Effect of ventricular dilatation on defibrillation threshold

P. Ott, M. J. Reiter

Research output: Contribution to journalArticle

Abstract

We studied the effects of acute ventricular dilatation (VD) on defibrillation thresholds (DFT) in 19 isolated, Tyrode perfused, rabbit hearts Methods: To achieve VD, a latex balloon, placed in the left ventricle (LV), was filled with 1.0 ml of normal saline [N=10], or 5% dextrose [N=9]. Ventricular fibrillation was induced by rapid ventricular stimulation, and a monophasic shock wave (12 msec pulse width) was delivered after 10 seconds. A circular, mesh-wire patch electrode (1.76 cm 2), placed over the posterior LV, served as cathode and the metallic aortic cannula served as anode. DFT was determined for zero volume [0] (defined as LV end-diastolic pressure of 0 mmHg)and dilated volume [d] (defined as "[0] plus 1.0 ml") using a modified down/up protocol, with voltage steps of 10 Volts. Results: (Data is snown in mean+/- Standard Error) DFT (volts) ERP (msec) EDP (mmHg) [0], N=19 96+1-4 117+/-3 0+/-1 [d], N=19 125+/-7 * 99 + /-3 * 35+/-3 * * p<0.001; paired two-sided t-test, [0] versus [d] volume. EDP= end-diastolic pressure, ERP= effective refractory period VD decreased ERP (15%) and increased DFT (30%). The increase in DFT was unaffected by the balloon solution (saline versus dextrose). Conclusion: (1) Acute VD, in this model, significantly increased DFT. (2) The precise mechanism remains unknown. (3) This may have implications for patients with the implantable cardioverter / defibrillator.

Original languageEnglish (US)
Pages (from-to)185A
JournalJournal of Investigative Medicine
Volume44
Issue number1
StatePublished - Jan 1 1996

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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