In their counterpoint, Dr Rivers and colleagues1 present the theoretical view that patients with septic shock present in very distinct “hemodynamic phases” and that Jones et al2 enrolled patients in a different phase of septic shock than did Rivers et al.3 According to their theory, decreased central venous oxygen saturation (Scvo2) always precedes the appearance of lactate—a concept not observed in my clinical practice. Clinicians who routinely care for the critically ill encounter patients with elevated lactate and normal Scvo2. Furthermore, as shown in Table 1,2-10 the hemodynamic patterns of the subjects enrolled by Rivers et al3 are markedly different from any other reported populations of patients with septic shock treated with quantitative resuscitation. The study by Rivers et al3 patients had much higher lactate, much lower Scvo2, and much higher mortality than described elsewhere. Possible explanations for this discrepancy may include that patients with septic shock in Detroit between 1997 and 2000 were markedly different than any other septic shock population reported in the world’s literature and/or that systematic selection bias was a significant problem in the their study. In such a scenario, their results have questionable external validity. Supporting either of these assertions is the fact that mortality in the control group of the Rivers et al3 study was 20% higher than any septic shock mortality reported in the recent literature, leaving one to question exactly what care they received.3 Little evidence supports the contention that Jones et al2 enrolled patients in a different phase of septic shock than did Rivers et al,3 because the population enrolled by Jones et al2 used inclusion criteria identical to the Rivers et al3 study. Furthermore, the population in the Jones et al3 study appears to be an accurate contemporaneous population from three US EDs; it has characteristics, including mortality rates, nearly identical to those described from other studies (Table 1).