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CARDIOVASCULAR ANESTHESIA

ß-Adrenergic Stimulation Restores Oxygen Extraction Reserve During Acute Normovolemic Hemodilution

George J. Crystal, PhD^*, and M. Ramez Salem, MD^*

*Department of Anesthesiology, Advocate Illinois Masonic Medical Center, Chicago, Illinois; and Departments of Anesthesiology and Physiology and Biophysics, University of Illinois College of Medicine, Chicago, Illinois

Address correspondence and reprint requests to George J. Crystal, PhD, Department of Anesthesiology, Advocate Illinois Masonic Medical Center, 836 W. Wellington Ave., Chicago, IL 60657-5193. Address e-mail to gcrystal{at}uic.edu

Compensatory increases in oxygen extraction (EO₂) during acute normovolemic hemodilution (ANH) have the effect of decreasing tissue oxygen tension values, thus increasing the threat of tissue hypoxia. We hypothesized that if the ß-adrenergic agonist isoproterenol (ISOP) could augment cardiac output (CO) during ANH, it could reverse the increases in EO₂ and restore the margin of safety for tissue oxygenation. Studies were performed in seven anesthetized (isoflurane) dogs. CO was measured by using thermodilution, and regional blood flow (RBF) was measured by using radioactive microspheres. Systemic oxygen delivery (DO₂), oxygen consumption (O₂), and EO₂, as well as regional DO₂, were calculated. Measurements were obtained under the following conditions in each dog: 1) baseline-1, 2) ISOP (0.1 µg · kg^-1 · min^-1 IV), 3) baseline-2, 4) ANH, and 5) ISOP during ANH. Hematocrit was 45% ± 3% under baseline conditions and 18% ± 3% during ANH. Before ANH, ISOP caused parallel increases in CO and systemic DO₂, which, in the presence of an unchanged O₂, reduced EO₂. RBF increased in myocardium and spleen, decreased in pancreas, and did not change in brain, spinal cord, or other tissues. ANH caused increases in CO, which were insufficient to offset the decrease in arterial oxygen content, and thus systemic DO₂ declined; systemic O₂ was maintained by an increase in EO₂. ANH-related increases in RBF maintained DO₂ in myocardium, brain, duodenum, and pancreas, whereas DO₂ declined in kidney and spleen. ISOP during ANH increased CO and systemic DO₂, which returned systemic EO₂ to baseline, and it increased RBF in myocardium, kidney, duodenum, and spleen. We conclude that 1) ß-adrenergic stimulation with ISOP restored the systemic EO₂ reserve during ANH, without apparent adverse effects in the individual body tissues, and that 2) the use of inotropic drugs, such as ISOP, may extend the limit to which hematocrit can be reduced safely during ANH.

IMPLICATIONS: By restoring the oxygen extraction reserve, isoproterenol and other inotropic drugs can enhance the margin of safety and extend the limit to which hematocrit can be reduced safely during acute normovolemic hemodilution. The use of this approach will depend on the degree of hemodilution, the extent of mixed venous oxygen desaturation, and whether increases in cardiac output are possible or desirable.

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