Anemia of Cancer and Its Cardiovascular Effects

Abstract

The principal obligation of blood, heart, and vessels is to maintain a steady and optimal oxygen supply to the tissues. These three organs are controlled by closely integrated feedback circuits, and a change in the function in any one will cause compensatory adjustment in the function of the others. In the case of blood, acute reduction in the oxygen-carrying capacity will result in tissue hypoxia, vascular dilatation, and decreased peripheral vascular resistance, which, abetted by lower blood viscosity, will cause an increase in cardiac output and, in turn, restoration to normal of oxygen supply to the tissues. However, such a primary response by the heart to anemia is metabolically and functionally expensive and is saved for conditions of acute and severe life-threatening anemia. In patients with cancer the associated anemia is usually chronic and of moderate severity, and here the compensatory adjustments in oxygen flow rarely demand an increase in cardiac work, but are accomplished by other means, such as changes in oxygen affinity and redistribution of blood among the tissues.