Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2020 Feb 24;12(2):e7090.
doi: 10.7759/cureus.7090.

The Role of Blood Viscosity in Infectious Diseases

Gregory D Sloop  1 , Quirijn De Mast  2 , Gheorghe Pop  3 , Joseph J Weidman  4 , John A St Cyr  5
Affiliations
Review

The Role of Blood Viscosity in Infectious Diseases

Gregory D Sloop et al. Cureus. .

Abstract

Blood viscosity is increased by elevated concentrations of acute phase reactants and hypergammaglobulinemia in inflammation. These increase blood viscosity by increasing plasma viscosity and fostering erythrocyte aggregation. Blood viscosity is also increased by decreased erythrocyte deformability, as occurs in malaria. Increased blood viscosity contributes to the association of acute infections with myocardial infarction (MI), venous thrombosis, and venous thromboembolism. It also increases vascular resistance, which decreases tissue perfusion and activates stretch receptors in the left ventricle, thereby initiating the systemic vascular resistance response. This compensates for the increased vascular resistance by vasodilation, lowering hematocrit, and decreasing intravascular volume. This physiological response causes the anemias associated with malaria, chronic inflammation, and other chronic diseases. Since tissue perfusion is inversely proportional to blood viscosity, anemia may be beneficial as it increases tissue perfusion when erythrocyte aggregating factors or erythrocytes with decreased deformability are present in the blood.

Keywords: acute phase response; anemia of chronic disease; atherosclerosis; atherothrombosis; blood viscosity; hemorheology; infection; inflammation; myocardial infarction; thrombosis.

PubMed Disclaimer

Conflict of interest statement

The authors have declared that no competing interests exist.

Figures

Figure 1
Figure 1. Shear rate
Flowing blood can be envisioned as an infinite number of independent layers sliding against each other. In this figure, the velocity of a layer is proportional to the length of an arrow. Shear rate is defined as the difference in velocities between any two layers divided by the distance between them. In a low viscosity fluid (left), the velocity gradient is greater than in a high viscosity fluid (right)
Figure 2
Figure 2. The relationship between blood viscosity and shear rate
As shear rate (and velocity) increases from left to right, blood viscosity decreases. Factors that affect blood viscosity are shown in the velocity domain in which their effect is most prominent Figure reprinted courtesy of www.BloodFlowOnline.com
See this image and copyright information in PMC

References

    1. Reducing cardiac after-load by lowering blood viscosity in patients with familial hypercholesterolemia - a pilot study. Possible mechanism for occurrence of anemia in chronic heart failure patients? Pop GAM, De Boer M-J, Stalenhoef AFH. Cor et Vasa. 2016;58:374–378.
    1. Sloop GD. Blood Viscosity: Its Role in Cardiovascular Pathophysiology and Hematology. Vol. 1. New York: Nova Science Publishers; 2017. The systemic vascular resistance response; pp. 67–82.
    1. Why atherothrombosis is in principle a hematologic disease: the effect of disorders and drugs which affect thrombosis on the development of atherosclerotic plaques. Sloop GD, Pop GAM, Weidman JJ, St Cyr JA. Int Arch Cardiovasc Dis. 2018;2
    1. Perspective: interesterified triglycerides, the recent increase in deaths from heart disease, and elevated blood viscosity. Sloop GD, Weidman JJ, St Cyr JA. Ther Adv Cardiovasc Dis. 2018;12:23–28. - PMC - PubMed
    1. Perspective: the failure of cholesteryl ester transfer protein inhibitors: is it due to increased blood viscosity? Sloop GD, Weidman JJ, St Cyr JA. Ther Adv Cardiovasc Dis. 2015;9:32–35. - PubMed

LinkOut - more resources