The factors that determine the rheological behavior of blood, a two-phase fluid, include the relative volume of each phase as reflected by the hematocrit value, plasma composition and the properties of cellular elements. The contribution of these factors to blood rheology has been detailed in previous chapters (Chapters II.2 and II.3.a). Thus it is not surprising that the mechanisms of blood rheology alterations are also related to these factors.

In a classification published by P.F. Leblond in an early, 1987 textbook of hemorheology, hyperviscosity syndromes were discussed from a pathophysiological point of view [1]: a) Polycythemic disorders to include erythrocytosis and leukocytosis. b) Sclerocythemic disorders to include conditions with impaired red blood cell (RBC) deformability. c) Plasmatic disorders to include alterations in plasma viscosity and red cell aggregation. Similar approaches have been used by others [2]. J-F. Stoltz classified hyperviscosity syndromes into five groups [3]: a) Increase in number of blood cells; b) Altered plasma protein levels; c) Increased RBC internal rigidity; d) Changes in RBC viscoelastic properties; e) Enhanced RBC aggregation.

These classifications, based on the mechanisms of hemorheological alterations, need to be revised in light of developments in the past twenty years. There has been a significant change in our understanding of the factors that determine the degree of RBC aggregation: in addition to plasma factors and local shear forces, RBC properties are now well established as an additional factor affecting the intensity of aggregation. Thus, enhanced RBC aggregation may not always be related to plasma composition changes, but can co-exist with plasma viscosity alterations. RBC properties therefore influence both cell deformability and aggregation.

Table 1 presents a classification of hemorheological alterations based upon the considerations described above.