Influence of shock strength and timing on induction of ventricular arrhythmias in dogs.
We delivered strong shocks via electrodes on the left ventricular apex and the right atrium in seven dogs during the T wave of atrial pacing while recordings were made from 56 epicardial electrodes. After shocks that induced arrhythmias were given, the earliest activation occurred in the middle of the ventricles for lower-energy shocks and in the base for higher-energy shocks. For shocks late in the vulnerable period, activation was recorded soon after the shock, whereas for shocks early in the vulnerable period activation was not recorded for a mean of 70 ms (+/- 17 ms SD) after the shock. We also gave 1-J shocks during right and left ventricular pacing. For shocks early in the vulnerable period, activation initiating fibrillation arose in a focal pattern from the paced region. For shocks during the midportion of the vulnerable period, fibrillation arose by two leading circle reentrant loops rotating in opposite directions, one on the left and the other on the right ventricle. For shocks at the end of the vulnerable period, the two reentrant loops fused on the side of the heart opposite the pacing site to again form a single focal activation pattern. Thus the initial activation patterns of arrhythmias initiated by shocks, the time from the shock until earliest postshock activation, and the site of earliest postshock activation are strongly influenced by the coupling interval and strength of the shock.
Shibata
N
N
Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710.
Chen
P S
PS
Dixon
E G
EG
Wolf
P D
PD
Danieley
N D
ND
Smith
W M
WM
Ideker
R E
RE
D000818:Animals; D004285:Dogs; D004554:Electric Countershock / Q000009:adverse effects; D004597:Electroshock; D006321:Heart / Q000502:physiology / Q000503:physiopathology*; D006325:Heart Atria / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology; D008955:Models, Cardiovascular; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000209:etiology / Q000503:physiopathology*