title: Acute circulatory actions of intravenous amiodarone loading in cardiac surgical patients.
abstract: BACKGROUND
  The duration, severity, and cause of hypotension after intravenous amiodarone has not been well characterized in anesthetized cardiac surgical patients. Because amiodarone is tolerated in patients with advanced cardiac disease, we hypothesized that left ventricular systolic performance is preserved despite hypotension during amiodarone loading.
  
  
  METHODS
  In a prospective double-blind trial, 30 patients undergoing coronary artery bypass graft (CABG) surgery were randomly assigned to receive intravenous amiodarone (n = 15) or placebo (n = 15). Cardiac output (CO), mixed venous oxygen saturation (SVO), arterial blood pressure (systolic blood pressure [SBP], diastolic blood pressure [DBP], mean arterial pressure [MAP]), pulmonary artery pressure, and central venous pressure (CVP) were recorded. Transesophageal echocardiographic left ventricular end-diastolic area (EDA), end-systolic area (ESA), fractional area change (FAC), and end-systolic wall stress (ESWS) were measured every 5 minutes.
  
  
  RESULTS
  Mean arterial pressure, SBP, and DBP decreased over time after drug administration in both groups (p < 0.05). At 6 minutes, amiodarone decreased the MAP by 14 mm Hg (p = 0.004) and placebo decreased the MAP by 4 mm Hg. The change in MAP, SBP, and DBP between groups was statistically different for the first 15 minutes after drug administration. Hypotension requiring intervention occurred in 3 of 15 after amiodarone and 0 of 15 after placebo (p = 0.22). The mean heart rate was 11.5 beats per minute less after amiodarone (p < 0.02), but pulmonary artery pressure, CVP, SVO, and FAC were not different between groups.
  
  
  CONCLUSIONS
  Intravenous amiodarone decreased heart rate and caused a significant, but transient decrease in arterial pressure in the first 15 minutes after administration. Left ventricular performance was maintained suggesting that selective arterial vasodilation was the primary cause of drug-induced hypotension.
authors.affiliation: Department of Anesthesiology, University of Pennsylvania, Philadelphia, Pennsylvania 19104-4283, USA. cheunga@uphs.upenn.edu
authors.forename: Albert T
authors.initials: AT
authors.lastname: Cheung
authors.forename: Stuart J
authors.initials: SJ
authors.lastname: Weiss
authors.forename: Joseph S
authors.initials: JS
authors.lastname: Savino
authors.forename: Warren J
authors.initials: WJ
authors.lastname: Levy
authors.forename: John G
authors.initials: JG
authors.lastname: Augoustides
authors.forename: Amy
authors.initials: A
authors.lastname: Harrington
authors.forename: Timothy J
authors.initials: TJ
authors.lastname: Gardner
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000638:Amiodarone / Q000008:administration & dosage*; D001795:Blood Pressure Determination; D002302:Cardiac Output; D001026:Coronary Artery Bypass / Q000379:methods*; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000601:surgery; D004305:Dose-Response Relationship, Drug; D004311:Double-Blind Method; D004334:Drug Administration Schedule; D017548:Echocardiography, Transesophageal; D005260:Female; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D007022:Hypotension / Q000175:diagnosis; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic; D010101:Oxygen Consumption / Q000502:physiology*; D011379:Prognosis; D011446:Prospective Studies; D012016:Reference Values; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D016896:Treatment Outcome; D014665:Vasodilator Agents / Q000008:administration & dosage*
chemical_list: D014665:Vasodilator Agents; D000638:Amiodarone