Coronary and cardiovascular dynamics and oxygen availability during acute normovolemic anemia

The hematocrit of 12 dogs was reduced from 43 to 30 and then to 20% by bleeding and simultaneous infusion of lactated Ringer's solution. At each level of anemia, blood volume, heart rate, cardiac output, left and right pressures, left ventricular (LV) work, aortic mean pressure, and systemic vascular resistance were at prebleeding values. Pulmonary arterial saturation decreased from 76 to 67 and 50%. LV coronary venous saturation fell from 46 to 31% at hematocrit 30, with no further reduction at hematocrit 20. Electromagnetically measured left coronary mean flow was 120 and 185% of control at hematocrits 30 and 20. Coronary flow reserve, or the ratio of peak increase in flow after 10 second occlusion to preocclusion flow, was 3.8 at hematocrit 43, 3.0 at 30, and 1.9 at 20. The change in ratio was due to increased resting flow with anemia, whereas peak reactive hyperemia flow did not change with hematocrit. Acute normovolemic anemia is not associated with significant changes in cardiac work. Despite lowered blood viscosity, systemic resistance is maintained by vasoconstriction. Systemic oxygen availability (Cardiac output X arterial O2 content) is decreased, but uptake is maintained by increased O2 extraction. LV O2 consumption is maintained by maximally increasing the already high myocardial O2 extraction and by increasing coronary flow. At half-normal hematocrit, coronary reserve is compromised significantly, indicating cardiac vulnerability at these levels of anemia, especially if coronary occlusive disease or higher work demands on the heart should coexist.