Circulatory shock is a common condition leading to ICU admission which occurs when there is a mismatch between oxygen supply and demand resulting in altered tissue perfusion, deficient oxygen, and nutrient delivery to tissues and ultimately to cellular and organ dysfunction (1). In addition to treating the underlying cause of the shock state (e.g., infection in septic shock), the initial hemodynamic goal of therapy is to provide adequate perfusion to the tissues and organs and normalize cellular metabolism (2).In patients with shock requiring vasopressor therapy, the mean arterial pressure (MAP) has been a long-standing hemodynamic variable targeted as a surrogate measure of tissue perfusion. A MAP goal is typically included in most clinical vasopressor order sets. Physiologic studies suggest that vascular bed autoregulation is compromised below a MAP of 60 mm Hg leading to a linear dependence of regional blood flow on MAP (2). These critical autoregulation MAP set points may vary by organ and depend on patient factors such as age and comorbidity (2). The most recent Surviving Sepsis Campaign (SSC) treatment guidelines recommend targeting an initial MAP of 65 mm Hg versus higher MAP targets in patients with septic shock requiring vasopressor support (3). These recommendations are based upon three recent multicenter prospective clinical trials in distributive shock looking at associations between MAP target goals and outcomes (4-6). The Sepsis and Mean Arterial Pressure (SEPSISPAM) (4) and Optimal Vasopressor Titration (OVATION) (5) studies randomized patients to target MAP goals of 65-70 mm Hg versus 80-85 mm Hg and 60-65 mm Hg versus 75-80 mm Hg, respectively, and found no significant difference in mortality between groups. Even though the SEPISPAM study found that targeting a higher MAP was associated with a higher occurrence rate of arrhythmia and more vasopressor exposure, it also reported that targeting a higher MAP was associated with a lower occurrence rate of renal impairment in the subgroup of patients with chronic hypertension. More recently, the 65 Trial (6) did not show a difference in mortality when comparing treatment aiming for a specified MAP target of 60-65 mm Hg versus "usual care" that was based on the SSC treatment guidelines. Similar to the SEPSISPAM study, the 65 Trial found that targeting a higher MAP was associated with more vasopressor exposure.A number of unanswered questions remain regarding the optimal MAP target and the balance between maintaining tissue perfusion and avoiding vasopressor-induced adverse effects. To that end, two independent systematic reviews and meta-analyses (SRMAs) in this issue of Critical Care Medicine provide further insight regarding optimal MAP targets for the treatment of shock *See also p. 241 and 254.