Anemia will lead to a decreased capacity of oxygen transport, eventually resulting in tissue hypoxia and even necrosis when compensatory mechanisms are insufficient. In response to tissue hypoxia, 2,3-diphosphoglycerate in the red cells will increase, leading to increased oxygen dissociation at any given PO2. Cardiac compensatory mechanisms, particularly an increase in heart rate, result in an increase in cardiac output. Blood loss followed by compensatory fluid replacement reduces blood viscosity, resulting in an increased tissue perfusion and a decreased cardiac workload.
In the patient with cardiopulmonary compromise, these compensatory mechanisms may not be sufficient and cardiac decompensation, angina pectoris, and even myocardial infarction may result.
There are no accurate means of predicting failure of the compensatory mechanisms to anemia. Thus it is essential to obtain information regarding the patient's medical history. In particular, any history of heart and/or vascular disease should influence the decision as to whether or not the anemia should be corrected. However, criteria for transfusion are arbitrary and vary considerably.
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