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.
Highlights
BackgroundThe role of blood viscosity in pathophysiology has been neglected even though increased blood viscosity affects the presentation and complications of many diseases
It 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
This review examines the fundamentals of blood viscosity and explores its role in several topics of interest to infectious disease specialists: the association of infectious diseases and immunization with myocardial infarction (MI) and venous thrombosis, and the anemias associated with malaria and chronic inflammation and disease
Summary
The role of blood viscosity in pathophysiology has been neglected even though increased blood viscosity affects the presentation and complications of many diseases. They found convincing evidence for a two-fold increase in the risk of venous thrombosis following pneumonia, urinary tract infection, and acute infectious diseases not otherwise specified They reviewed a study that showed a decreased prevalence of deep vein thrombosis in subjects vaccinated against influenza. They noted that the treatment of anemia of chronic disease should have a negative effect if it is a homeostatic response They reported that a metaanalysis of 51 studies of erythropoiesis-stimulating agents in cancer showed higher mortality and risk of venous thromboembolism when the therapeutic goal was a normal hemoglobin concentration compared to a lower one. Arteriovenous shunt thrombosis, and poorly controlled hypertension are all attributable to increased blood viscosity These results support the theory that anemia of chronic disease is a beneficial response as it decreases systemic vascular resistance, increases cardiac output, and improves tissue perfusion. Treatment of the anemia of chronic disease with erythropoiesis-stimulating agents or transfusion should be undertaken cautiously and guided by monitoring of blood viscosity
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