Modification of the electrophysiologic matrix by antiarrhythmic drugs.
Evidence from many experiments and observations suggests that the likelihood of ventricular fibrillation is increased in some proportion to the magnitude of local differences in the electrophysiologic state of the ventricular myocardium. Many local anesthetic antiarrhythmic drugs have differing affinities for resting, open and inactivated fast channels. In ischemic or otherwise damaged hearts, local differences in resting potential, action potential upstroke and action potential duration will result in differing degrees of block of fast channels by local anesthetic antiarrhythmic drugs. Such drugs can be expected to add to the preexisting local inhomogeneities of electrophysiologic state and thereby increase the likelihood of fibrillation.
D000200:Action Potentials / Q000187:drug effects; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D001566:Benzocaine / Q000494:pharmacology; D004594:Electrophysiology; D006329:Heart Conduction System / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D008012:Lidocaine / Q000031:analogs & derivatives / Q000494:pharmacology; D013997:Time Factors; D016677:Tocainide; D014693:Ventricular Fibrillation / Q000503:physiopathology
D000889:Anti-Arrhythmia Agents; D016677:Tocainide; D008012:Lidocaine; D001566:Benzocaine