R A Malkin1, B K Hoffmeister. 1. Joint Program in Biomedical Engineering at The University of Memphis and The University of Tennessee-Memphis, 38152-3210, USA. ramalkin@memphis.edu
Abstract
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 microA. 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 microA; minimum 50 microA in two animals) occurs below the VF threshold (108+/-28 microA) by causing rapid, regular excitation.
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 microA. 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 microA; minimum 50 microA in two animals) occurs below the VF threshold (108+/-28 microA) by causing rapid, regular excitation.