The clinical syndrome of gastrointestinal hemorrhagic necrosis is relatively frequent. The appearance of abdominal pain and distention, and adynamic ileus with or without evidence of overt hemorrhagic tendency in a patient with chronic congestive heart failure should arouse the suspicion of this disorder especially when accompanied by hypotension or arrhythmias and when there is a history of antecedent treatment with large doses of digitalis or norepinephrine. The importance of clinical recognition of this syndrome, to avoid unnecessary surgery, is stressed. The pathologic findings in these cases include absence of demonstrable mesenteric obstruction (intrinsic or extrinsic); the presence of diffuse or patchy hemorrhagic lesions in the gastrointestinal tract distributed throughout the stomach, small and large bowel, localized in most cases to the mucosa and submucosa but potentially involving all layers, causing perforation; and marked vasodilation of the arterioles, venules and capillaries around the affected areas. Although the pathogenesis of gastrointestinal hemorrhagic necrosis is not known, there is enough information to show that the following factors could be among the more important ones: diminished cardiac output and mesenteric capillary vasoconstriction, with blood slowing and sludging. The presence of microscopic vascular dilatation and hemorrhagic necrosis points to the possibility that liberation of vasoactive amines could be one of the mechanisms producing vasodilatation and hemorrhagic necrosis of the gastrointestinal tract. © 1969.