[Theoretical limits of "permissive anemia"]

The limiting factor for acute anemia is myocardial oxygen supply, since arterial oxygen content is decreased by isovolemic hemodilution while myocardial oxygen demand is increased as a result of a compensatory increase of cardiac output. A theoretical model was developed which describes the relation between hematocrit, myocardial oxygen demand and the required coronary blood flow during progressive hemodilution. Using this model, the determinants of critical hematocrit and the limits of intentional acute anemia (= "permissive anemia") can be calculated based on the limits of coronary vasodilator reserve. For a normal systemic oxygen consumption of 120 ml min-1 m-2 a critical degree of hemodilution is achieved at an hematocrit of 14% and an hemoglobin content of 4.7 g dl-1, respectively. Hyperoxia with an arterial pO2 of 400 mmHg will shift the critical hematocrit to 12%. An increase of systemic oxygen consumption by a factor of three (460 ml min-1 m-2), which might be typical for a patient during the postoperative recovery phase, increases the critical hematocrit to 21%. In patients with coronary artery disease critical hematocrit levels might be much higher. We conclude that a fixed critical hematocrit as a transfusion trigger is not appropriate in most patients. Rather the indication for blood transfusions must individually appreciate the specific circumstances of the patient, such as expected blood loss and required oxygen transport capacity reserves, hemodynamic stability, coronary artery disease and systemic oxygen consumption. It is suggested that the model presented herein might be valuable for estimation of the individual critical hematocrit in a particular patient.