Advertisement

Cardiopulmonary evaluation of the use of medetomidine hydrochloride in cats

Leigh A. LamontDepartment of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, IL 61801.

Search for other papers by Leigh A. Lamont in
Current site
Google Scholar
PubMed
Close
 DVM
,
Barret J. BulmerDepartment of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, IL 61801.

Search for other papers by Barret J. Bulmer in
Current site
Google Scholar
PubMed
Close
 DVM
,
Kurt A. GrimmDepartment of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, IL 61801.

Search for other papers by Kurt A. Grimm in
Current site
Google Scholar
PubMed
Close
 DVM, MS
,
William J. TranquilliDepartment of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, IL 61801.

Search for other papers by William J. Tranquilli in
Current site
Google Scholar
PubMed
Close
 DVM, MS
, and
David D. SissonDepartment of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, IL 61801.

Search for other papers by David D. Sisson in
Current site
Google Scholar
PubMed
Close
 DVM, MS

Abstract

Objective—To evaluate the cardiovascular effects of the α2-adrenergic receptor agonist medetomidine hydrochloride in clinically normal cats.

Animals—7 clinically normal cats.

Procedure—Cats were anesthetized with isoflurane, and thermodilution catheters were placed for measurement of central venous, pulmonary, and pulmonary capillary wedge pressures and for determination of cardiac output. The dorsal pedal artery was catheterized for measurement of arterial blood pressures and blood gas tensions. Baseline variables were recorded, and medetomidine (20 µg/kg of body weight, IM) was administered. Hemodynamic measurements were repeated 15 and 30 minutes after medetomidine administration.

Results—Heart rate, cardiac index, stroke index, ratepressure product, and right and left ventricular stroke work index significantly decreased from baseline after medetomidine administration, whereas systemic vascular resistance and central venous pressure increased. However, systolic, mean, and diastolic arterial pressures as well as arterial pH, and oxygen and carbon dioxide tensions were not significantly different from baseline values.

Conclusions and Clinical Relevance—When administered alone to clinically normal cats, medetomidine (20 µg/kg, IM) induced a significant decrease in cardiac output, stroke volume, and heart rate. Arterial blood pressures did not increase, which may reflect a predominant central α2-adrenergic effect over peripheral vascular effects. (Am J Vet Res 2001;62:1745–1762)

Abstract

Objective—To evaluate the cardiovascular effects of the α2-adrenergic receptor agonist medetomidine hydrochloride in clinically normal cats.

Animals—7 clinically normal cats.

Procedure—Cats were anesthetized with isoflurane, and thermodilution catheters were placed for measurement of central venous, pulmonary, and pulmonary capillary wedge pressures and for determination of cardiac output. The dorsal pedal artery was catheterized for measurement of arterial blood pressures and blood gas tensions. Baseline variables were recorded, and medetomidine (20 µg/kg of body weight, IM) was administered. Hemodynamic measurements were repeated 15 and 30 minutes after medetomidine administration.

Results—Heart rate, cardiac index, stroke index, ratepressure product, and right and left ventricular stroke work index significantly decreased from baseline after medetomidine administration, whereas systemic vascular resistance and central venous pressure increased. However, systolic, mean, and diastolic arterial pressures as well as arterial pH, and oxygen and carbon dioxide tensions were not significantly different from baseline values.

Conclusions and Clinical Relevance—When administered alone to clinically normal cats, medetomidine (20 µg/kg, IM) induced a significant decrease in cardiac output, stroke volume, and heart rate. Arterial blood pressures did not increase, which may reflect a predominant central α2-adrenergic effect over peripheral vascular effects. (Am J Vet Res 2001;62:1745–1762)