Abstract: Subarachnoid hemorrhage is a common disease in neurosurgery with a high mortality. Researches on delayed cerebral vasospasm(CVS) after subarachnoid hemorrhage are explored in China at home and abroad. However, clinical work finds patients with early death after SAH. There is a widespread ischemic injury in the brain that involves the pathophysiological events that occur in the brain tissue prior to late onset of cerebral vasospasm (3 days to 2 weeks).It includs changes in cerebral perfusion, microcirculation, matrix metalloproteinases, digestion of plasminogen activator and other enzymes lead to the loss of type IV collagen in the basilar membrane, distribution in the subarachnoid serum, platelet rich plasma to promote acute vasoconstriction after SAH, platelet activation and aggregation in the microvascular break Cerebral circulation lead to insufficient cerebral perfusion, ischemia and a series of pathophysiological changes. This article reviews the mechanism and progress of EBI after SAH, in order to provide a preliminary theoretical basis for better control of these secondary events and effective treatment of acute SAH in future.