Synchronized repolarization after defibrillation shocks. A possible component of the defibrillation process demonstrated by optical recordings in rabbit heart.
BACKGROUND
It is currently believed that defibrillation shocks act primarily by stimulating excitable myocardium to abolish wave fronts. Recent studies have shown that shocks applied during pacing not only stimulate excitable myocardium but also prolong the depolarization and refractoriness of myocardium already in a depolarized state. This study investigates the effects of shocks on fibrillation action potentials.


RESULTS
Recordings of membrane action potentials free of shock artifact were obtained using the voltage-sensitive dye WW781 during defibrillation of isolated rabbit hearts. These records showed that the shocks caused an additional phase of depolarization beginning with an initial rapid depolarization of the optical signal followed by a slow phase of repolarization. This occurred throughout all phases of the fibrillation action potential from just after completion of the upstroke to a time of near maximal repolarization. Defibrillation shocks, however, had the additional effect of causing the myocardium to repolarize at a constant time after the shock regardless of its prior electrical activity--the constant repolarization time response. This effect was not dependent on the presence of D600 (methoxyverapamil) or continuous coronary perfusion. It was accompanied by a similar constancy in the return of myocardial excitability. Recordings taken from multiple adjacent recording sites also showed a constant repolarization time among them.


CONCLUSIONS
A simple model of reentry is used to illustrate how the constant repolarization response, in addition to wave front termination and refractoriness extension, could play a role in the successful termination of fibrillation by electrical shock.
Dillon
S M
SM
Department of Pharmacology, College of Physicians and Surgeons, Columbia University, New York City, NY 10032.
D000818:Animals; D004554:Electric Countershock; D005711:Gallopamil / Q000494:pharmacology; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D055095:Optics and Photonics; D011817:Rabbits; D013997:Time Factors
D005711:Gallopamil