Cardiac electrophysiological and hemodynamic effects of β-adrenoceptor blockade and thoracic epidural analgesia in the dog

• Published in: Anesthesia and analgesia Vol. 63; no. 9; pp. 817 - 824
• Main Authors: HOTVEDT, R, REFSUM, H, PLATOU, E. S
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott 01-09-1984
• Subjects: Anesthesia; Anesthesia, Epidural; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Animals; Atenolol - pharmacology; Biological and medical sciences; Bupivacaine - blood; Bupivacaine - pharmacology; Cardiac Catheterization; Dogs; Electrophysiology; Female; Heart Conduction System - drug effects; Hemodynamics - drug effects; Injections, Intravenous; Local anesthesia. Pain (treatment); Male; Medical sciences; Fissipedia; Carnivora; Vertebrata; Mammalia; Regional anesthesia; Extradural administration; Hemodynamics; Experimental study; Dog; Sympathic nervous system
• ISSN: 0003-2999; 1526-7598

To investigate whether thoracic epidural analgesia (TEA) has additional cardiac electrophysiological and hemodynamic effects when induced after beta-adrenergic blockade, bupivacaine (0.7-1.2 mg/kg) was injected into the epidural space at T2-3 after intravenous injection of atenolol (1.0 mg/kg) in anesthetized dogs. Cardiac electrophysiology was studied by His bundle electrography, programmed electrical stimulation, and monophasic action potential recordings. Atenolol reduced heart rate, prolonged atrio-ventricular (AV) nodal impulse conduction time and refractoriness, prolonged ventricular refractoriness and action potential duration, and decreased left ventricular (LV) dP/dt max. Addition of TEA further reduced heart rate, prolonged AV nodal conduction time and refractoriness, decreased LV dP/dt max and arterial blood pressure, but had no effect on atrial and ventricular electrophysiology. Induction of TEA during beta-blockade may thus have additive depressive effects on sinoatrial and AV nodal functions, as well as on left ventricular inotropy. The study indicates that the cardiac electrophysiological effects induced by TEA are mainly caused by decreased beta-receptor stimulation, but increased vagal activity may also contribute.