There Is More to Postcraniotomy Emergence Hypertension Than Simply Blood Pressure Control—Why Nicardipine May Not Be the Drug of Choice

To the Editor We read with great interest the article by Bebawy et al.1 concluding that nicardipine is superior to esmolol for the prevention of emergence hypertension. Although superior blood pressure control may be evident for nicardipine, blood pressure is perhaps not the most appropriate hemodynamic variable to predict the potential for postcraniotomy bleeding. Nicardipine may be inferior to esmolol for reducing bleeding and other adverse events. The study was underpowered to evaluate these endpoints. Esmolol is a β1-selective antagonist that decreases chronotropy and inotropy. Esmolol’s mechanism leads to decreases in left ventricular work and ejection velocity throughout systole. Nicardipine, a peripherally acting calcium channel blocker, decreases blood pressure by vasodilation. These hemodynamic principles are well recognized in the literature regarding the acute care of patients with aortic aneurysms.2,3 The initial treatment goal in the context of aneurysm pathology is to decrease the pulsatile load or the aortic wall stress (a function of change in pressure with time [dP/dT]) with β-blockade. In the acute setting, only after effective control of dP/dT should one initiate vasodilator therapy. The sole use of a vasodilator may decrease blood pressure, but without β-blockade, the pulsatile load will actually increase, potentially leading to adverse events including bleeding. The morbidity from emergence hypertension is primarily caused by bleeding. The likely mechanism is clot dislodgement after ineffective control of dP/dT. Hence, attenuating dP/dT should be the primary perioperative hemodynamic objective. Perhaps a more useful variable to measure would be cerebral blood flow. Cerebral blood flow will increase at emergence with the sympathetic surge and the release of endogenous catecholamines and is a good surrogate for dP/dT. Two studies have addressed this in the setting of emergence from anesthesia. Nicardipine decreased blood pressure but increased cerebral blood flow, likely secondary to cerebral vasodilation.4 Esmolol decreased heart rate, cardiac output, and, most importantly, cerebral blood flow.5 We all agree that blood pressure must be aggressively controlled to mitigate the untoward effects of emergency hypertension. However, in our view, it should begin with β-blockade. Michael Christopher Carey, MD Neal Stuart Gerstein, MD, FASE Department of Anesthesiology and Critical Care Medicine University of New Mexico Albuquerque, New Mexico [email protected] Amber D.