title: Systemic vascular resistance during high-volume plasmapheresis in patients with fulminant hepatic failure: relationship with oxygen consumption.
abstract: BACKGROUND
  In patients with fulminant hepatic failure, systemic vascular resistance and blood pressure are often reduced.
  
  
  OBJECTIVE
  To determine whether systemic vascular resistance increases during high-volume plasmapheresis, which is assumed to eliminate endogenous vasodilatory substances from the bloodstream.
  
  
  METHODS
  A prospective study.
  
  
  METHODS
  Ten patients [median age 48 (range 21-53) years] were admitted for liver transplantation. Systemic haemodynamic variables were determined using a catheter in a radial artery and a thermodilution catheter placed in a pulmonary artery. Ten (range 8-15) litres of fresh frozen plasma were exchanged, while body temperature [37.6 (range 36.6-38.4) degrees C], blood partial pressure of carbon dioxide [3.75 (range 3.30-4.50) kPa] and peak inspiratory ventilatory pressure [24 (range 20-26) mmHg] were kept constant.
  
  
  RESULTS
  Mean arterial pressure increased from 74 (range 61-110) to 96 (range 68-103) mmHg and cardiac index decreased from 5.2 (range 3.6-7.5) to 4.2 (range 3.4-6.6) l/min/m2. The systemic vascular resistance index increased from 662 (range 430-1270) to 1060 (range 621-1520) dyn s/cm5/m2. In contrast, the pulmonary vascular resistance index [42 (range 20-110) dyn s/cm5/m2) remained constant. As cardiac index decreased, oxygen delivery decreased from 939 (range 680-1496) to 745 (range 601-1189) ml/min/m2 with no effect on oxygen consumption [171 (87-231) ml/min/m2], as the arteriovenous oxygen extraction ratio increased from 17 (range 9-22) to 25 (range 8-31)% (P < 0.02).
  
  
  CONCLUSIONS
  In patients with fulminant hepatic failure, cardiac output, systemic vascular resistance and arterial blood pressure improved during high-volume plasmapheresis.
authors.affiliation: Department of Hepatology, Rigshospitalet, University of Copenhagen, Denmark.
authors.forename: F S
authors.initials: FS
authors.lastname: Larsen
authors.forename: E
authors.initials: E
authors.lastname: Ejlersen
authors.forename: B A
authors.initials: BA
authors.lastname: Hansen
authors.forename: T
authors.initials: T
authors.lastname: Mogensen
authors.forename: N
authors.initials: N
authors.lastname: Tygstrup
authors.forename: N H
authors.initials: NH
authors.lastname: Secher
mesh_terms: D000208:Acute Disease; D000328:Adult; D005260:Female; D006439:Hemodynamics; D006501:Hepatic Encephalopathy / Q000378:metabolism / Q000503:physiopathology* / Q000628:therapy; D006801:Humans; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption / Q000502:physiology*; D010956:Plasmapheresis; D011446:Prospective Studies; D014655:Vascular Resistance / Q000502:physiology*