Mechanisms responsible for countershock-induced ventricular tachycardia in the intact canine heart.
To determine the mechanism for postcountershock ventricular ectopy, internal and external shocks were delivered to 20 anesthetized dogs. Shock energies of 25 and 50 joules were employed internally while 100 and 200 joules were delivered externally. Experiments were performed in both the presence and absence of a nearly toxic dose of ouabain. All shocks resulted in the occurrence of nonsustained (less than 15 seconds) ventricular tachycardia. When bursts of rapid ventricular pacing were synchronized with a shock, the pacing stimuli invariably captured the ventricles and overdrove the shock-induced ventricular tachycardia. However, the burst pacing never appeared to break a tachycardia, since the termination of pacing was followed immediately by the resumption of the shock-induced ventricular tachycardia. The presence of ouabain did not alter the response of the ventricles to postshock burst pacing. Administration of verapamil (0.5 mg/kg) had no effect on the duration of shock-induced ventricular arrhythmia. Elevation of the serum potassium level to 8.5 +/- 0.6 mEq/L drastically reduced the duration of postshock ventricular tachycardia in both the presence and absence of ouabain. The results suggest that postshock ventricular ectopy results from an abnormality of impulse initiation rather than reentry.
D000818:Animals; D004285:Dogs; D004554:Electric Countershock / Q000009:adverse effects*; D006947:Hyperkalemia / Q000150:complications; D010042:Ouabain / Q000494:pharmacology; D013610:Tachycardia / Q000209:etiology* / Q000503:physiopathology
D010042:Ouabain