title: Model-based study of the effects of the hemodialysis technique on the compensatory response to hypovolemia.
abstract: BACKGROUND
  Hemodialysis technique (dialysate composition, filter, convection/diffusion ratio, etc.) can have an impact on the patient's tendency to acute hypotension. We have examined the hypothesis that the dialysis technique affects the hypotension risk by altering the cardiovascular compensatory response to hemodialysis-induced hypovolemia.
  
  
  METHODS
  Twelve hypotension-prone subjects were studied during six sessions of conventional bicarbonate dialysis (BD) and six sessions of acetate-free biofiltration (AFB). Blood volume (BV) control system was used in AFB to provide a BV change equivalent to the BV change observed in BD. The efficacy of reflex compensatory mechanisms was assessed by a model-based computer analysis of the BD and AFB sessions.
  
  
  RESULTS
  BD sessions were complicated by hypotension more frequently than the AFB ones (34/66 BD vs. 18/66 AFB). Hypotension arose about 60 minutes earlier in BD (123 +/- 41 minutes in BD vs. 183 +/- 25 minutes in AFB, P < 0.01), and after a smaller BV reduction (hypotension BV 7.9%+/- 2.0% in BD vs. 10.9%+/- 2.6% in AFB, P < 0.05). Model-based computer analysis of the sessions without hypotension revealed differences in peripheral resistance adaptation (9%+/- 9% BD vs. 19%+/- 7% AFB, P < 0.05) as well as in the stroke volume reduction (19%+/- 8% BD vs. 10%+/- 8% AFB, P < 0.001). Model analysis of sessions with hypotension indicated that compensatory mechanisms were almost inoperative in BD, whereas a residual capacity to control peripheral resistance and cardiac contractility was present in AFB. Model simulations demonstrated that hypotension occurred later in AFB since the residual compensatory capacity in AFB was able to sustain the arterial pressure for larger BV reductions (8.3% BD vs. 11.2% AFB).
  
  
  CONCLUSIONS
  The increased risk of acute hypotension in BD compared to AFB is caused by a therapy-induced inhibition of reflex compensatory response to hypovolemia.
authors.affiliation: Bioengineering Laboratory-DEIS, University of Bologna, Bologna, Italy. silvio.cavalcanti@unibo.it
authors.forename: Silvio
authors.initials: S
authors.lastname: Cavalcanti
authors.forename: Andrea
authors.initials: A
authors.lastname: Ciandrini
authors.forename: Stefano
authors.initials: S
authors.lastname: Severi
authors.forename: Fabio
authors.initials: F
authors.lastname: Badiali
authors.forename: Stefano
authors.initials: S
authors.lastname: Bini
authors.forename: Andrea
authors.initials: A
authors.lastname: Gattiani
authors.forename: Leonardo
authors.initials: L
authors.lastname: Cagnoli
authors.forename: Antonio
authors.initials: A
authors.lastname: Santoro
mesh_terms: D000222:Adaptation, Physiological; D000368:Aged; D000369:Aged, 80 and over; D001639:Bicarbonates / Q000009:adverse effects; D001794:Blood Pressure; D002319:Cardiovascular System / Q000503:physiopathology*; D003198:Computer Simulation; D018592:Cross-Over Studies; D005260:Female; D006339:Heart Rate; D017583:Hemodiafiltration / Q000009:adverse effects; D006801:Humans; D007022:Hypotension / Q000209:etiology; D020896:Hypovolemia / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D008955:Models, Cardiovascular; D009200:Myocardial Contraction; D011446:Prospective Studies; D006435:Renal Dialysis / Q000009:adverse effects / Q000379:methods*; D012306:Risk; D014655:Vascular Resistance
chemical_list: D001639:Bicarbonates