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Elevated cardiac output in anemia occurs independently of right atrial pressure or tissue oxygen tension; leaves open mechanisms for clinical translation.
Several measures of cardiovascular function were made in nine dogs before, during, and after the production of anemia by daily venesections. Stress is laid on the time sequence of the various changes in the circulation and their relation to each other. From the results obtained it was concluded that the elevated cardiac output observed in anemia was not the result of an increase in right atrial pressure or a decrease in tissue oxygen tension, per se. It is suggested that the increased cardiac output may be due to a slowly elaborated or slow-acting humoral agent produced as a result of tissue anoxia.
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Hatcher et al. (1954) studied this question.
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