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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
1992-1-14
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pubmed:abstractText |
Patients with automatic defibrillators frequently require chronic antiarrhythmic drug therapy or receive acute therapy with the onset of symptoms. The effects on energy requirements for defibrillation of lidocaine hydrochloride and verapamil hydrochloride, two commonly used antiarrhythmic agents, were examined in 20 successive patients undergoing corrective arrhythmia surgery. The minimum energy requirement for ventricular defibrillation before and 5 minutes after the administration of 150 mg of lidocaine intravenously (n = 8), or 10 minutes after 10 mg of verapamil intravenously (n = 12), were determined. Each patient was assigned to receive either verapamil or lidocaine. Three mesh coil defibrillating electrodes (Medtronic 6891, 6892) were sutured to the epicardium of the right and left ventricles. Ventricular fibrillation was induced using alternating current. After a minimum of 10 seconds of fibrillation, the minimum energy for defibrillation was established using sequential pulse defibrillation. The preselected drug was then infused and the ventricular defibrillation energy was again determined after 5 or 10 minutes circulation time. Lidocaine did not alter the minimum energy for defibrillation (3.0 +/- 1.4 J vs. 3.0 +/- 1.8 J, mean +/- SD), despite plasma levels of lidocaine that averaged 13.2 +/- 1.9 mumol/l. In contrast, verapamil significantly increased (3.9 +/- 2.2 J vs. 6.5 +/- 2.9 J) the minimum energy necessary for defibrillation. The difference in defibrillation energy was significantly correlated to the fall in systolic blood pressure induced by verapamil administration (r = 0.72). These data reinforce the necessity for determining efficacy of defibrillation when medication changes are instituted. Verapamil should be used with caution in patients with automatic defibrillators and marginal defibrillation threshold.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-0736
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
24
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
299-305
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pubmed:dateRevised |
2009-11-11
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pubmed:meshHeading |
pubmed-meshheading:1744543-Adult,
pubmed-meshheading:1744543-Blood Pressure,
pubmed-meshheading:1744543-Electric Countershock,
pubmed-meshheading:1744543-Electrocardiography,
pubmed-meshheading:1744543-Female,
pubmed-meshheading:1744543-Heart,
pubmed-meshheading:1744543-Heart Rate,
pubmed-meshheading:1744543-Humans,
pubmed-meshheading:1744543-Lidocaine,
pubmed-meshheading:1744543-Male,
pubmed-meshheading:1744543-Middle Aged,
pubmed-meshheading:1744543-Ventricular Fibrillation,
pubmed-meshheading:1744543-Verapamil
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pubmed:year |
1991
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pubmed:articleTitle |
Effects of lidocaine and verapamil on defibrillation in humans.
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pubmed:affiliation |
Department of Medicine, University of Western Ontario, University Hospital, London, Canada.
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pubmed:publicationType |
Journal Article
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