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  (defined as LV end-diastolic pressure of 0 mmHg)and dilated volume [d] (defined as " 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) , 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,  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 language||English (US)|
|Journal||Journal of Investigative Medicine|
|State||Published - Jan 1 1996|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)