The question of whether the Scvo2 is a numeric equivalent to Sv̄o2 has been examined in a number of studies,9–12 which continues to fuel this debate. These studies, including the trial by Chawla et al,11 have consistently shown that Scvo2 values are (on average) approximately 5% higher than Sv̄o2 values, which is likely secondary to the contributions of deoxygenated blood from the coronary sinus. Recognizing this minor, yet consistent, difference allows the clinician to make an accurate assessment of global tissue hypoxia. Furthermore, the clinical utility of an end point of resuscitation is determined by whether it changes clinical practice, morbidity, and mortality in a cohort of patients under the rigors of an appropriately designed clinical trial. In other words, has this end point been calibrated to have clinical utility in the setting in which it is to be used? This was done with Scvo2 in the EGDT study,,4 in which the range of Scvo2 values was 48.6 to 49.2%, with lactate levels of 6.9 to 7.7 mmol/L indicating significant supply dependency. Using the finding from Chawla et al,,11 the Sv̄o2 values would be extrapolated to 43 to 45%. Thus, irrespective of whether the Scvo2 value equals the Sv̄o2 value, the presence of a low Scvo2 level in patients with early sepsis portends increased morbidity and mortality, and correcting this value according to a consensus-derived algorithm,13 improves morbidity and mortality. It should be further noted that, in this well-designed study by Chawla et al,11 the majority of the 51 patients were not supply-dependent as the mean Sv̄o2 values ranged from 67.6 to 70.5, and the corresponding Scvo2 values ranged from 71.9 to 77.0 with no mention of lactate levels.