The authors' objectives were as follows: 1) to characterize for the first time the relationship between whole body O2delivery (Do2) and O2consumption (Vo2in adult conscious dogs; and 2) to assess the effects of the inhalational anesthetic, halothane, on that relationship. Do2was varied over a wide range in chronically instrumented dogs by gradual inflation and deflation of a hydraulic occluder implanted around the thoracic inferior vena cava to alter venous return and cardiac output. Vo2was measured at different values of Do2in dogs in the folly conscious state and again during halothane anesthesia. A “binning‘’ technique indicated that halothane decreased Vo2(P< 0.01) at any given value of Do2over a broad range of Vo2. A twoline piecewise linear regression analysis technique indicated that halothane decreased (P< 0.01) the critical O2delivery (GOD) from 20 ± 3 to 10 ± 1 ml.kg−1.min−1and increased (P< 0.01) O2extraction at COD from 31 ± 3 to 40 ± 2% However, the Do2-Vo2plots measured in both conscious and halothane-anesthetized dogs did not exhibit a discrete discontinuity but rather were closely fit (correlation coefficient = 0.98) by an exponential equation of the following form:O2extraction = B1.(1 - exp (-Do2/B2))/Do2where B1 if the delivery-Independent estimate of Vo2and B2 is the “delivery constant,‘’i.e., the Do2associated with a Vo2equal to 63% of B1. Halothane decreased B1 (P< 0.01) from 5.3 ± 0.1 to 3.9 ± 0.1 ml. kg−1. min−1and decreased B2 (P< 0.01) from 5.6 ± 0.3 to 3.6 ± 0.3 ml.kg−1.min−1compared with that measured in conscious dogs. Thus, compared with the conscious state, halothane anesthesia alters the fundamental relationship between Do2and Vo2and may have a beneficial effect on tissue oxygenation at low values of Do2.