title: Blood pressure and sympathetic nerve tone relation during hemodialysis may reflect cardiovascular dysfunction.
abstract: BACKGROUND
  The blood pressure response to the rapid removal of fluid during hemodialysis is complex and the pathophysiological mechanisms underlying intradialytic hypotension are not clear and sometimes these mechanisms render dialysis difficult to continue.
  
  
  OBJECTIVE
  We analyzed the changes in blood pressure and sympathetic nerve tone and attempted to clarify whether the dynamic pattern of this relationship reflects cardiovascular dysfunction.
  
  
  METHODS
  The dynamic pattern of sympathetic nerve activity throughout dialysis was analyzed by frequency analysis of RR intervals recorded by 24 hours Holter electrocardiography in 64 patients and 3 minutes ECG every 15 minutes during dialysis in 121 stable end-stage renal failure patients who underwent maintenance hemodialysis. Blood pressure and fluid volume removed was measured every 15-30 minutes during dialysis and the average value of the ratio of low to high frequency components (LF/HF) was calculated as an index of sympathetic nerve tone. The relationship between removed fluid volume, systolic blood pressure (Bp) and LF/HF was analyzed.
  
  
  RESULTS
  The patients were classified into 3 groups based on the correlation between the LF/HF and Bp as follows: positive (52 cases), inverse (54 cases), and not significant (NS; 61 cases). Eighteen patients who showed multiple arrhythmias, atrial fibrillation and other artifacts or noises were eliminated as they were inadequate for frequency analysis of RR intervals. The positive group was characterized by a hypotension-resistant response with a low LF/HF, whereas the inverse group was characterized by a hypotension-prone response with high LF/HF. These results suggest that cardiovascular dysfunction is responsible for the inverse correlation.
  
  
  CONCLUSIONS
  Analysis of the relationship between sympathetic nerve tone and Bp is effective in predicting the existing of cardiovascular dysfunction.
authors.affiliation: Kohjinkai Kimachi Hospital, Japan. ino-oka@koujinkai-med.or.jp
authors.forename: Eiji
authors.initials: E
authors.lastname: Ino-Oka
authors.forename: Jyun
authors.initials: J
authors.lastname: Urae
authors.forename: Makoto
authors.initials: M
authors.lastname: Sekino
authors.forename: Masatsugu
authors.initials: M
authors.lastname: Satoh
authors.forename: Kazuhisa
authors.initials: K
authors.lastname: Takeuchi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Sekino
authors.forename: Yasuaki
authors.initials: Y
authors.lastname: Ohtaki
authors.forename: Hikaru
authors.initials: H
authors.lastname: Inooka
mesh_terms: D000368:Aged; D001794:Blood Pressure / Q000502:physiology*; D001810:Blood Volume; D002319:Cardiovascular System / Q000503:physiopathology*; D015716:Electrocardiography, Ambulatory; D005260:Female; D006801:Humans; D007022:Hypotension / Q000209:etiology / Q000503:physiopathology; D007676:Kidney Failure, Chronic / Q000503:physiopathology / Q000628:therapy; D008297:Male; D008875:Middle Aged; D006435:Renal Dialysis / Q000009:adverse effects*; D013564:Sympathetic Nervous System / Q000503:physiopathology*