Anemia induces significant compensatory circulatory changes, primarily an increase in cardiac output driven by increased systolic output and moderate cardiac acceleration.
Marked cardiac output rises in anemia warrant monitoring for strain; leaves open relevance to modern transfusion thresholds.
Profound circulatory changes occur in both primary and secondary anemia. With a decrease in the hemoglobin content of the blood the output of the heart is increased.¹This is the outstanding compensatory mechanism for the loss of oxygen-carrying power of the blood. The cardiac rate is also increased in anemia.²Although the cardiac acceleration is moderate, rarely more than 120 per minute, it results in a certain increase in cardiac output. This increase in minute volume output is due, likewise, in part, to lowering of the viscosity of the blood.1c Nevertheless, the increased cardiac output observed in anemia is due mainly to the increased systolic output of the heart. This increase in cardiac output is directly proportional to the decrease in hemoglobin content of the blood. A 200 per cent and a 300 per cent increase are reported to occur with hemoglobin levels of 30 per cent and
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J. BAILEY CARTER (1943) studied this question.
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