Abstract
The influence of severe chronic anemia on cardiovascular dynamics has long been recognized. The decreased blood viscosity and vascular tone that accompany the reduced oxygen-carrying capacity lead to increased venous return and preload, with increased cardiac output. When oxygen demand exceeds oxygen supply, congestive heart failure develops. In the absence of cardiac disease, mild anemia is generally well tolerated through such compensatory mechanisms as the increased cardiac output and a decreased affinity of hemoglobin for oxygen. However, the combination of anemia with an intracardiac defect may enhance or precipitate cardiopulmonary compromise — effects not anticipated with a normal heart.In . . .