title: Atrial, SA nodal, and AV nodal electrophysiology in standing horses: normal findings and electrophysiologic effects of quinidine and diltiazem.
abstract: BACKGROUND
  Although atrial arrhythmias are clinically important in horses, atrial electrophysiology has been incompletely studied.
  
  
  OBJECTIVE
  Standard electrophysiologic methods can be used to study drug effects in horses. Specifically, the effects of diltiazem on atrioventricular (AV) nodal conduction are rate-dependent and allow control of ventricular response rate during rapid atrial pacing in horses undergoing quinidine treatment.
  
  
  METHODS
  Fourteen healthy horses.
  
  
  METHODS
  Arterial blood pressure, surface electrocardiogram, and right atrial electrogram were recorded during sinus rhythm and during programmed electrical stimulation at baseline, after administration of quinidine gluconate (10 mg/kg IV over 30 minutes, n = 7; and 12 mg/kg IV over 5 minutes followed by 5 mg/kg/h constant rate infusion for the remaining duration of the study, n = 7), and after coadministration of diltiazem (0.125 mg/kg IV over 2 minutes repeated every 12 minutes to effect).
  
  
  RESULTS
  Quinidine significantly prolonged the atrial effective refractory period, shortened the functional refractory period (FRP) of the AV node, and increased the ventricular response rate during atrial pacing. Diltiazem increased the FRP, controlled ventricular rate in a rate-dependent manner, caused dose-dependent suppression of the sinoatrial node and produced a significant, but well tolerated decrease in blood pressure. Effective doses of diltiazem ranged from 0.125 to 1.125 mg/kg.
  
  
  CONCLUSIONS
  Standard electrophysiologic techniques allow characterization of drug effects in standing horses. Diltiazem is effective for ventricular rate control in this pacing model of supraventricular tachycardia. The use of diltiazem for rate control in horses with atrial fibrillation merits further investigation.
authors.affiliation: Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, 43210, USA. schwarzwald.4@osu.edu
authors.forename: Colin C
authors.initials: CC
authors.lastname: Schwarzwald
authors.forename: Robert L
authors.initials: RL
authors.lastname: Hamlin
authors.forename: John D
authors.initials: JD
authors.lastname: Bonagura
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Nishijima
authors.forename: Cheyney
authors.initials: C
authors.lastname: Meadows
authors.forename: Cynthia A
authors.initials: CA
authors.lastname: Carnes
mesh_terms: D000818:Animals; D016275:Atrial Function / Q000187:drug effects / Q000502:physiology; D001283:Atrioventricular Node / Q000187:drug effects* / Q000502:physiology; D002317:Cardiovascular Agents / Q000494:pharmacology; D004110:Diltiazem / Q000008:administration & dosage / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D022062:Electrophysiologic Techniques, Cardiac; D005260:Female; D006325:Heart Atria / Q000187:drug effects*; D006736:Horses / Q000502:physiology*; D008297:Male; D011802:Quinidine / Q000008:administration & dosage / Q000494:pharmacology*; D012849:Sinoatrial Node / Q000187:drug effects* / Q000502:physiology
chemical_list: D002317:Cardiovascular Agents; D004110:Diltiazem; D011802:Quinidine