Abstract
Summary
Numerous recent studies have emphasized the potential adverse effects of increased oxyhemoglobin affinity on oxygen delivery. Respiratory alkalosis increases the affinity of hemoglobin for oxygen, and is also associated with increased oxygen consumption. This study was designed to evaluate the effect of increased hemoglobin affinity for oxygen on oxygen transport and consumption during a period of respiratory alkalosis in a group of animals whose oxygen delivery system was already stressed by a decrease in red cell mass. Nine rhesus monkeys were anesthetized and studied before, during and 40 min after being hyperventilated. With hyperventilation, the arterial pH increased to 7.56 while base excess decreased from 3.5 to 1.3 mequiv/liter. Oxygen consumption increased from 5.5 to 11.4 cm3/min/kg and the in vivo P 50 (the PO 2 at which hemoglobin is 50% saturated) fell from 34.8 to 27.8 mm Hg as the oxyhemoglobin dissociation curve shifted to the left. No change was observed in 2, 3-diphosphoglycerate or in P 50 when corrected to pH 7.40. The increased oxygen consumption was maintained by an increase in the arterial-venous oxygen difference; cardiac output did not change with hyperventilation. The mixed venous PO 2 fell from 44 to 29 mm Hg: approximately half of the 15 mm Hg fall was due to the increased oxyhemoglobin affinity and half to the increased oxygen consumption.
Thus, in this experimental model, oxygen consumption significantly increased during hyperventilation without changes in the cardiac output or evidence of anaerobic metabolism, even though hemoglobin's affinity for oxygen had also increased. This resulted in a marked fall in the mixed venous PO 2.
We express appreciation to Mr. Larry Tague, Mrs. Geraldine Imundo, Mr. Earle Berrell, and Miss Jane Harris for valuable technical assistance.
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