title: Defibrillation shocks produce different effects on Purkinje fibers and ventricular muscle: implications for successful defibrillation, refibrillation and postshock arrhythmia.
abstract: OBJECTIVE
  To understand the mechanisms of postdefibrillation arrhythmias and failed defibrillation, we studied the cellular effects of high voltage shocks on different cardiomyocytes in the dog.
  
  
  BACKGROUND
  The causes of postdefibrillation arrhythmias and unsuccessful defibrillation are not clear.
  
  
  METHODS
  High voltage shocks with voltage differentials of 9.3 to 97.6 V/cm were delivered to isolated canine papillary muscles with attached Purkinje fibers. Transmembrane potentials were recorded simultaneously from the Purkinje fiber and the ventricular muscle using standard microelectrode techniques.
  
  
  RESULTS
  After delivery of high voltage shocks, significant depolarization and rapid firing were observed in Purkinje fibers. The maximal rate of the rapid firing in the Purkinje fibers correlated with shock intensity (r = 0.69, p < 0.05). In contrast, in ventricular muscle, only slight depolarization and a transient refractory state were observed after the shock. The incidence of the refractory state was correlated with both the shock intensity and the rate of the rapid firing in the Purkinje fiber (r = 0.89 and 0.74, p < 0.01 and 0.05, respectively). Propranolol at a concentration sufficient for complete beta-blockade (1 mg/liter) did not change the tissue response to shocks but suppressed or abolished the shock-induced rapid firing of Purkinje fibers at a higher concentration (3 mg/liter). Blockade of the slow calcium channel with verapamil (400 micrograms/dl) did not alter the responsiveness of the preparation to shocks.
  
  
  CONCLUSIONS
  These results indicate that high voltage shocks induce different responses in Purkinje fibers and ventricular muscle. The shock-induced rapid firing in the Purkinje fiber may contribute to postshock arrhythmias and possibly refibrillation in some cases. The shock-induced transient refractory state in the ventricular muscle may prevent the ventricle from responding to the rapid firing and thus may decrease the incidence of postshock arrhythmias.
authors.affiliation: Department of Physiology, University of Western Ontario, London, Canada.
authors.forename: H G
authors.initials: HG
authors.lastname: Li
authors.forename: D L
authors.initials: DL
authors.lastname: Jones
authors.forename: R
authors.initials: R
authors.lastname: Yee
authors.forename: G J
authors.initials: GJ
authors.lastname: Klein
mesh_terms: D000200:Action Potentials; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D004285:Dogs; D004554:Electric Countershock; D066298:In Vitro Techniques; D008564:Membrane Potentials; D009206:Myocardium / Q000166:cytology; D011690:Purkinje Fibers / Q000502:physiology*; D016276:Ventricular Function