2001
DOI: 10.1097/00000542-200107000-00023
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Effects of Thoracic Epidural Anesthesia with and without Autonomic Nervous System Blockade on Cardiac Monophasic Action Potentials and Effective Refractoriness in Awake Dogs

Abstract: This model helps to study the role of TEA on ventricular repolarization and arrhythmogenicity. Because lengthening of repolarization and prolongation of refractoriness may, in some circumstances, be antiarrhythmic, TEA may be protective against generation of ventricular arrhythmias mediated, e.g., by increased sympathetic tone. The results also imply that the beneficial role of TEA might be stronger at the ventricular site as compared with the atrium. At atrial sites there was only a trend toward prolongation … Show more

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Cited by 48 publications
(32 citation statements)
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“…There are several potential reasons for failure of TEA and LCSD in arrhythmia control: (i) a sympathetic trigger may not be responsible for initiation or perpetuation of the arrhythmia and therefore its elimination may not impact on arrhythmia burden, (ii) sympathetic blockade secondary to TEA may be incomplete, the addition of autonomic nervous system blockade by simultaneous administration of propranolol, atropine and hexamethonium during TEA has been shown to augment the effects of TEA on repolarization and effective refractory period (ERP) in an animal model6 (iii) denervation secondary to LCSD may also be incomplete, resection of the lower half of the left stellate ganglion to T4 has been suggested7 -this level of denervation was not carried out in five of the patients in our cohort, (iv) the nerve of Kuntz (an inconstant intra-thoracic nerve which connects the first and second thoracic nerves, bypassing the sympathetic chain between the T2 ganglion and stellate ganglion)27 should be sought out and divided if sympathectomy is to be complete (v) remaining sympathetic innervation via the right stellate ganglion (which contributes to varying degrees) may also contribute to the failure of LCSD in controlling arrhythmias in some patients. These limitations of LCSD have also been reported in the LQTS population, LCSD was shown to reduce but not abolish sudden cardiac death in two large studies7,9 and in a small series 28 LCSD proved inadequate for control of symptoms despite addition of beta blockade.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…There are several potential reasons for failure of TEA and LCSD in arrhythmia control: (i) a sympathetic trigger may not be responsible for initiation or perpetuation of the arrhythmia and therefore its elimination may not impact on arrhythmia burden, (ii) sympathetic blockade secondary to TEA may be incomplete, the addition of autonomic nervous system blockade by simultaneous administration of propranolol, atropine and hexamethonium during TEA has been shown to augment the effects of TEA on repolarization and effective refractory period (ERP) in an animal model6 (iii) denervation secondary to LCSD may also be incomplete, resection of the lower half of the left stellate ganglion to T4 has been suggested7 -this level of denervation was not carried out in five of the patients in our cohort, (iv) the nerve of Kuntz (an inconstant intra-thoracic nerve which connects the first and second thoracic nerves, bypassing the sympathetic chain between the T2 ganglion and stellate ganglion)27 should be sought out and divided if sympathectomy is to be complete (v) remaining sympathetic innervation via the right stellate ganglion (which contributes to varying degrees) may also contribute to the failure of LCSD in controlling arrhythmias in some patients. These limitations of LCSD have also been reported in the LQTS population, LCSD was shown to reduce but not abolish sudden cardiac death in two large studies7,9 and in a small series 28 LCSD proved inadequate for control of symptoms despite addition of beta blockade.…”
Section: Discussionmentioning
confidence: 99%
“…The antiarrhythmic effects of TEA have been demonstrated in animal studies,4,5 effects include lengthening of repolarization and prolongation of refractory periods 6…”
Section: Introductionmentioning
confidence: 98%
“…In cardiac and thoracic surgery, epidural anesthesia has not been clearly associated with either a higher or lower incidence of atrial fibrillation [15][16][17]. Finally, in animal models, thoracic epidural anesthesia has been suggested to have an antiarrhythmic effect due to sympathetic nervous system blockade [18,19].…”
Section: Discussionmentioning
confidence: 99%
“…Sympathetic hyperactivity is an important modulator of ventricular arrhythmias, including electrical storm [14], therefore selective modulation of neural efferents to the heart is an attractive option for arrhythmia management. The antiarrhythmic effect of thoracic epidural anesthesia (TEA), including lengthening of repolarization and prolongation of refractory periods [15], has been demonstrated in animal studies [16] and its clinical utility in controlling arrhythmias in human subjects has also been described by our research team [17,18].…”
Section: Thoracic Epidural Anesthesiamentioning
confidence: 99%