title: Parasympathetic activity in brain death: effect of apnea on heart rate variability.
abstract: BACKGROUND
  Power spectral analysis of heart rate variability is a useful monitoring of brain-damaged patients. However, the effect of artificial ventilation is not clearly demonstrated in assessing vagal activity because the locus of its activity is originated close to the respiratory center in the brain stem. We studied heart rate variability during artificial ventilation and apnea test as part of an assessment of brain death.
  
  
  METHODS
  Ten adult patients with severe brain damage were studied. Power spectral analysis of heart rate variability from electrocardiographic R-R intervals was integrated to compare spectral components before, during and after the apnea test. Before the test, circulatory and blood gas variables and electrocardiographic recording were obtained under controlled mechanical ventilation at a rate of 12 and 18 (/min), each for 5 min. Measurements were made for 10 min during the apnea test, and repeated thereafter as before the test. Power spectral analysis based on fast Fourier transformation was made by integrating each low- (LF: 0.04-0.15 Hz) and high- (HF: 0.15-0.40 Hz) frequency band areas. LF was assessed as sympathetic and parasympathetic nervous activity, and HF as respiratory-related parasympathetic vagal activity. The HF/LF ratio showed sympathovagal balance.
  
  
  RESULTS
  All patients were assessed as brain dead. During apnea, PaCO2 (P<0.01) and LF (P<0.05) increased, and pH (P<0.01) and HF/LF ratio (P<0.05) decreased. Heart rate, mean arterial pressure, PaO2 and HF remained consistent throughout.
  
  
  CONCLUSIONS
  It was shown that sympathovagal balance was inclined to be sympathotonic during apnea, and that there were no changes in the respiratory-related vagal activity in spite of stopping artificial ventilation.
authors.affiliation: Department of Anesthesiology and Critical Care, Hiroshima University Hospital, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Kawamoto
authors.forename: A
authors.initials: A
authors.lastname: Sera
authors.forename: K
authors.initials: K
authors.lastname: Kaneko
authors.forename: O
authors.initials: O
authors.lastname: Yuge
authors.forename: M
authors.initials: M
authors.lastname: Ohtani
mesh_terms: D000293:Adolescent; D000328:Adult; D001049:Apnea / Q000503:physiopathology*; D001775:Blood Circulation / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology; D001925:Brain Damage, Chronic / Q000503:physiopathology; D001926:Brain Death / Q000503:physiopathology*; D001933:Brain Stem / Q000503:physiopathology; D002245:Carbon Dioxide / Q000097:blood; D004562:Electrocardiography; D005260:Female; D005583:Fourier Analysis; D006329:Heart Conduction System / Q000503:physiopathology*; D006339:Heart Rate / Q000502:physiology*; D006801:Humans; D006863:Hydrogen-Ion Concentration; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic; D010100:Oxygen / Q000097:blood; D010275:Parasympathetic Nervous System / Q000503:physiopathology*; D012121:Respiration, Artificial; D012125:Respiratory Center / Q000503:physiopathology; D012815:Signal Processing, Computer-Assisted; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014630:Vagus Nerve / Q000503:physiopathology
chemical_list: D002245:Carbon Dioxide; D010100:Oxygen