High and low strength nonsynchronized shocks given during canine ventricular tachycardia.

Published

Journal Article

UNLABELLED: Cardioversion shocks given during ventricular tachycardia may cause ventricular fibrillation or acceleration of ventricular tachycardia, or arrest the tachycardia. A recently proposed theory may explain why the former two phenomena may occur. Briefly, this theory states that potential gradient shock fields of a critical strength delivered to tissue with a critical degree of refractoriness will cause circulating wave fronts of ventricular activation ("rotors") manifest as ventricular arrhythmia. We tested this theory by delivering nonsynchronized shocks 50% higher than defibrillation threshold or 50% lower than defibrillation threshold during 275 episodes of ventricular tachycardia in eight dogs with 5- to 7-day-old myocardial infarcts. Shocks stronger than the defibrillation threshold are likely to create shock fields in the ventricles everywhere stronger than this critical value, and therefore would not generate rotors. Shocks less strong than the defibrillation threshold may create shock fields within the ventricles that include the critical value, and therefore cause rotors if given when critically refractory tissue is present. Nonsynchronized shocks were used to increase the likelihood of encountering tissue with a critical degree of refractoriness. Ventricular fibrillation or acceleration of ventricular tachycardia occurred following 83 of 138 (60%) low strength shocks and following 20 of 137 (14.6%) high strength shocks. The pooled odds ratio for induction of ventricular fibrillation or accelerated ventricular tachycardia after low strength shocks as compared to high strength shocks was 8.9. CONCLUSION: when given during ventricular tachycardia, low strength shocks are much more likely to cause ventricular fibrillation or accelerated ventricular tachycardia than are high strength shocks (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Full Text

Duke Authors

Cited Authors

  • McClelland, JH; Daubert, JP; Kavanagh, KM; Harrell, FE; Ideker, RE

Published Date

  • July 1992

Published In

Volume / Issue

  • 15 / 7

Start / End Page

  • 986 - 992

PubMed ID

  • 1378609

Pubmed Central ID

  • 1378609

International Standard Serial Number (ISSN)

  • 0147-8389

Digital Object Identifier (DOI)

  • 10.1111/j.1540-8159.1992.tb03091.x

Language

  • eng

Conference Location

  • United States