Ventricular Fibrillation after Myocardial Revascularization

摘要

We read with interest Dr. Beaudet's comments concerning ultrastructural damage associated with the use of lidocaine as a component of his cold hyperkalemic cardioplegic solution. As we did not obtain either biochemical or electron microscopic data in our study, it is not possible to comment on potential ultrastructural myocardial damage associated with the use of lidocaine in our patients. It should be noted, however, that our method of delivery of lidocaine, i.e., a single dose given through the cardiopulmonary bypass circuit shortly before the removal of the aortic cross-clamp, undoubtedly presents the lidocaine to the myocardium under different conditions (lower concentration, more rapid washout, warmer temperature) that may ameliorate or prevent the deleterious effects described by Dr. Beaudet. As noted in the discussion of our study, we did not observe the high incidence of transient atrioventricular block and increased requirements for inotropic support noted by Tchervenkov and colleagues when lidocaine was added to the cardioplegic solution. Khuri and associates showed that, while all patients with ventricular fibrillation during reperfusion do not necessarily have low intramyocardian pH, those who did were adversely affected and tended to have a higher operative mortality. Prompt defibrillation in that group significantly minimized the acidosis, and presumably the prevention of ventricular fibrillation would have the same effect.