Correspondence  |   April 2004
Hemodynamic Compensation during Acute Normovolemic Hemodilution: In Reply
Author Affiliations & Notes
  • Philippe Van der Linden, M.D., Ph.D.
  • * CHU Brugmann-HUDERF, Brussels, Belgium.
Article Information
Correspondence   |   April 2004
Hemodynamic Compensation during Acute Normovolemic Hemodilution: In Reply
Anesthesiology 4 2004, Vol.100, 1034-1035. doi:
Anesthesiology 4 2004, Vol.100, 1034-1035. doi:
We thank Drs. Crystal and Ramez Salem for their interesting comments regarding our article. 1 This experimental study tested the hypothesis that the cardiodepressive effects of some anesthetic agents may exceed their effects on tissue oxygen demand, so that deepening the level of anesthesia may actually reduce tolerance to acute isovolemic anemia, as reflected by an increase in the critical hemoglobin concentration (i.e.  , the value of hemoglobin below which oxygen consumption becomes supply dependent).
We agree with Drs. Crystal and Ramez Salem that the impaired cardiac output response observed during isovolemic hemodilution in our experiments was not exclusively related to the more pronounced negative inotropic effect of the higher anesthetic dose. In the halothane study, we discussed the possible contribution of the depressant effect of halothane on the sympathetic system. Several authors emphasized the role the sympathetic system in the physiologic response to acute isovolemic anemia. 2,3 The impact of reduced arterial blood pressure must also be considered. However, we think that the lower mean arterial pressure in the higher-dose halothane group was essentially related to the lower cardiac output because systemic vascular resistances were similar in the two halothane groups. Halothane is known to have only minimal effects on vascular tone and, in particular, on coronary vascular tone. 4 In addition, systemic vascular resistance decreased during acute isovolemic hemodilution, and the maintenance of arterial pressure in these conditions depends mainly on the increase in cardiac output. 5,6 
In both the halothane and the ketamine studies, heart rate at critical point was lower in the higher-dose anesthetic group. Although these results might have been expected with halothane, they are more astonishing with ketamine. Other authors 7 have observed a surprisingly low heart rate response in a dog model of hemorrhage. The mechanisms responsible for the effects of ketamine on the circulatory system are not completely understood because of its complexity and the lack of systematic investigation in this area. A better understanding of the effects of ketamine on the physiologic response to isovolemic hemodilution requires further investigation.
In contrast to Dr. Crystal and Ramez Salem, we think the maintenance of tissue oxygenation during acute isovolemic anemia depends on both an increase in cardiac output and an increase in tissue oxygen extraction. Several studies have shown that both mechanisms are already involved in the early stages of normovolemic hemodilution. 8 Similar observations have been reported in a recent article evaluating the effects of β-adrenergic stimulation in fentanyl-isoflurane–anesthetized dogs undergoing severe normovolemic hemodilution. 9 This interesting article showed that isoproterenol significantly increases the cardiac output response to hemodilution in the anesthetized animals. These observations may indicate that, during anesthesia, sympathetic stimulation may improve the tolerance of individuals to acute isovolemic anemia.
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Crystal GJ, Ramez Salem M:β-Adrenergic stimulation restores oxygen extraction reserve during acute normovolemic hemodilution. Anesth Analg 2002; 95: 851–7Crystal, GJ Ramez Salem, M