BACKGROUND AND RATIONALE Patients successfully resuscitated after cardiac arrest experience a "sepsis-like" syndrome characterized by cytokine storm, endotoxemia, coagulopathy, and various degrees of adrenal insufficiency. These pathophysiological mechanisms contribute to the development of circulatory failure, i.e. post-resuscitation shock. Post-resuscitation shock patients resuscitated from vasopressor-requiring cardiac arrest are frequently poorly responsive to high-rate vasopressor infusions (e.g. norepinephrine ≥0.5 μg/kg/min) and intravenous fluids.