PubMed Health⌕ Search

PubMed · 11397530

Sources of error in maximum velocity estimation using linear phased-array Doppler systems with steady flow.

Abstract

Using linear-array Doppler ultrasound (US) transducers, the measured maximum velocity may be in error and lead to incorrect clinical diagnosis. This study investigates the existence and cause of maximum velocity estimation errors for steady flow of a blood-mimicking fluid in a tissue-mimicking phantom. A specially designed system was used that enabled fine control of flow rate, transducer positioning and transducer angle relative to the flow phantom. Doppler machine settings (transducer aperture size, focal depth, beam-steering, gain) were varied to investigate a wide range of clinical applications. To estimate the maximum velocity, a new signal-to-noise ratio (SNR) independent method was developed to calculate the maximum frequency from an ensemble averaged Doppler power spectrum. This enabled the impact of each factor on the total Doppler error to be determined. When using the new maximum frequency estimator, it was found that the effect of transducer focal depth, intratransducer, intramachine, intermachine (that was tested) and beam-steering did not significantly contribute to maximum velocity estimation errors. Instead, it was the dependence of the maximum velocity on the Doppler angle that made, by far, the greatest contribution to the estimation error. Because our maximum frequency estimator took into account the effect of intrinsic spectral broadening, the degree of overestimation error was not as great as that previously published. Thus, the effects of Doppler angle and intrinsic spectral broadening are the chief sources of Doppler US error and should be the focus of future efforts to improve the accuracy.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

A H Steinman, J Tavakkoli, J G Myers, R S Cobbold, K W Johnston. 2001. Sources of error in maximum velocity estimation using linear phased-array Doppler systems with steady flow.. https://doi.org/10.1016/s0301-5629(01)00352-0

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Vascular bed origin dictates flow pattern regulation of endothelial adhesion molecule expression.

Endothelial cell phenotypes markedly differ, depending upon function and vascular bed of origin. Differences might account for specific susceptibility to pathological conditions. As leukocyte adhesion to activated endothelium is the initiating event in a range of diseases, we compared the influence of vascular bed-specific flow patterns on adhesion molecule expression in human saphenous vein (HSVEC) and coronary artery endothelial cells (HCAEC). In vitro, immune cell attachment was increased 1.6-fold when tumor necrosis factor (TNF)-alpha-stimulated HSVEC were exposed to coronary artery flow in place of physiological venous flow and 1.9-fold higher compared with attachment to cytokine-stimulated HCAEC exposed to coronary artery flow. This was associated with increased concentrations of soluble E-selectin, VCAM-1, and ICAM-1 in supernatants of HSVEC exposed to coronary artery flow compared with HCAEC exposed to the same flow pattern. Venous and coronary artery flow both increased TNF-alpha-induced E-selectin and ICAM-1 expression on HSVEC, but only coronary artery flow increased VCAM-1 expression. In marked contrast to HSVEC, venous and coronary artery flow attenuated TNF-alpha-induced E-selectin and VCAM-1 expression on HCAEC, whereas coronary artery flow further induced ICAM-1 on cytokine-stimulated HCAEC. With the exception of cytokine-induced ICAM-1, adhesion molecule expression on HSVEC exposed to coronary artery flow exceeded expression on HCAEC. Thus ICAM-1 expression involves complex flow-dependent and -independent pathways with marked dissimilarities between the two endothelial cell types studied. Interestingly, Kruppel-like factor (KLF) 4 overexpression in HCAEC and HSVEC significantly reduced TNF-alpha-induced E-selectin and VCAM-1 expression in static conditions, while ICAM-1 expression remained constant. Furthermore, both flow patterns induced KLF2 and KLF4 expression in HCAEC and HSVEC. Venous and coronary artery flow differentially influence endothelial adhesion molecule and transcription factor expression, depending on the vascular bed of origin. Differences in adhesion molecule expression and subsequent immune cell adhesion between HSVEC and HCAEC may contribute to different susceptibility to pathological conditions.

Blood Flow Velocity↗

Mesoscale simulation of blood flow in small vessels.

Computational modeling of blood flow in microvessels with internal diameter 20-500 microm is a major challenge. It is because blood in such vessels behaves as a multiphase suspension of deformable particles. A continuum model of blood is not adequate if the motion of individual red blood cells in the suspension is of interest. At the same time, multiple cells, often a few thousands in number, must also be considered to account for cell-cell hydrodynamic interaction. Moreover, the red blood cells (RBCs) are highly deformable. Deformation of the cells must also be considered in the model, as it is a major determinant of many physiologically significant phenomena, such as formation of a cell-free layer, and the Fahraeus-Lindqvist effect. In this article, we present two-dimensional computational simulation of blood flow in vessels of size 20-300 microm at discharge hematocrit of 10-60%, taking into consideration the particulate nature of blood and cell deformation. The numerical model is based on the immersed boundary method, and the red blood cells are modeled as liquid capsules. A large RBC population comprising of as many as 2500 cells are simulated. Migration of the cells normal to the wall of the vessel and the formation of the cell-free layer are studied. Results on the trajectory and velocity traces of the RBCs, and their fluctuations are presented. Also presented are the results on the plug-flow velocity profile of blood, the apparent viscosity, and the Fahraeus-Lindqvist effect. The numerical results also allow us to investigate the variation of apparent blood viscosity along the cross-section of a vessel. The computational results are compared with the experimental results. To the best of our knowledge, this article presents the first simulation to simultaneously consider a large ensemble of red blood cells and the cell deformation.

Blood Flow Velocity↗

Doppler sonography evaluation of flow velocity and volume of the extracranial internal carotid and vertebral arteries in healthy adults.

PURPOSE: To measure with Doppler sonography the velocity and volume of blood flow in the extracranial internal carotid artery (ICA) and vertebral artery (VA) of healthy adults and to calculate total cerebral blood flow volume (tCBFV). METHODS: Bilateral ICA and VA were examined sonographically in 180 healthy adults. Angle-corrected peak systolic (Vps), end-diastolic (Ved), and time-averaged maximum blood flow velocity (TAV) were measured in pulsed Doppler mode, and the resistance index (RI) and pulsatility index (PI) were calculated. The cross-sectional area (A) was measured on gray-scale images. Volume flow was calculated as FV = TAV x A, and tCBFV was calculated as the sum of the right and left ICA and VA volume flow. RESULTS: tCBFV was 651 +/- 96 ml/min for the entire population. There was a significant decrease in Vps, Ved, TAV, and tCBFV with age in all arteries. RI and PI values initially declined and then increased with age. Cross-sectional area increased with age in ICA but not in VA. PI and RI were higher in men than in women. Blood flow velocity and volume were higher, and RI was lower in the left than in the right VA. CONCLUSION: The Doppler sonographic assessment of extracranial ICA and VA blood flow volume may be useful for the study of cerebral hemodynamic changes in patients with cerebrovascular disorders. Age-dependent changes should be considered, for instance, in the management of intensive care patients with impaired cerebral perfusion.

Blood Flow Velocity↗