Abstract
The term hyperviscosity cannot be understood without some knowledge of how blood viscosity is defined and measured. Viscosity (V) is a flow property defined as resistance (R) to the movement of blood: R = VZ, where Z is the resistance resulting from the vessel geometry [1]. Blood viscosity is usually measured in flow devices with fixed geometry (e.g., in a rotational viscometer with a defined gap or in a tube viscometer with defined tube diameter and length). In these devices, the blood flow resistance increases linearly with the blood viscosity, and blood flow resistance is measured as pressure (P) or force required to achieve a defined blood flow (F) in the device (V ≈ R = P/F). Blood viscosity decreases with increasing shear forces due to red blood cell (RBC) aggregation at low shear rates and ellipsoidal deformation of RBCs at high shear. In tube viscometers with diameters below 300 μ, blood viscosity decreases linearly with decreasing tube diameter. Without this so called Fahraus-Lindqvist effect, blood with a hematocrit of 50% and higher could probably not pass through arterioles and capillaries with diameters below 50 µm.
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Linderkamp, O. (2012). Polycythemia and Hyperviscosity. In: Buonocore, G., Bracci, R., Weindling, M. (eds) Neonatology. Springer, Milano. https://doi.org/10.1007/978-88-470-1405-3_79
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