement is virtually negligible in the presence of mild external constraints, while the phase angles between pressure and fluid mass flow are at most 45 degrees . The corresponding phase angles for the fast waves exhibit much larger variations with changes in the elastic properties of the surrounding medium.
The theoretical predictions described in part I of this study are compared with in vivo data from anesthetized dogs. It is shown that the observed attenuation of the pressure and axial waves cannot be accounted for by fluid viscosity alone. For large values of the frequency parameter alpha = radicalrhoomegaR(2) (0)/mu, the analysis of part I is extended to include the effects of viscoelasticity of the vessel wall. The results indicate that the speeds of both types of waves are essentially not affected by a realistic viscoelasticity model while the attenuation per wavelength is significantly increased and becomes frequency independent. The application of this analysis to in vivo data from the carotid arteries of anesthetized dogs demonstrates partial agreement between theory and experiment and suggests that the carotid arteries are anisotropically viscoelastic.
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Theoretical and experimental evidence suggests that the dissipation of high frequency pressure waves in blood vessels is caused primarily by the viscoelastic behavior of the vessel wall. In this theoretical analysis the vessels are considered as fluid-filled circular cylindrical shells whose walls have isotropic and homogeneous viscoelastic properties and are subjected to an initial axial stretch and a transmural pressure. If the wall material is incompressible and behaves as a Voigt solid in shear, the results predict a decrease in wave amplitude per wavelength which is essentially independent of frequency over a wide range. This finding is in qualitative agreement with recent experiments on anesthetized dogs. A parametric study also shows a great sensitivity of the dissipation to changes in transmural pressure and axial stretch. Axisymmetric waves are only mildly dispersive, while all nonaxisymmetric waves are highly dispersive and exhibit much stronger damping per wavelength at low frequencies than do axisymmetric waves.
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A computer-controlled 14-channel pulsed Doppler ultrasound instrument was used as a noninvasive means to evaluate instantaneous velocity profiles and flow in the comlon carotid arteries of 22 healthy persons and in 22 patients. Of the later, 13 had severe obstructions of the extracranial portion of the carotid artery, four had obstruction of the intracranial portion, and five had severe aortic valve insufficiency (AI), with more than 60% regurgitation in all cases. Measurements could be performed within an accuracy of about +/- 20% under clinical conditions and revealed perfusion values of 5 to 8 ml per second (300 to 480 ml per minute) in healthy persons. Of the patients, values less than 3 ml per second (180 ml per minute) were detected in nine, between 3 and 5 mm per second (180 to 300 ml per minute) in four, and normal values in another four, while significant backflow was observed only in patients with severe AI. Consecutive blood flow profiles were recorded every 4 msec; these demonstratedthat, for a period lasting from 40 msec to 280 msec after the initial systolic peak, blood flow decelerated more rapidly in the central portion of the vessel lumen than near the wall. This situation was present in all healthy persons and in most patients with pathological flow. In patients with AI, flow reinversion from reverse to normal began near the vessel wall, while in the middle third of the vessel lumen, blood was still flowing backward. These phenomena seem to be in agreement with the theoretical and experimental findings of Wormersly, Müller, and others. The AI patients who underwent artificial valve implantation were studied ten days after operation and showed no or little backflow in the common carotid artery at that time.