Mechanisms by which AC leakage currents cause complete hemodynamic collapse without inducing fibrillation

TitleMechanisms by which AC leakage currents cause complete hemodynamic collapse without inducing fibrillation
Publication TypeJournal Article
Year of Publication2001
AuthorsMalkin RA, Hoffmeister BK
JournalJournal of Cardiovascular Electrophysiology
Start Page1154
Pagination1154 - 1161
Date Published01/2001

Introduction: The first study of weak alternating current (AC) stimulation in closed chest humans showed that complete hemodynamic collapse can occur below the threshold for inducing ventricular fibrillation (VF), a heretofore unknown danger to patients. This article, and the accompanying simulation article, explore the mechanisms responsible for the collapse. Methods and Results: A quadripolar pacing catheter was placed in the right ventricle (RV) of six dogs. The tip of the catheter (17 mm2) carried 5 seconds of AC stimulation ranging from 10 to 160 Hz and 10 to 1,000 μA. The lead II body surface ECG, femoral artery pressure, and a bipole from the proximal pair of electrodes on the RV catheter were recorded 2 seconds before, during, and 2 seconds after stimulation. Based on the blood pressure, every episode was categorized as VF, COLLAPSE without VF, extrasystolic without COLLAPSE (EFFECT), or having caused no effect (NSR). The electrical activation interval (interspike interval [ISI]) from the RV bipole was compared with the mechanical activation interval, determined from M-mode ultrasound. COLLAPSE is associated with a short ISI (NSR = 408 ± 110 msec; EFFECT = 305 ± 113 msec; COLLAPSE = 179 ± 25 msec; P < 0.001) with a high degree of regularity (P < 0.001): coefficient of variation of ISI for COLLAPSE (0.038 ± 0.069) versus VF (0.389 ± 0.222), EFFECT (0.420 ± 0.241), and NSR (0.016 ± 0.048). Electrical activation and mechanical activation rates occurred at integer multiples of the AC stimulation period. Conclusion: COLLAPSE (86 ± 37 μA; minimum 50 μA in two animals) occurs below the VF threshold (108 ± 28 μA) by causing rapid, regular excitation.

Short TitleJournal of Cardiovascular Electrophysiology