
Changes in Cerebral Hemodynamics After a Single Dose of Clonidine in Severely Head-Injured Patients
Author(s) -
Aram Ter Minassian,
L. Beydon,
Philippe Decq,
Francis Bonnet
Publication year - 1997
Publication title -
anesthesia and analgesia/anesthesia and analgesia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.404
H-Index - 201
eISSN - 1526-7598
pISSN - 0003-2999
DOI - 10.1097/00000539-199701000-00024
Subject(s) - medicine , clonidine , anesthesia , cerebral perfusion pressure , hemodynamics , cerebral blood flow , mean arterial pressure , cerebral circulation , intracranial pressure , vasoconstriction , glasgow coma scale , blood pressure , middle cerebral artery , vasodilation , heart rate , ischemia , cardiology
alpha 2-Adrenergic agonists induce cerebral vasoconstriction, reduce intracranial pressure (ICP) in experimental animals and may be useful in the hemodynamic management of head-injured patients. We studied the effects of the alpha 2 agonist clonidine on the cerebral circulation in 12 head-injured patients (Glasgow Coma Scale score < 8). Middle cerebral artery flow velocity (MCAV), ICP, mean arterial pressure (MAP), and cerebral perfusion pressure (CPP), were continuously recorded before (T0), at the end (T1), and 30 min after (T2) a 10-min intravenous (i.v.) infusion of 2.5 micrograms/kg clonidine. The cerebral arteriovenous oxygen content difference (AVDO2) and Paco2 were sequentially obtained. ICP, Paco2, AVDO2, and MCAV did not change after clonidine administration. In contrast, MAP and CPP decreased (P < 0.05 and P < 0.05, respectively, at T1 and T2). Three subjects displayed a transient increase in ICP (> 10 mm Hg) at T1; this increase was concomitant with the decrease in MAP. Clonidine administered as an i.v. infusion may induce a critical but transient increase in ICP in some severely head-injured patients. This effect may result from cerebral autoregulatory vasodilation and increased cerebral blood volume as a response to the hypotensive effects of clonidine.