title: Effects of increasing blood hemoglobin levels on systemic hemodynamics of acutely anemic cirrhotic patients.
abstract: OBJECTIVE
  In experimental portal hypertension, blood hemoglobin levels have been shown to influence the hyperdynamic circulatory state. The aim of this study was to assess the hemodynamic effects of increasing hemoglobin concentration in human portal hypertension.
  
  
  METHODS
  Sixteen cirrhotic patients recovering from a variceal bleeding episode were randomly assigned to receive two units of packed red cells or 500 ml of a protein solution. Systemic and portal hemodynamics, and rheological and hormonal parameters were measured at baseline and after expansion.
  
  
  RESULTS
  Both groups were similar with respect to the degree of liver failure, severity of the bleeding episode, activation of the endogenous vasopressor systems, and hemodynamic parameters. The administration of either erythrocytes or a protein solution prompted a similar increase in total blood volume and suppression of vasopressor systems. Both groups of patients experienced similar increases in wedged hepatic venous pressure. Hepatic venous pressure gradient was not significantly modified but tended to increase in erythrocyte-transfused patients. Cardiopulmonary pressures increased, but this increment was significant in the non-blood-transfused patients only. Cardiac output decreased in erythrocyte-transfused patients, while it increased in the group receiving a protein solution. Red blood cell transfusion resulted in an increase in systemic vascular hindrance (resistance/blood viscosity), whereas the administration of a protein solution prompted a decrease in this parameter, thus reflecting true vasoconstriction and vasodilation, respectively.
  
  
  CONCLUSIONS
  An increase in blood hemoglobin in acutely anemic cirrhotic patients attenuates their hyperdynamic circulation beyond viscosity-dependent changes, an effect which might be counteracted by the effects on portal venous pressure gradient.
authors.affiliation: Gastroenterology Department, Institut Clínic de Malalties Digestives, Hospital Clínic, Universitat de Barcelona, Spain.
authors.forename: J I
authors.initials: JI
authors.lastname: Elizalde
authors.forename: E
authors.initials: E
authors.lastname: Moitinho
authors.forename: J C
authors.initials: JC
authors.lastname: García-Pagán
authors.forename: I
authors.initials: I
authors.lastname: Cirera
authors.forename: A
authors.initials: A
authors.lastname: Escorsell
authors.forename: J C
authors.initials: JC
authors.lastname: Bandi
authors.forename: W
authors.initials: W
authors.lastname: Jiménez
authors.forename: J
authors.initials: J
authors.lastname: Bosch
authors.forename: J M
authors.initials: JM
authors.lastname: Piqué
authors.forename: J
authors.initials: J
authors.lastname: Rodés
mesh_terms: D000368:Aged; D001810:Blood Volume; D017707:Erythrocyte Transfusion; D004932:Esophageal and Gastric Varices; D005260:Female; D006471:Gastrointestinal Hemorrhage / Q000097:blood* / Q000209:etiology / Q000628:therapy; D006439:Hemodynamics; D006454:Hemoglobins / Q000378:metabolism*; D006801:Humans; D008103:Liver Cirrhosis / Q000150:complications*; D008297:Male; D008875:Middle Aged
chemical_list: D006454:Hemoglobins