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The fluid mechanics of artificial blood pumps has been studied since the early 1970s in an attempt to understand and mitigate hemolysis and thrombus formation by the device. Pulsatile pumps are characterized by inlet jets that set up a rotational "washing" pattern during filling. Strong regurgitant jets through the closed artificial heart valves have Reynolds stresses on the order of 10,000 dynes/cm 2 and are the most likely cause of red blood cell damage and platelet activation. Although the flow in the pump chamber appears benign, low wall shear stresses throughout the pump cycle can lead to thrombus formation at the wall of the smaller pumps (10-50 cc). The local fluid mechanics is critical. There is a need to rapidly measure or calculate the wall shear stress throughout the device so that the results may be easily incorporated into the design process. 65 Annu. Rev. Fluid Mech. 2006.38:65-86. Downloaded from www.annualreviews.org Access provided by University of California -San Diego on 02/04/15. For personal use only.

a b s t r a c tThis paper reviews key issues in the physical and numerical modelling of marine renewable energy systems, including wave energy devices, current turbines, and offshore wind turbines. The paper starts with an overview of the types of devices considered, and introduces some key studies in marine renewable energy modelling research. The development of new International Towing Tank Conference (ITTC) guidelines for model testing these devices is placed in the context of guidelines developed or under development by other international bodies as well as via research projects. Some particular challenges are introduced in the experimental and numerical modelling and testing of these devices, including the simulation of Power-Take-Off systems (PTOs) for physical models of all devices, approaches for numerical modelling of devices, and the correct modelling of wind load on offshore wind turbines. Finally, issues related to the uncertainty in performance prediction from model test results are discussed.

Recent developments indicate that the forces acting on the papillary muscles can be a measure of the severity of mitral valve regurgitation. Pathological conditions, such as ischemic heart disease, cause changes in the geometry of the left ventricle and the mitral valve annulus, often resulting in displacement of the papillary muscles relative to the annulus. This can lead to increased tension in the chordae tendineae. This increased tension is transferred to the leaflets, and can disturb the coaptation pattern of the mitral valve. The force balance on the individual components governs the function of the mitral valve. The ability to measure changes in the force distribution from normal to pathological conditions may give insight into the mechanisms of mitral valve insufficiency. A unique in vitro model has been developed that allows quantification of the papillary muscle spatial position and quantification of the three-dimensional force vector applied to the left ventricular wall by the papillary muscles. This system allows for the quantification of the global force exerted on the posterior left ventricular wall from the papillary muscles during simulation of normal and diseased conditions.

Flow stasis in an artificial heart may provide a situation where thrombus develops. Should part, or all, of the clot dislodge, a thromboembolism may lead to stroke(s), neurologic deficits, or even death. In an effort to determine if the regime of low shear or stasis exists, a two-dimensional particle image velocimetry (PIV) system was implemented to measure the velocity field within the 50 cc Penn State Artificial Heart. The velocity measurements were decomposed nearest the wall to obtain wall shear rates along the bottom of the chamber. The PIV measurements were made in three image planes across the depth of the chamber to reconstruct a surface distribution of the wall shear rates at the bottom over the entire heart cycle. The wall shear rate is shown to be spatially nonuniform, with persistently low wall shear rates. An area near the front edge of the chamber at the bottom showed wall shear rates not exceeding 250 s(-1). This was an area of clot formation seen in vivo, suggesting a link may exist between the low wall shear rate zone and thrombus formation.