title: Small bolus of esmolol effectively prevents sodium nitroprusside-induced reflex tachycardia without adversely affecting blood pressure.
abstract: OBJECTIVE
  Hypotensive anesthesia with sodium nitroprusside (SNP) often is associated with reflex tachycardia. The purpose of this study was to investigate whether a small bolus of esmolol could counteract SNP-induced reflex tachycardia and sympathetic activation without affecting blood pressure.
  
  
  METHODS
  Using a time-series study design, 27 healthy young patients scheduled for mandibular osteotomy were enrolled in this study. General anesthesia was maintained with 2% sevoflurane and 67% nitrous oxide in oxygen. SNP was administered to decrease the mean arterial pressure to 55 to 65 mm Hg. When heart rate (HR) increased reflexively to higher than 95 beats/min from SNP-induced hypotension, esmolol 0.5 mg/kg was given. Blood pressure and HR were measured, and the low-frequency component (0.04 to 0.15 Hz) of systolic blood pressure variability and high-frequency component (0.15 to 0.4 Hz) of HR variability were calculated to evaluate the autonomic condition. Data were analyzed using 1-way analysis of variance after multiple comparisons or t test. P < .05 was considered statistically significant.
  
  
  RESULTS
  Of the 27 patients analyzed, 19 patients (70%) required esmolol. In these patients, SNP caused an increase in the low-frequency component of systolic blood pressure variability and a decrease in the high-frequency component of HR variability, leading to tachycardia (HR range, 95.9 ± 7.3 to 106.7 ± 7.4 beats/min; P < .001). Esmolol suppressed the effects of SNP on the low-frequency component of systolic blood pressure variability and high-frequency component of HR variability, resulting in an immediate decrease in HR to 86.9 ± 6.2 beats/min (P < .001), whereas mean arterial pressure remained unchanged.
  
  
  CONCLUSIONS
  A small bolus of esmolol can suppress reflex tachycardia without significantly changing mean arterial pressure. Thus, esmolol restores the autonomic imbalance induced by SNP during hypotensive anesthesia.
authors.affiliation: Department of Dental Anesthesiology, Osaka University Graduate School of Dentistry, Osaka, Japan. hanamoto@dent.osaka-u.ac.jp
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Hanamoto
authors.forename: Mitsutaka
authors.initials: M
authors.lastname: Sugimura
authors.forename: Yoshinari
authors.initials: Y
authors.lastname: Morimoto
authors.forename: Chiho
authors.initials: C
authors.lastname: Kudo
authors.forename: Aiji
authors.initials: A
authors.lastname: Boku
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Niwa
mesh_terms: D058671:Adrenergic beta-1 Receptor Antagonists / Q000008:administration & dosage*; D018685:Anesthetics, Inhalation / Q000008:administration & dosage; D001794:Blood Pressure / Q000187:drug effects*; D004562:Electrocardiography / Q000187:drug effects; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D007023:Hypotension, Controlled / Q000379:methods*; D008297:Male; D008334:Mandible / Q000601:surgery; D008738:Methyl Ethers / Q000008:administration & dosage; D009599:Nitroprusside / Q000009:adverse effects*; D009609:Nitrous Oxide / Q000008:administration & dosage; D010027:Osteotomy / Q000379:methods; D010100:Oxygen / Q000008:administration & dosage; D010275:Parasympathetic Nervous System / Q000187:drug effects; D011412:Propanolamines / Q000008:administration & dosage*; D000077149:Sevoflurane; D012815:Signal Processing, Computer-Assisted; D013564:Sympathetic Nervous System / Q000187:drug effects; D013610:Tachycardia / Q000517:prevention & control*; D013997:Time Factors; D014665:Vasodilator Agents / Q000009:adverse effects*; D055815:Young Adult
chemical_list: D058671:Adrenergic beta-1 Receptor Antagonists; D018685:Anesthetics, Inhalation; D008738:Methyl Ethers; D011412:Propanolamines; D014665:Vasodilator Agents; D009599:Nitroprusside; D000077149:Sevoflurane; D009609:Nitrous Oxide; C036604:esmolol; D010100:Oxygen