Delayed vasospasm and secondary injury due to ischemia occur frequently in the setting of subarachnoid hemorrhage (SAH), and these changes have been well characterized within the last decades. Considerable effort has also been put into the development of therapeutic strategies and appropriate monitoring modalities. However, although in particular acute injury is known to contribute significantly to overall outcome in SAH, these immediate alterations still remain largely neglected in current research. Few studies exist to date which mainly describe rapid alterations in perfusion and metabolism. As the main characteristic of the very first minutes and hours after SAH, an immediate phase of CPP-independent hypoperfusion has been observed repeatedly both experimentally and clinically, and it has mostly been attributed to the development of acute vasospasm. Endothelin and nitric oxide, prime suspect in the pathogenesis of chronic vasospasm, may play a pivotal role in this early scenario, possibly being promoted by the drastic ICP increase and extravasation of blood compounds. The much disputed concept of inflammation in chronic vasospasm may not be applicable this early after the ictus, but mechanisms of cellular and structural changes causing microvascular platelet aggregation and immediate disruption of the basal lamina, however, are thought to contribute significantly to the imminent cascade of disturbances in perfusion and metabolism. This review is intended to summarize current insights and illustrate recent efforts to better understand alterations in cerebral perfusion in these very first minutes and hours after SAH which – at some point – may also be amenable to early therapeutic intervention.