Intravascular volume expansion has been shown to improve cardiac output in experimental cardiac tamponade. To determine the limitations of intravascular volume manipulation, acute tamponade was created in 20 anesthetized, spontaneously breathing dogs. The intrapericardial volume causing tamponade was determined for each animal, and kept constant. Hemodynamics were recorded with and without tamponade at multiple levels of intravascular volume. During cardiac tamponade, intravascular volume expansion increased cardiac output only in animals which were initially volume-depleted. Volume expansion of normovolemic or hypervolemic animals caused minimal changes in cardiac output, but increased atrial and aortic pressures. Intravascular volume depletion of the normovolemic animal caused a significant decline in cardiac output, in contrast to the trend towards an increased output following phlebotomy of the volume-expanded animals. In general, the benefit of intravascular volume expansion during cardiac tamponade could only be demonstrated when atrial pressures were below 12 mm Hg.