Intracellular calcium during pacing-induced ventricular fibrillation. Effects of lidocaine.
Hemodynamics and endocardial [Ca2+]i transients were studied during ventricular fibrillation in isolated perfused rat hearts. During 1 minute of pacing-induced ventricular fibrillation, the diastolic fibrillatory [Ca2+]i level increased significantly (p less than 0.001) above the end-systolic [Ca2+]i concentration of the last regular contraction. A bolus of lidocaine led to a decrease in the [Ca2+]i level during fibrillation (p less than 0.007) to the end-diastolic level of baseline conditions and then subsequently converted the heart to sinus rhythm. In 13 (62%) of the 21 studies described, post-lidocaine ventricular fibrillation converted to a brief period of asystole followed by sinus rhythm; in 8 (38%) of the studies, post-lidocaine ventricular fibrillation switched to ventricular tachycardia. Postfibrillatory cardiac dysfunction was related to the duration and degree of elevated diastolic [Ca2+]i. The authors conclude that [Ca2+]i levels are increased during ventricular fibrillation, and that lidocaine treatment leads to a prompt decrease in [Ca2+]i preceding conversion to sinus rhythm.
Stefenelli
T
T
Department of Medicine, University of California, San Francisco 94143.
Wikman-Coffelt
J
J
Wu
S T
ST
Parmley
W W
WW
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002304:Cardiac Pacing, Artificial; D004699:Endocardium / Q000378:metabolism; D006329:Heart Conduction System / Q000187:drug effects* / Q000503:physiopathology; D008012:Lidocaine / Q000494:pharmacology*; D009200:Myocardial Contraction / Q000187:drug effects; D010477:Perfusion; D051381:Rats; D011919:Rats, Inbred Strains; D014693:Ventricular Fibrillation / Q000209:etiology / Q000378:metabolism*
D008012:Lidocaine; D002118:Calcium