Objectives: Clonidine is an antihypertensive drug used for analgosedation in the PICU. Lack of reliable data on its hemodynamic tolerance limits its use. This study explores the hemodynamic tolerance of IV clonidine infusion in a broad population of children with high severity of disease.
Design: Retrospective analysis of prospectively collected data.
Setting: A tertiary and quaternary referral PICU.
Patients: Critically ill children age 0-18 years old who received an IV clonidine infusion for analgosedation of at least 1 hour.
Interventions: None.
Measurements And Main Results: The primary endpoints were the prevalences of bradycardia and hypotension. Secondary endpoints were changes in heart rate, blood pressure, Vasoactive-Inotropic Score, COMFORT Behavior score (a sedation scoring scale), and body temperature during the infusion. The association of bradycardia with other hemodynamic variables was explored, as well as potential risk factors for severe bradycardia. One-hundred eighty-six children (median age, 12.9 mo [interquartile range, 3.5-60.6 mo]) receiving a maximum median clonidine infusion of 0.7 µg/kg/hr (interquartile range, 0.3-1.5) were included. Severe bradycardia and systolic hypotension occurred in 72 patients (40.2%) and 105 patients (58%), respectively. Clonidine-associated bradycardia was hemodynamically well tolerated, as it was not related with hypotension and the need for vasoactive drugs decreased in parallel with a sedation score guided clonidine infusion rate increase. Younger age was the only identified risk factor for clonidine-associated bradycardia.
Conclusions: Although administration of clonidine is often associated with bradycardia and hypotension, these complications do not seem clinically significant in a mixed PICU population with a high degree of disease severity. Clonidine may have a vasoactive-inotropic sparing effect.
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http://dx.doi.org/10.1097/PCC.0000000000001602 | DOI Listing |
Brain Res
January 2025
Cognitive and Neuroscience Research Center (CNRC), Tehran Medical Sciences, Islamic Azad University, Tehran, Iran; Department of Physiology, Faculty of Medicine, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran. Electronic address:
The present research examined the possible role of α-2 adrenergic receptor drugs (clonidine, selective α-2 adrenergic receptor agonist, and yohimbine, competitive α-2 adrenoreceptor antagonist,) on the effect of arachidonylcyclopropylamide (ACPA), a cannabinoid CB1 receptor agonist, in non-acute restraint stress (NARS) and acute restraint stress (ARS) mice. The animals were unilaterally implanted with a cannula in the left lateral ventricle. ARS was carried out by movement restraint at a period of 4 h.
View Article and Find Full Text PDFClin Ther
December 2024
Department of Pharmacy, Brigham and Women's Hospital, Boston, Massachusetts.
Intensive Care Med
November 2024
Level 9, Medical School, University of Queensland Health Sciences Building, Brisbane, QLD, Australia.
Purpose: Dexmedetomidine increases sleep and reduces delirium in postoperative patients, but it is expensive and requires a monitored environment. Clonidine, another 2-agonist, is cheaper and is used safely for other purposes in wards. We assessed whether clonidine would improve sleep in postoperative high-dependency unit (HDU) patients.
View Article and Find Full Text PDFJ Pediatr Pharmacol Ther
August 2024
Pharmacy Services, Alberta Health Services, Calgary, Alberta, Canada.
Objective: To determine a conversion factor for use when switching from dexmedetomidine infusion to enteral clonidine in critically ill neonates.
Methods: This was an observational, retrospective review of conversions from dexmedetomidine to -clonidine, performed in a neonatal intensive care unit (NICU) between January 2020 and December 2021. Both initial conversion factors and those resulting after a 48-hour titration period were examined.
INNOSC Theranostics Pharmacol Sci
July 2024
Department of Psychiatry, Mt. Sinai School of Medicine, New York City, New York, United States of America.
Clonidine operates through agonism at the alpha-2A receptor, a specific subtype of the alpha-2-adrenergic receptor located predominantly in the prefrontal cortex. By inhibiting the release of norepinephrine, which is responsible for withdrawal symptoms, clonidine effectively addresses withdrawal-related conditions such as anxiety, hypertension, and tachycardia. The groundbreaking work by Gold .
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