Effects of Thoracic Epidural Anesthesia with and without Autonomic Nervous System Blockade on Cardiac Monophasic Action Potentials and Effective Refractoriness in Awake Dogs

2001 ◽  
Vol 95 (1) ◽  
pp. 132-138 ◽  
Author(s):  
Andreas Meissner ◽  
Lars Eckardt ◽  
Paulus Kirchhof ◽  
Thomas Weber ◽  
Norbert Rolf ◽  
...  
Keyword(s):  
Action Potential ◽  
Epidural Anesthesia ◽  
Action Potential Duration ◽  
Action Potentials ◽  
Monophasic Action Potential ◽  
Thoracic Epidural Anesthesia ◽  
Thoracic Epidural ◽  
Monophasic Action Potentials ◽  
Cycle Lengths

Background The effects of thoracic epidural anesthesia (TEA) on myocardial repolarization and arrhythmogenicity are only incompletely understood. This is primarily because of the lack of appropriate experimental models. In most of the studies performed thus far, TEA was used in anesthetized animals. Baseline anesthesia itself may have modified the effects of TEA. This study investigates right atrial and ventricular repolarization by recording monophasic action potentials after TEA in awake dogs. The authors hypothesized that an antiarrhythmic role of TEA exists, which may be related to a direct effect of TEA on myocardial repolarization. Methods The hypothesis was tested in an in vivo canine model, in which atrial and ventricular myocardial action potential duration and refractoriness are recorded by means of monophasic action potential catheters. Results Thoracic epidural anesthesia significantly increased ventricular monophasic action potential duration for cycle lengths shorter than 350 ms. Changes in monophasic action potential duration were paralleled by a concomitant prolongation of effective refractory period (ERP) at higher rates so that the ratio of ERP to action potential duration was unaffected. Conclusions 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 of repolarization even at short cycle lengths.

Monophasic action potentials and activation recovery intervals as measures of ventricular action potential duration: Experimental evidence to resolve some controversies

Heart Rhythm ◽  
2006 ◽  
Vol 3 (9) ◽  
pp. 1043-1050 ◽  
Author(s):  
Ruben Coronel ◽  
Jacques M.T. de Bakker ◽  
Francien J.G. Wilms-Schopman ◽  
Tobias Opthof ◽  
André C. Linnenbank ◽  
...  
Keyword(s):  
Action Potential ◽  
Experimental Evidence ◽  
Action Potential Duration ◽  
Action Potentials ◽  
Monophasic Action Potentials ◽  
Ventricular Action Potential

Monophasic action potential recordings in response to graded hyperkalemia in dogs

1989 ◽  
Vol 256 (4) ◽  
pp. H956-H961
Author(s):  
P. M. Sutton ◽  
P. Taggart ◽  
D. W. Spear ◽  
H. F. Drake ◽  
R. H. Swanton ◽  
...  
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Regional Differences ◽  
Monophasic Action Potential ◽  
Extracellular Potassium ◽  
Activation Time ◽  
Biphasic Response ◽  
The Difference ◽  
Alpha Chloralose

Recent interest in sudden cardiac death during exercise in normal healthy people has highlighted the possible role of swings of extracellular potassium in arrhythmogenesis in conditions other than ischemia. Regional differences in action potential duration and conduction may be important. We have recorded monophasic action potentials (MAPs) from the endocardium and epicardium in nine open-chest dogs during graded intravenous infusion of potassium up to a plasma level of 9 mM. The animals were anesthetized with alpha-chloralose and urethan. Continuous, online arterial potassium monitoring was employed. MAP duration showed a biphasic response with initial shortening up to 7 mM, which tended to be more obvious on the epicardium. Regional activation time was measured as the difference between the onset of depolarization of the endocardial and epicardial MAP. Regional activation time also showed a biphasic response with initial shortening and subsequent delay. The QRS width of the scalar lead II electrocardiogram also showed biphasic changes, and the T wave amplitude progressively decreased. Our results suggest that regional differences in repolarization time may develop in the nonischemic myocardium in response to increased extracellular potassium levels mainly as a result of local changes in regional activation time rather than as a result of a direct effect on action potential duration.

Isoproterenol antagonizes drug-induced prolongation of action potential duration in humans

1993 ◽  
Vol 71 (10-11) ◽  
pp. 755-760 ◽  
Author(s):  
David Newman ◽  
Paul Dorian ◽  
Randi Feder-Elituv
Keyword(s):  
Steady State ◽  
Action Potential ◽  
Action Potential Duration ◽  
Refractory Period ◽  
Cycle Length ◽  
Monophasic Action Potential ◽  
Class Iii ◽  
State Action ◽  
Cycle Lengths ◽  
Prolongation Of Action Potential

The effects of an isoproterenol infusion on the duration of the human right ventricular endocardial monophasic action potential at 90% repolarization were recorded in the absence and in the presence of an antiarrhythmic drag regimen containing class III effects in two similar groups of patients. The drugs used were amiodarone (N = 3, 300 ± 50 mg), sotalol plus quinidine (N = 11, 156 ± 13 mg sotalol, 1688 ± 594 mg quinidine), and sotalol alone (N = 3, 300 ± 20 mg). All patients had underlying coronary disease but no evidence of inducible ischemia. In the absence of antiarrhythmic drug, isoproterenol did not significantly change the relationship of action potential duration at 90% repolarization to cycle length; there was a linear decrease in action potential duration by 19.8% between a paced cycle length of 600 and 300 ms. Isoproterenol did not significantly shorten the action potential duration at any cycle length. However, isoproterenol decreased the ventricular effective refractory period at 400 ms drive from 240 ± 5.0 to 225 ± 6.0 ms (p < 0.05) accompanied by no change in the ratio of refractory period to steady-state action potential duration. In the presence of class III drug effects, the action potential duration was increased by an average of 9.2% at all paced cycle lengths longer than 300 ms (p < 0.05). The ventricular refractory period was increased from 240 ± 5 to 269 ± 9.0 ms (p < 0.05 compared with baseline) with a concomitant increase in the ratio of refractory period to action potential duration from 96 ± 2 to 103 ± 2% (p < 0.05 compared with baseline). With infusion of isoproterenol in the presence of a class III containing regimen, the drug-prolonged action potential duration was shortened (p < 0.05) by an average of 8.1% at all cycle lengths longer than 300 ms. These results suggest that isoproterenol simulation of enhanced sympathetic tone can antagonize drug prolongation of action potential duration and that in the absence of drugs, the effects of isoproterenol on the steady-state action potential duration are modest. The clinical utility of class III agents may be augmented by the addition of concomitant β-blockade.Key words: action potential duration, antiarrhythmic drugs, isoproterenol.

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