1 From the Department of Medicine, School of Medicine, Medical College of Virginia, Richmond, Va.
Editors: HERRMAN L. BLUMGART, M.D. and A. STONE FREEDBERG, M.D..
The following brief summary seems justified from the large volume of accumulated data dealing with the reaction of the cardiovascular system in the anemic patient. There are four mechanisms operating in the anemic patient which may increase the supply of oxygen to the tissues when the oxygen carrying capacity of the blood is reduced. Under conditions of rest, a rapid velocity flow and tachycardia with an increase in minute volume of cardiac output is the first response to anemia. As compensation develops, tachycardia and increased velocity flow are largely replaced by selective shunting of blood and the removal of an increasing percentage of oxygen in the tissue capillaries from each gram of circulating hemoglobin. These later physiologic mechanisms are best illustrated by patients with chronic parasitic anemias. Under conditions of physical stress each of the four physiologic mechanisms contribute in meeting the demands for increased oxygen requirements. Compensation is, however, never perfect; the status of the patient is determined by the reduction in hemoglobin, the tissue oxygen requirements, the presence of physical changes in the cardiovascular and pulmonary systems, degree of oxygen abstraction from the blood, and the selective shunting of blood. In relatively acute anemia, dyspnea readily occurs on physical exercise. Reduction in the ventilatory capacity of the lung occurring in some anemic patients results from an over-all reduction in physical fitness due to the anemic state rather than to physical changes in the lung. In well compensated, chronic anemia, the vital capacity of the lungs is frequently above normal and similar to that observed in athletes and completely acclimatized, high altitude inhabitants. In the absence of cardiovascular disease or physical or metabolic factors requiring increased cardiac output, true congestive heart failure rarely results from the anemic state. Effort angina is uncommon in anemic patients and when present is usually related to underlying coronary artery disease. Cardiac hypertrophy under certain conditions results from prolonged anemia. Since cardiac hypertrophy is rightly placed in the category of organic heart disease, one is justified in classifying chronic anemia as one of the etiologic factors in the production of heart disease.
© 1953 American Heart Association, Inc.
The Heart in Anemia