Viscosity of Blood
Viscosity is a property of fluid related to the internal friction of adjacent fluid layers sliding past one another (see laminar flow) as well as the friction generated between the fluid and the wall of the vessel. This internal friction contributes to the resistance to flow. The viscosity of plasma is about 1.8-times the viscosity of water (termed relative viscosity) at 37°C and is related to the protein composition of the plasma. Whole blood has a relative viscosity of 3-4 depending upon hematocrit, temperature, and flow rate.
The viscosity of whole blood is strongly influenced by four factors: hematocrit, temperature, flow and vessel diameter as described below.
- Hematocrit is an important determinant of the viscosity of blood. As hematocrit increases, there is a disproportionate increase in viscosity (see figure to right). For example, at a hematocrit of 40%, the relative viscosity is 4 when measure in vitro in a viscometer. At a hematocrit of 60%, the relative viscosity is about 8. Therefore, a 50% increase in hematocrit from a normal value increases blood viscosity by about 100%. Such changes in hematocrit and blood viscosity occur in a patients with polycythemia.
- Temperature also has a significant effect on viscosity. As temperature decreases, viscosity increases. Viscosity increases approximate 2% for each °C decrease in temperature. This effect has several implications. For example, when a person's hand is cooled by exposure to a cold environment, the increase in blood viscosity contributes to the decrease in blood flow (along with neural-mediated thermoregulatory mechanisms that constrict the vessels). The use of whole body hypothermia during certain surgical procedures also increases blood viscosity and therefore increases resistance to blood flow.
- The flow rate of blood also affects viscosity. At very low flow states in the microcirculation, as occurs during circulatory shock, the blood viscosity can increase quite significantly. This occurs because at low flow states there are increased cell-to-cell and protein-to-cell adhesive interactions that can cause erythrocytes to adhere to one another (rouleau formation) and increase the blood viscosity.
- At small vessel diameters (e.g., in arterioles less than 300 microns), there is a paradoxical decrease in blood viscosity (Fahraeus-Lindqvist effect). This occurs because the hemotocrit decreases in small vessels relative to the hemotocrit of large feed arteries.
Based upon in vitro experiments using blood viscometers, it is not surprising that as blood flows from distributing arteries into the microcirculation the progressive decrease in vessel diameters and flow velcocities alter blood viscosity, although in opposite directions. The net effect of these changes is that blood flow in the microcirculation has a lower viscosity than what is predicted by in vitro blood viscometer measurements. In vivo measurements of blood viscosity were made in dog hindlimbs in 1933 by Whittaker and Winton (J. Physiol. 78:339, 1933). At a given arterial blood hemotocrit, the relative viscosity of blood is much lower than predicted from in vitro experiement (cp figure at right with previous figure that used a viscometer). Although not shown in this figure, one could predict that as total hindlimb blood flow decreases (as occurs in hypotensive shock) that the relative viscosity would increase at any given feed artery hemotocrit.
Revised 03/23/10


