title: Increased oxygen consumption after cardiac surgery is associated with the inflammatory response to endotoxemia.
abstract: OBJECTIVE
  The aim of this study was to determine whether the increase in post-operative oxygen consumption (delta VO2) in cardiac surgery patients is related to endotoxemia and subsequent cytokine release and whether delta VO2 can be used as a parameter of post-perfusion syndrome.
  
  
  METHODS
  Prospective study.
  
  
  METHODS
  Operating room and intensive care unit of a university hospital.
  
  
  METHODS
  Twenty-one consecutive male patients undergoing elective coronary artery bypass surgery without major organ dysfunction and not receiving corticosteroids.
  
  
  RESULTS
  Plasma levels of endotoxin, tumor necrosis factor (TNF) and interleukin-6 (IL-6) were measured before, during and for 18 h after cardiac surgery. Oxygen consumption, haemodynamics, the use of IV fluids and dopamine, body temperature and the time of extubation were also measured. Measurements from patients with high delta VO2 (> or = median value of the entire group) were compared with measurements from patients with low delta VO2 (< median). Patients with high delta VO2 had higher levels of circulating endotoxin (P = 0.004), TNF (P = 0.04) and IL-6 (P = 0.009) received more IV fluids and dopamine while in the ICU, and were extubated later than patients with low delta VO2. Several hours after delta VO2 the patient's body temperature rose. Forward stepwise regression analysis showed that circulating endotoxin and TNF explained 50% of the variability of delta VO2.
  
  
  CONCLUSIONS
  This study demonstrates that patients with high post operative oxygen consumption after elective cardiac surgery have higher circulating levels of endotoxin, TNF and IL-6 and also have more symptoms of post-perfusion syndrome. Early detection of high VO2 might be used as a clinical signal to improve circulation in order to meet the high oxygen demand of inflammation. In addition, continuous measurement of VO2 provides us with a clinical parameter of inflammation in interventional studies aiming at a reduction of endotoxemia or circulating cytokines.
authors.affiliation: Intensive Care Department, Onze Lieve Vrouwe Gasthuis, Amsterdam, The Netherlands.
authors.forename: H M
authors.initials: HM
authors.lastname: Oudemans-van Straaten
authors.forename: P G
authors.initials: PG
authors.lastname: Jansen
authors.forename: H
authors.initials: H
authors.lastname: te Velthuis
authors.forename: I C
authors.initials: IC
authors.lastname: Beenakkers
authors.forename: C P
authors.initials: CP
authors.lastname: Stoutenbeek
authors.forename: S J
authors.initials: SJ
authors.lastname: van Deventer
authors.forename: A
authors.initials: A
authors.lastname: Sturk
authors.forename: L
authors.initials: L
authors.lastname: Eysman
authors.forename: C R
authors.initials: CR
authors.lastname: Wildevuur
mesh_terms: D000328:Adult; D001026:Coronary Artery Bypass; D004731:Endotoxins / Q000097:blood*; D006801:Humans; D015850:Interleukin-6 / Q000097:blood; D008297:Male; D010101:Oxygen Consumption / Q000276:immunology* / Q000502:physiology; D011183:Postoperative Complications / Q000209:etiology*; D011446:Prospective Studies; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology*; D014115:Toxemia / Q000150:complications; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D004731:Endotoxins; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha