The Effects of Lidocaine on the Vulnerable Period During Ventricular Fibrillation
Yong‐Mei Cha, Barry Peters, PENG‐SHENG CHEN
Abstract
Yong‐Mei Cha, Barry Peters, PENG‐SHENG CHEN
Abstract
INTRODUCTION: It was postulated that a subthreshold defibrillation shock failed to halt ventricular fibrillation because the shock itself reinitiated ventricular fibrillation by falling into the vulnerable period of the wavefronts. Whether or not the timing of the vulnerable period is determined by the ventricular fibrillation cycle length is unknown. METHODS AND RESULTS: We determined the patterns of epicardial activation in ten dogs by computerized mapping techniques during unsuccessful defibrillation. Lidocaine was then given to prolong the ventricular fibrillation cycle length, and the computerized mapping studies were repeated. The results showed that lidocaine increased the ventricular fibrillation cycle length from 110 +/- 13 msec to 156 +/- 5 msec (P < 0.001). Among 55 episodes of unsuccessful defibrillation, the site of the earliest postshock activation occurred in the center of the mapped tissue 12 times at baseline and 14 times during lidocaine infusion. At electrodes that registered as postshock early sites, the preshock intervals clustered within a narrow range both before (58 +/- 14 msec) and during (101 +/- 18 msec, P < 0.001) lidocaine infusion. The correlation between the preshock intervals and the ventricular fibrillation cycle length was significant for these 26 sites (r = 0.87, P < 0.001). CONCLUSION: We conclude that a vulnerable period is present during ventricular fibrillation, and the timing of the vulnerable period is determined by the ventricular fibrillation cycle length.
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INTRODUCTION: It was postulated that a subthreshold defibrillation shock failed to halt ventricular fibrillation because the shock itself reinitiated ventricular fibrillation by falling into the vulnerable period of the wavefronts. Whether or not the timing of the vulnerable period is determined by the ventricular fibrillation cycle length is unknown. METHODS AND RESULTS: We determined the patterns of epicardial activation in ten dogs by computerized mapping techniques during unsuccessful defibrillation. Lidocaine was then given to prolong the ventricular fibrillation cycle length, and the computerized mapping studies were repeated. The results showed that lidocaine increased the ventricular fibrillation cycle length from 110 +/- 13 msec to 156 +/- 5 msec (P < 0.001). Among 55 episodes of unsuccessful defibrillation, the site of the earliest postshock activation occurred in the center of the mapped tissue 12 times at baseline and 14 times during lidocaine infusion. At electrodes that registered as postshock early sites, the preshock intervals clustered within a narrow range both before (58 +/- 14 msec) and during (101 +/- 18 msec, P < 0.001) lidocaine infusion. The correlation between the preshock intervals and the ventricular fibrillation cycle length was significant for these 26 sites (r = 0.87, P < 0.001). CONCLUSION: We conclude that a vulnerable period is present during ventricular fibrillation, and the timing of the vulnerable period is determined by the ventricular fibrillation cycle length.
Key concepts: Ventricular fibrillation, Defibrillation, Medicine, Lidocaine, Cardiology, Fibrillation, Defibrillation threshold, Shock (circulatory)