Cerebral precapillary arterioles, under normal circumstances, accommodate to changes in BP (in the range of mean arterial pressures between 60 and 150 mm Hg) by changing arteriolar diameter, which maintains constant cerebral perfusion in the capillary bed.18 Such response to pressure pulsations is usually initiated by a fast dynamic response, followed by a slow static response that restores cerebral perfusion.19 The mechanism underlying this response is myogenic and metabolic.19 Arterioles respond to a decrease in BP by vasodilation to restore blood flow, but when vasodilation reaches a maximal limit blood flow decreases (perfusion pressure ≤ 60 mm Hg). If perfusion pressure continues to fall, an increase in the oxygen extraction fraction maintains cerebral oxygen metabolism.20 Once this mechanism becomes maximal, usually at perfusion pressures ≤ 30 mm Hg, further decline in blood flow leads to substrate depletion, energy failure, disruption of cellular homeostasis, and ultimately, ischemic necrosis.20