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Metabolic, cardiovascular, and acid‐base status after hepatic artery or portal vein reperfusion during orthotopic liver transplantation
Author(s) -
Walsh Timothy S.,
Garden O. James,
Lee Alistair
Publication year - 2002
Publication title -
liver transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.814
H-Index - 150
eISSN - 1527-6473
pISSN - 1527-6465
DOI - 10.1053/jlts.2002.33481
Subject(s) - medicine , liver transplantation , transplantation , artery , cardiology , portal venous pressure , cardiac index , anesthesia , vein , hemodynamics , surgery , cardiac output , portal hypertension , cirrhosis
During liver transplantation, reperfusion traditionally is performed through the portal vein. After anecdotal observations that patients who underwent reperfusion first through the hepatic artery were more hemodynamically stable, we performed an exploratory, prospective, observational, nonrandomized study to compare cardiovascular stability, acid‐base status, and metabolic gas exchange between patients who underwent reperfusion through either the portal vein or hepatic artery. We studied 20 patients undergoing liver transplantation (10 patients, reperfusion first through the portal vein; 10 patients, reperfusion first through the hepatic artery). Cardiovascular and acid‐base parameters were compared at times before and after anastomosis of each vessel, and epinephrine use was recorded. Oxygen consumption (V O 2 ) and carbon dioxide elimination (V CO 2 ) were measured continuously by using an indirect calorimeter. Alanine aminotransferase (ALT) concentrations 24 hours after transplantation were compared as an index of reperfusion injury. Cardiovascular changes (mean arterial pressure, cardiac output) were similar for both groups, but more epinephrine was administered to the portal‐vein group ( P = .014). There was a greater increase in Pa CO 2 after portal reperfusion (median portal vein, 1.01 kPa; hepatic artery, 0.29 kPa; P = .015) and a trend toward more severe acidemia. V O 2 increased more rapidly in the portal‐vein group ( P = .005), but overall changes in V O 2 during the study period were similar. There were no differences in V CO 2 between the groups or ALT concentrations 24 hours posttransplantation. These observational data suggest that hepatic arterial reperfusion may be associated with reduced epinephrine requirements and a slower rate of acid release, which could be advantageous in unstable patients. V O 2 increases more slowly after hepatic artery reperfusion, which could indicate slower reoxygenation of the graft. Further studies of the relative merits of each technique are warranted.