Prosthetic heart valves, heart-assist devices, oxygenators, dialyzers and other biomedical devices that repair, replace or support various organ systems of the human body are in wide clinical use. These devices are responsible for saving, extending, and enhancing the lives of patients with otherwise hopeless medical conditions. The safety and efficacy of these blood-contacting biomedical devices strongly depends on the extent to which they damage blood. Unfortunately, in many cases these devices cause dangerous complications triggered by non-physiological factors within the blood flow.

The precise mechanisms of blood damage in blood-contacting devices are heterogeneous and are not well understood in spite of numerous investigations of blood trauma conducted over several decades by investigators worldwide. This body of research has revealed that blood trauma is related to non-physiological flow conditions such as elevated shear forces, turbulence, cavitation, prolonged contact and collision between blood cells and foreign surfaces. These factors may induce a variety of damage mechanisms: overstretching or fragmentation of a subpopulation of erythrocytes causing free hemoglobin to be released into plasma (i.e., hemolysis); activation or dysfunction of platelets and leukocytes; increased concentrations of inflammatory mediators; complement activation; and sub-lethal blood trauma such as alterations in mechanical properties of erythrocytes as manifested by an increase in RBC aggregation and decrease in their deformability (see Figure 1). This latter sublethal RBC mechanical damage causes a shortening of RBC life span, a decrease in density of functioning capillaries and area of contact surface of RBC with capillary walls, and may lead to anemia, tissue hypoxia and other complications. Even moderate hemolysis, which is not an immediate threat to renal function, is an important warning sign of other potential blood cell damage such as platelet activation, white blood cell (WBC) dysfunction, and other serious complications such as scavenging of nitric oxide [1], damage to glycocalyx and endothelial cells, and impairment of the vascular smooth muscle tone [2]. Although damage to platelets and WBC is an extremely important topic, this chapter concentrates on the mechanical trauma to RBC and related changes in rheological properties of whole blood. In summary, in vitro experimental studies and clinical experience with artificial organs presented in this chapter substantiate the assertion that mechanical stress substantially impairs the mechanical properties of RBC and adversely affects whole blood rheology, and that this impairment may contribute to various medical complications in dialysis, prosthetic heart valve and circulation-assist device recipients.