Defibrillation shocks increase myocardial pacing threshold: an intracellular microelectrode study.
Defibrillation is known to cause inability to pace the heart acutely, but the mechanism is unknown. This study used microelectrode techniques to directly evaluate the effect of defibrillation shocks on the pacing threshold and membrane potentials from superfused guinea pig papillary muscles. Failure of pacing stimuli to induce action potentials (pacing failure) followed shocks of 50-200 V/cm, with pacing failure duration correlated with shock intensity. Increasing pacing strength from one to three times diastolic threshold decreased the incidence and duration of pacing failure. Decreased extracellular calcium concentration and verapamil added to the superfusate increased the duration of pacing failure. Membrane potential depolarization occurred after shock, but pacing failure did not correlate with depolarization magnitude. We conclude that defibrillation shocks directly cause shock intensity-dependent increase of myocardial pacing threshold. The pacing threshold of the myocardium can be increased after defibrillation shock independent of hypoxia or shock-induced depolarization and may involve membrane changes in calcium handling.
Li
H G
HG
Department of Physiology, University of Western Ontario, London, Canada.
Jones
D L
DL
Yee
R
R
Klein
G J
GJ
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D002304:Cardiac Pacing, Artificial; D004554:Electric Countershock; D005260:Female; D006168:Guinea Pigs; D006321:Heart / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D008839:Microelectrodes; D009206:Myocardium / Q000166:cytology*; D010210:Papillary Muscles / Q000166:cytology / Q000502:physiology; D014700:Verapamil / Q000494:pharmacology
D014700:Verapamil; D002118:Calcium