Probability of induction and stabilization of ventricular fibrillation with epinephrine

Clinical studies suggest that epinephrine facilitates ventricular fibrillation (VF) although mechanisms remain unclear. We tested the hypothesis that epinephrine increases the probability of inducing VF and stabilizes VF in association with shortening of fibrillation action potential duration. VF was induced in isolated, New Zealand White rabbit hearts (n=16) under control conditions and in the presence of 0.9 micro M/l epinephrine. Monophasic action potentials were recorded during sinus rhythm, pacing, and fibrillation. Epinephrine reduced fibrillation p80 by 80%, from 23+/-4 to 4.6+/-1 V (P<0.05); and reduced fibrillation p90 by 82%, from 29.3+/-5.4 to 5.4+/-1.9 V (P<0.05). Epinephrine also reduced the probability of spontaneous termination of VF during the first 5 s of VF from 29 to 8% (P<0.05). Epinephrine significantly decreased mean fibrillation cycle length from 104.5+/-2 to 75.7+/-2.3 ms (P<0.001). Mean action potential duration (60% repolarization) decreased from 76+/-3 to 40+/-3 ms (P<0.0003). Frequency analysis showed a mean dominant frequency during VF of 10.0+/-0.2 Hz under control conditions and 13. 3+/-0.3 Hz with epinephrine (P<0.0001). These results suggest that epinephrine increases the probability of VF induction and decreases the probability of spontaneous defibrillation. Stabilization of fibrillation is associated with shortening of action potential duration and fibrillation cycle length, which may allow a greater number of fibrillation waves in the ventricle.