Document Detail


Regional hyperkalemia increases ventricular defibrillation energy requirements: role of electrical heterogeneity in defibrillation.
MedLine Citation:
PMID:  10868736     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
INTRODUCTION: Increased spatial electrical heterogeneity has been associated with impaired defibrillation efficacy. The current study investigated the relationship between electrical heterogeneity and defibrillation efficacy by manipulating spatial electrical heterogeneity. METHODS AND RESULTS: We increased spatial electrical heterogeneity by infusing potassium chloride (2 to 4 mEq/hour) or placebo in the left anterior descending artery in 13 pentobarbital anesthetized swine. Electrophysiologic measurements at five myocardial sites and defibrillation energy requirement (DER) values were determined at baseline and during regional hyperkalemia (n = 7) or placebo (n = 6). Regional potassium infusion was titrated to a 20% reduction in action potential duration in the perfused region. Regional hyperkalemia increased biphasic DER values by 87% (P = 0.02), whereas infusion of placebo did not alter defibrillation efficacy. Regional hyperkalemia decreased myocardial repolarization and refractoriness in the perfused region by 21% (P < 0.001) and 18% (P = 0.01), respectively. However, regional hyperkalemia increased ventricular fibrillation cycle length (VFCL) by 39% (P = 0.008). Consequently, dispersions of repolarization, refractoriness, and VFCL were significantly increased by 169%, 92%, and 200%, respectively. Regional hyperkalemia also increased ventricular conduction time to the perfused region by 54% (P = 0.006), indicating conduction velocity dispersion, while not affecting local pacing threshold or local voltage gradient. CONCLUSION: Regional hyperkalemia increased DER values. Regional hyperkalemia likely impairs defibrillation by increasing myocardial electrical heterogeneity, which supports the theory that electrical heterogeneity promotes nonuniform propagation of early postshock activations, thereby inhibiting defibrillation.
Authors:
J J Sims; A W Miller; M R Ujhelyi
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cardiovascular electrophysiology     Volume:  11     ISSN:  1045-3873     ISO Abbreviation:  J. Cardiovasc. Electrophysiol.     Publication Date:  2000 Jun 
Date Detail:
Created Date:  2000-10-19     Completed Date:  2000-10-19     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9010756     Medline TA:  J Cardiovasc Electrophysiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  634-41     Citation Subset:  IM    
Affiliation:
University of Georgia College of Pharmacy, Medical College of Georgia School of Medicine, and Augusta VA Medical Center, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Electric Countershock*
Electricity
Electrophysiology
Heart Conduction System / physiopathology
Hyperkalemia / complications*,  physiopathology
Osmolar Concentration
Potassium / blood
Refractory Period, Electrophysiological
Swine
Ventricular Fibrillation / complications*,  physiopathology,  therapy*
Chemical
Reg. No./Substance:
7440-09-7/Potassium
Comments/Corrections
Comment In:
J Cardiovasc Electrophysiol. 2000 Jun;11(6):642-4   [PMID:  10868737 ]

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