Viscosity of Blood
Viscosity is an intrinsic property of fluid related to the internal friction of adjacent fluid layers sliding past one another (see laminar flow). This internal friction contributes to the resistance to flow. The interactions between fluid layers depend on the chemical nature of the fluid, and whether it is homogeneous or heterogeneous in composition. For example, water is a homogeneous fluid and its viscosity is determined by molecular interactions between water molecules. Water behaves as a Newtonian fluid and therefore under non-turbulent conditions, its viscosity is independent of flow velocity (i.e., does not change with changes in velocity). Although plasma is mostly water, it also contains other molecules such as electrolytes, proteins (especially albumin and fibrinogen), and other macromolecules. Because of various molecular interactions between these many different components of plasma, it is not surprising that plasma has a higher viscosity than water. In fact, plasma at 37°C is about 1.8-times more viscous than water at the same temperature; therefore, the relative viscosity of plasma (compared to water) is about 1.8.
The addition of formed elements to the plasma (red cells, white cells, and platelets) further increases the viscosity. Of these formed elements, red cells have the greatest effect on viscosity under normal conditions. As shown in the figure to the right in which whole blood viscosity is determined in vitro using a viscometer, an increase in red cell hematocrit leads to an increase in relative viscosity. Note that the increase is non-linear, so that doubling hematocrit more than doubles the relative viscosity. Therefore, blood viscosity strongly depends on hematocrit. At a normal hematocrit of 40-45%, the relative viscosity of blood is 4-5. Patients with a condition called polycythemia, which is a abnormal elevation in red cell hematocrit, have much higher blood viscosities. This increases the resistance to blood flow and therefore increases the work of the heart and can impair organ perfusion. Some patients with anemia have low hematocrits, and therefore reduced blood viscosities.
A second important factor that influences blood viscosity is temperature. Just like molasses, when blood gets cold, it get "thicker" and flows more slowly. Therefore, there is an inverse relationship between temperature and viscosity. Viscosity increases about 2% for each degree centigrade decrease in temperature. Normally, blood temperature does not change much in the body. However, if a person's hand is exposed to a cold environment and the fingers become cold, the blood temperature in the fingers will fall and viscosity increase, which together with sympathetic-mediated vasoconstriction will decrease blood flow in the cooled region. When whole body hypothermia is induced in critical care or surgical situations, this will also lead to an increase in blood viscosity and therefore affect systemic hemodynamics and organ blood flow.
Unlike water, blood is non-Newtonian, meaning that viscosity is not independent of flow at all flow velocities. In fact, during conditions such as circulatory shock where microcirculatory flow in tissues is reduced because of decreased arterial pressure, low flow states can lead to several-fold increases in viscosity. Low flow states permit increased molecular interactions to occur between red cells and between plasma proteins and red cells. This can cause red cells to stick together and form chains of several cells (rouleau formation) within the microcirculation, which increases the blood viscosity.
If clotting mechanisms are stimulated in the blood, platelet aggregation and interactions with plasma proteins occur. This leads to entrapment of red cells and clot formation, which dramatically increase blood viscosity.
There is a microcirculatory phenomenon called the Fahraeus-Lindqvist effect that leads to a reduction in hematocrit in small arterioles (less than 200 microns in diameter) and capillaries relative to the hematocrit of large feed arteries. This decrease in hematocrit in these flow vessels reduces the relative blood viscosity in the small vessels, which helps to offset the increase in viscosity that can occur because of reduced velocity in these same vessels. 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 hematocrit, the relative viscosity of blood is much lower than predicted from in vitro experiments (compare figure at right with previous figure that used a viscometer).