Blood Viscosity Influence on Flow

Blood Viscosity Influence on Flow is the effect that the internal frictional resistance of blood itself, referred to as viscosity, has on the flow of blood through the circulatory system, acting as one of the three physical variables, alongside vessel radius and vessel length, that together determine the resistance a given vessel offers to flow. Unlike vessel radius, which can be rapidly and precisely regulated through smooth muscle contraction, blood viscosity changes more slowly and is governed primarily by the cellular and protein composition of blood, making its influence on flow somewhat less amenable to rapid physiological adjustment but nonetheless clinically and physiologically significant.

Physical Basis of Blood Viscosity

Viscosity as Internal Fluid Friction

Viscosity describes the internal friction that arises between adjacent layers of a fluid as they move at different velocities relative to one another, with more viscous fluids requiring a greater force to produce a given rate of deformation or flow than less viscous fluids. In the context of blood flowing through a vessel, viscosity determines how much of the driving pressure gradient is dissipated as internal friction rather than converted into the kinetic energy of forward moving blood.

Contribution of Hematocrit to Whole Blood Viscosity

Whole blood viscosity is determined predominantly by hematocrit, the proportion of blood volume occupied by red blood cells, since red blood cells are considerably more viscous as a suspended phase than the surrounding plasma, and increasing hematocrit increases the frequency and intensity of cell to cell and cell to plasma interactions that generate internal friction within the flowing blood.

Contribution of Plasma Protein Concentration

Plasma itself possesses a baseline viscosity somewhat greater than that of pure water, attributable primarily to the presence of plasma proteins, particularly fibrinogen, and conditions that alter plasma protein concentration, such as dehydration or certain inflammatory and hematologic disorders, can measurably alter plasma viscosity even independent of any change in hematocrit.

Non-Newtonian Behavior of Blood

Shear Thinning Property

Unlike an idealized Newtonian fluid, whose viscosity remains constant regardless of the rate at which it is sheared, whole blood exhibits shear thinning behavior, meaning that its apparent viscosity decreases as shear rate increases, a property attributable largely to the deformability of red blood cells and their tendency to align with the direction of flow and to disaggregate from clumped formations at higher shear rates.

The Fahraeus-Lindqvist Effect

In vessels of very small diameter, approaching the size of individual capillaries and small arterioles, the apparent viscosity of blood decreases further as vessel diameter decreases, a phenomenon known as the Fahraeus-Lindqvist effect, attributed to the tendency of red blood cells to migrate toward the center of the vessel lumen in narrow vessels, leaving a relatively cell poor layer of plasma adjacent to the vessel wall that reduces the effective friction experienced by the bulk of the flowing blood. This effect means that blood flowing through the smallest vessels of the circulation experiences somewhat lower resistance than would be predicted from its viscosity as measured in larger diameter vessels or in bulk laboratory conditions.

Consequences of Altered Viscosity for Flow and Resistance

Direct Proportionality Between Viscosity and Resistance

According to the Hagen-Poiseuille relationship, resistance is directly proportional to viscosity, so that an increase in blood viscosity, all else held constant, produces a proportional increase in resistance and a corresponding proportional decrease in flow for any given pressure gradient.

Comparison to Radius as a Flow Determinant

Although viscosity affects resistance and flow according to a simple linear relationship, this influence is considerably weaker than the fourth power relationship governing radius, meaning that clinically significant changes in blood viscosity, such as the substantial elevation of hematocrit seen in polycythemia, typically produce a more modest effect on flow than would result from a comparably significant change in vessel radius, even though both variables act through the same underlying resistance equation.

Visual Representation of Viscosity Influence on Flow

Physiological and Clinical Relevance

Regulation of Hematocrit as an Indirect Flow Regulator

Because viscosity is closely tied to hematocrit, physiological or pathological processes that alter red blood cell mass, including the erythropoietin driven increase in red cell production at high altitude or in chronic hypoxic states, produce corresponding changes in blood viscosity that must be balanced against the beneficial effect of increased oxygen carrying capacity, since an excessive rise in hematocrit can raise viscosity enough to meaningfully impair flow and increase cardiac workload despite the increased oxygen content of each unit of blood.

Clinical Significance of Viscosity Altering Conditions

Conditions that substantially alter blood viscosity, including severe dehydration, polycythemia, and disorders of plasma protein concentration such as multiple myeloma, can produce clinically significant increases in vascular resistance and cardiac workload as a direct consequence of the viscosity term within the resistance equation, illustrating that blood viscosity, while a comparatively weaker determinant of flow than vessel radius, remains a physiologically and clinically meaningful variable within the overall hemodynamic framework.