title: Lidocaine's effect on defibrillation threshold are dependent on the defibrillation electrode system: epicardial versus endocardial.
abstract: BACKGROUND
  Epicardial and endocardial defibrillation electrode systems affect myocardial electrophysiology and sympathetic function differently. Thus, we postulate that antiarrhythmic drugs will interact with these electrode systems differently.
  
  
  RESULTS
  Defibrillation energy requirements (DER) at 20% (ED20), 50% (ED50), and 80% (ED80) success were measured at baseline and during lidocaine (10 mg/kg per hour) or D5W treatment for epicardial and endocardial electrodes. Pigs were randomized to treatment (lidocaine or D5W) and electrode system, which resulted in four experimental groups: (1) epicardial electrode + D5W; (2) epicardial electrode + lidocaine; (3) endocardial electrode + D5W; and (4) endocardial electrode + lidocaine. ED50 DER (mean +/- SEM) values at baseline for groups 1-4 were 10.6+/-1, 8.5+/-1, 12.6+/-1, and 12.3+/-1 J, respectively. DER values for groups 1 and 3 during D5W were similar to baseline. Conversely, lidocaine increased ED50 DER values from 8.5+/-1 to 13.5+/-2 J (P < 0.05) in group 2 animals (epicardial electrodes). When lidocaine was administered to group 4 animals (endocardial electrodes), however, ED50 DER values remained similar to baseline values (12.3+/-1 to 14.3+/-2 J, P = NS). Lidocaine increased ED50 DER values by 59% with the epicardial electrode system, which was significantly greater than the 16% increase with the endocardial electrode system (P < 0.05). Electrophysiologic response and electrode impedance were similar between electrode systems.
  
  
  CONCLUSIONS
  Lidocaine increases DER values to a greater extent when using epicardial versus endocardial electrode system. Thus, drug-device interactions are dependent on the electrode system. These data suggest that the electrophysiologic milieu created by endocardial defibrillation mitigates the effects that lidocaine has on DER values.
authors.affiliation: The University of Georgia College of Pharmacy, Augusta VA Medical Center, USA.
authors.forename: A P
authors.initials: AP
authors.lastname: Winecoff Miller
authors.forename: J J
authors.initials: JJ
authors.lastname: Sims
authors.forename: R
authors.initials: R
authors.lastname: McSwain
authors.forename: M R
authors.initials: MR
authors.lastname: Ujhelyi
mesh_terms: D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D004554:Electric Countershock / Q000295:instrumentation*; D004558:Electric Stimulation; D004562:Electrocardiography / Q000187:drug effects; D004566:Electrodes; D004594:Electrophysiology; D004699:Endocardium / Q000187:drug effects / Q000502:physiology*; D006329:Heart Conduction System / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D066298:In Vitro Techniques; D008012:Lidocaine / Q000494:pharmacology*; D010496:Pericardium / Q000187:drug effects / Q000502:physiology*; D013552:Swine
chemical_list: D000889:Anti-Arrhythmia Agents; D008012:Lidocaine