Background: Maintaining an adequate mean arterial pressure (MAP) and cerebral perfusion pressure to ensure proper perfusion and oxygen delivery to all major organs is crucial—especially for neurosurgical patients after subarachnoid hemorrhage or traumatic brain injury—for preventing secondary brain damage or delayed cerebral ischemia. Currently, most neurosurgical intensive care units rely on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) values to guide therapy. Fluid resuscitation and norepinephrine are standard treatments for achieving a CPP between 60 and 70 mmHg; however, patients sometimes experience norepinephrine-refractory hypotension. In such cases, vasopressin is often the preferred medication; it is widely utilized and has gained interest in treating septic shock or refractory hypotension following cardiac surgery or hypovolemic shock. Recent studies have also shown the significant impact of vasopressin on resuscitation after traumatic brain injury (TBI) and its effect on CPP during ICU care. Nevertheless, little is known about how vasopressin affects cerebral perfusion and oxygenation, especially in patients with subarachnoid hemorrhage. Methods: This preliminary retrospective single-arm study examined how vasopressin affects PbtO2 and cerebral blood flow using the non-invasive QuantixND® device. After administering vasopressin for treating catecholamine-refractory hypotension, MAP, CPP, ICP, PbtO2, and cerebral blood flow were measured over a 20-min period. Results: In this small cohort, vasopressin sufficiently improved MAP and CPP over a 20 min period following AVP bolus administration with a slight decline at later time points. The ICP decreased throughout this period, indicating some level of autoregulation. In contrast, cerebral blood flow did not improve despite the rise in CPP, and PbtO2 levels remained below 20 mmHg. Conclusions: We conclude that vasopressin could be a viable option for maintaining MAP and CPP, but caution should be exercised in patients with already impaired cerebral perfusion. Furthermore, relying solely on CPP as the therapeutic guide in subarachnoid hemorrhage patients appears to be at least questionable.