Is Dexmedetomidine a Favorable Agent for Cerebral Hemodynamics?

Georgia Tsaousi,Federico Bilotta

doi:10.21767/2471-8505.10007

Abstract

Hemodynamic stability, with special attention to arterial pressure in order to warrant an adequate cerebral perfusion, is a cornerstone of Neurocritical care (NCC) management. An abrupt elevation of arterial blood pressure can aggravate cerebral edema or induce cerebral hematoma, resulting in a prolonged NCC unit stay, on the other hand, hypotension is associated with an increased risk for cerebral ischemia that is more pronounced when auto regulation of cerebral blood flow (CBF) is impaired and there is a compromised cerebral compliance [1, 2]. Moreover, any derangement of cerebrovascular hemodynamics may contribute to intracranial pressure (ICP) elevation with concomitant cerebral perfusion pressure (CPP) deterioration, which can further exacerbate ischemic damage [3].

Highlights

Hemodynamic stability, with special attention to arterial pressure in order to warrant an adequate cerebral perfusion, is a cornerstone of Neurocritical care (NCC) management
The appealing performance of Dex in NCC practice is tempered by the reported unfavorable hemodynamic sequelae, consisting of bradycardia, hypotension, and hypertension
Existing evidence supports a dose-dependent decline in cerebral blood flow (CBF) after Dex administration secondary to cerebrovascular vasoconstriction, being almost 30% at clinically relevant Dex concentrations [4]

Summary

Introduction

Hemodynamic stability, with special attention to arterial pressure in order to warrant an adequate cerebral perfusion, is a cornerstone of Neurocritical care (NCC) management. The ideal sedative agent in NCC setting should have minimal impact on hemodynamics. The appealing performance of Dex in NCC practice is tempered by the reported unfavorable hemodynamic sequelae, consisting of bradycardia, hypotension, and hypertension.

Results

Conclusion