Cardiovascular disease, mostly atherosclerosis, is responsible for one third of all deaths globally, rising to more than 50% in the Western World. Risk factors include smoking, diet, and familial history. Doppler ultrasound can provide estimates of blood velocity and wall shear rate. Clinically, maximum velocity is used to categorise patients for surgery, although Doppler velocity measurement is prone to errors and in need of validation. Wall shear stress—which can be derived from wall shear rate—plays a role in disease initiation and progression, although its clinical utility is unclear due to difficulties associated with its measurement. This thesis investigates the use of Doppler ultrasound as a tool to estimate blood velocity and wall shear rate. A simplified method for estimation of wall shear rate in healthy arteries is developed that uses spectral Doppler ultrasound. This method is based upon the theory of oscillatory flow in rigid pipes, requiring two measurements that are readily available with clinical ultrasound machines. This method is compared to a similar method based on colour flow imaging. The spectral Doppler method underestimated the theoretic value of wall shear rate by between 7 and 22%, with results varying between phantoms. Errors for the colour method were on average 35% greater. Test measurements from one healthy volunteer demonstrated that this method can be applied in-vivo. In more advanced stages of disease, peak velocity distal to a stenosis is of clinical interest and the simplified method for wall shear rate estimation is invalid. Steady flow in a series of simplified stenosis geometries was studied using a dual-beam Doppler system to obtain velocity vectors. These measurements were compared with data from an equivalent system that used particle image velocimetry (PIV) and was considered the gold standard. For Reynolds numbers at the stenosis throat of less than 800, flow remained laminar over the region studied, although distal flow separation did occur. For higher throat Reynolds numbers—corresponding to more severe stenoses or increased flow rates—asymmetric recirculation regions developed; the transition to turbulence occurred more proximally, with a corresponding reduction in stenotic jet and recirculation length. Qualitative agreement was observed in the velocity profile shapes measured using ultrasound and PIV at throat Reynolds numbers less than 800. Above this threshold the qualitative agreement between the velocity profiles became poorer as both downstream distance and the degree of stenosis increased. Peak axial velocity distal to the stenosis was underestimated, on average, by 15% in the ultrasound system. Estimation of shear rate remained difficult with both experimental techniques. Under a Newtonian approximation, the normalised wall shear stresses agree qualitatively. Under pulsatile flow conditions using an idealised flow waveform, superior qualitative agreement was observed in the velocity profiles at diastole than at systole. Similar to the steady flow behaviour, this agreement deteriorated with stenosis severity. The current generation of clinical ultrasound machines are capable of estimating the wall shear rate in healthy arteries. In the presence of significant arterial disease, errors in the peak velocity may result in mis-selection of patients for surgery, while estimation of the wall shear stress remains extremely problematic; particularly with identifying the wall location and measuring velocities close to the wall.

Red blood cells (RBCs) form approximately 40 to 45% of the human blood volume, and their behaviour and characteristics are the main determinant of blood properties, such as viscosity. RBCs are deformable species and stack together under low shear rate to form aggregates or rouleaux. Flowing RBCs migrate away from the wall leaving a cell-depleted layer known as the cell-free layer (CFL). This layer contributes to the blood viscosity and exchange between the RBCs and the target cells: a thinner CFL enhances the exchange process by reducing the diffusion distance. The formation of this CFL, however, is not yet completely understood. The goal of this study is to improve the understanding of the formation of the CFL in the micro-flow. This was accomplished by studying the effects of changing both the flow rate and the microchannel geometry on blood flow in microchannels. In this work, 10% hematocrit human blood suspensions were prepared in native plasma and flowed through poly-dimethylsiloxane (PDMS) microchannels of 100 μm x 34 μm cross-section. Investigation of the flowing cells was performed by using micro particle image velocimetry (μPIV) coupled with a high-speed camera. First, the high-speed camera images were processed with customized Matlab programs to detect and measure the CFL thickness and the RBC aggregates sizes. Second, the blood flow velocity profiles were measured using μPIV in order to determine the actual flow rate, the RBCs’ centerline velocity, and the shear rate. The results showed that the increase in both flow rate and shear rate significantly reduced the CFL thickness and RBC aggregates size. Comparison of the upstream and downstream measurements in the bifurcating microchannel showed that the change in microchannel geometry did not significantly influence CFL thickness and RBC aggregate size, while within the daughter branches, RBCs tended to flow close to the inner wall resulting in an undetectable CFL at the inner wall and in a larger CFL at the outer wall of the branch. These in vitro results quantitatively relate CFL thickness and RBC aggregate size at different shear rates. The findings are of immediate interest regarding the understanding of microcirculation and improved designs of microchips.