title: Plasminogen activator inhibitor activity is associated with raised lactate levels after cardiac surgery with cardiopulmonary bypass.
abstract: OBJECTIVE
  To investigate the pathophysiology underlying raised lactate levels after cardiac surgery with cardiopulmonary bypass (CPB).
  
  
  METHODS
  Prospective observational study.
  
  
  METHODS
  Medical and surgical intensive care unit of a tertiary hospital.
  
  
  METHODS
  A total of 40 patients undergoing first-time coronary artery bypass grafting with CPB.
  
  
  METHODS
  The prothrombotic response to cardiac surgery with CPB was assessed by measuring plasma levels of prothrombin fragment 1 + 2 and plasminogen activator inhibitor (PAI) activity. The hemodynamic responses to cardiac surgery with CPB were also measured using standard techniques.
  
  
  RESULTS
  After cardiac surgery, prothrombin fragment 1 + 2 levels increased 6-fold and PAI activity increase 2- to 3-fold (p <.0001). Lactate levels were not associated with prothrombin fragment 1 + 2 and PAI activity levels after CPB. Lactate levels were associated with baseline PAI activity (p =.006), a history of hypertension (p =.02), raised baseline lactate levels (p =.02), an early increase in body temperature after CPB (p =.05), a late increase in oxygen consumption after CPB (p =.03), and a raised white cell count after CPB (p =.06). Lactate levels were inversely associated with the maximum activated clotting time level reached during CPB (p =.02). Multivariate linear regression demonstrated lactate levels were independently associated with baseline PAI activity.
  
  
  CONCLUSIONS
  We found cardiac surgery with CPB was associated with a marked prothrombotic response. Lactate levels were associated with elevated baseline PAI activity and evidence of an amplified inflammatory response to cardiac surgery with CPB. Our findings implicate aspects of the inflammatory response, including microvascular thrombosis, in the development of raised lactate levels after cardiac surgery with CPB.
authors.affiliation: Intensive Care Centre, St. Vincent's Hospital, St. Vincent's Institute of Medical Research, Fitzroy, Australia.
authors.forename: Barry
authors.initials: B
authors.lastname: Dixon
authors.forename: John D
authors.initials: JD
authors.lastname: Santamaria
authors.forename: Duncan J
authors.initials: DJ
authors.lastname: Campbell
mesh_terms: D000368:Aged; D001831:Body Temperature; D002315:Cardiopulmonary Bypass / Q000009:adverse effects; D001026:Coronary Artery Bypass / Q000009:adverse effects; D005260:Female; D006801:Humans; D019344:Lactic Acid / Q000097:blood*; D007958:Leukocyte Count; D008297:Male; D010101:Oxygen Consumption; D010446:Peptide Fragments / Q000097:blood; D015849:Plasminogen Inactivators / Q000097:blood*; D011498:Protein Precursors / Q000097:blood; D011516:Prothrombin; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology; D014914:Whole Blood Coagulation Time
chemical_list: D010446:Peptide Fragments; D015849:Plasminogen Inactivators; D011498:Protein Precursors; D019344:Lactic Acid; C029733:prothrombin fragment 1; C044183:prothrombin fragment 2; D011516:Prothrombin