Increased defibrillation threshold due to ventricular fibrillation duration. Potential mechanisms

The duration of ventricular fibrillation (VF) that precedes a high energy shock has been recognized as a critical determinant of defibrillation outcome. Factors such as metabolic acidosis or alkalosis do not affect outcome. The authors hypothesized that release of myocardial adenosine during VF coul...

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Veröffentlicht in:Journal of electrocardiology 1995, Vol.28 Suppl, p.21-24
Hauptverfasser: Lerman, B B, Engelstein, E D
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description The duration of ventricular fibrillation (VF) that precedes a high energy shock has been recognized as a critical determinant of defibrillation outcome. Factors such as metabolic acidosis or alkalosis do not affect outcome. The authors hypothesized that release of myocardial adenosine during VF could potentially mediate the time-dependent effects of VF duration on defibrillation. Defibrillation threshold (DFT) was therefore determined in dogs during concurrent infusion of adenosine and dipyridamole (a nucleoside transport blocker). Transthoracic DFT increased by approximately 50%, whereas transmyocardial DFT increased by approximately 100% in a separate group of dogs. These effects of adenosine on DFT were abolished when the dogs were autonomically denervated, suggesting that the deleterious effects of adenosine on DFT are due to its antiadrenergic mechanism of action. These data indicate that adenosine release during VF can markedly increase DFT. Since adenosine myocardial release during VF is time dependent, it is likely that adenosine plays a significant role in mediating the increase in threshold that is dependent on the duration of VF.
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These effects of adenosine on DFT were abolished when the dogs were autonomically denervated, suggesting that the deleterious effects of adenosine on DFT are due to its antiadrenergic mechanism of action. These data indicate that adenosine release during VF can markedly increase DFT. Since adenosine myocardial release during VF is time dependent, it is likely that adenosine plays a significant role in mediating the increase in threshold that is dependent on the duration of VF.</description><identifier>ISSN: 0022-0736</identifier><identifier>DOI: 10.1016/S0022-0736(95)80004-2</identifier><identifier>PMID: 8656114</identifier><language>eng</language><publisher>United States</publisher><subject>Adenosine - antagonists &amp; inhibitors ; Adenosine - metabolism ; Adenosine - pharmacology ; Adenosine - physiology ; Adrenergic Antagonists - pharmacology ; Animals ; Autonomic Nervous System - physiopathology ; Cardiovascular Agents - pharmacology ; Denervation ; Dipyridamole - pharmacology ; Dogs ; Electric Countershock ; Epinephrine - metabolism ; Lactates - metabolism ; Myocardium - metabolism ; Norepinephrine - metabolism ; Nucleosides - antagonists &amp; inhibitors ; Time Factors ; Vagotomy ; Ventricular Fibrillation - metabolism ; Ventricular Fibrillation - physiopathology ; Ventricular Fibrillation - therapy</subject><ispartof>Journal of electrocardiology, 1995, Vol.28 Suppl, p.21-24</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,4010,27902,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8656114$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lerman, B B</creatorcontrib><creatorcontrib>Engelstein, E D</creatorcontrib><title>Increased defibrillation threshold due to ventricular fibrillation duration. Potential mechanisms</title><title>Journal of electrocardiology</title><addtitle>J Electrocardiol</addtitle><description>The duration of ventricular fibrillation (VF) that precedes a high energy shock has been recognized as a critical determinant of defibrillation outcome. Factors such as metabolic acidosis or alkalosis do not affect outcome. The authors hypothesized that release of myocardial adenosine during VF could potentially mediate the time-dependent effects of VF duration on defibrillation. Defibrillation threshold (DFT) was therefore determined in dogs during concurrent infusion of adenosine and dipyridamole (a nucleoside transport blocker). Transthoracic DFT increased by approximately 50%, whereas transmyocardial DFT increased by approximately 100% in a separate group of dogs. 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subjects Adenosine - antagonists & inhibitors
Adenosine - metabolism
Adenosine - pharmacology
Adenosine - physiology
Adrenergic Antagonists - pharmacology
Animals
Autonomic Nervous System - physiopathology
Cardiovascular Agents - pharmacology
Denervation
Dipyridamole - pharmacology
Dogs
Electric Countershock
Epinephrine - metabolism
Lactates - metabolism
Myocardium - metabolism
Norepinephrine - metabolism
Nucleosides - antagonists & inhibitors
Time Factors
Vagotomy
Ventricular Fibrillation - metabolism
Ventricular Fibrillation - physiopathology
Ventricular Fibrillation - therapy
title Increased defibrillation threshold due to ventricular fibrillation duration. Potential mechanisms
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