title: Detection of organ ischemia during hemorrhagic shock.
abstract: BACKGROUND
  In a porcine hemorrhagic shock model we aimed to determine: (a) whether blood flow to the intestine and kidney was more reduced than cardiac output; (b) whether parameters of anaerobic metabolism correlated with regional blood flow; and (c) whether metabolic parameters in intestine, kidney and skeletal muscles detected a compromised metabolic state at an earlier stage than did systemic parameters.
  
  
  METHODS
  In an animal research laboratory at a university hospital six domestic pigs were subjected to volume-controlled hemorrhage. Every 30 min samples of blood were withdrawn. Systemic and regional hemodynamic parameters and tissue levels of PCO2 were monitored. Whole body and organ-specific oxygen consumption (VO2) and veno-arterial (VA) differences of lactate, glucose, potassium (K+), PCO2, H+ and base excess (BE) were calculated every 30 min.
  
  
  RESULTS
  With progressive hemorrhage, intestinal blood flow decreased to the same extent as cardiac output, whereas the reduction in renal blood flow was more pronounced. We found a concomitant reduction in VO2 (onset of supply dependent metabolism) in intestine, kidney and skeletal muscles. In muscular tissue PCO2 increased to levels three times higher than baseline, while renal and intestinal PCO2 increased eightfold. Supply dependency was associated with a concomitant increase in VA CO2 and VA H+. Also, VA lactate increased, mostly in intestine and least in skeletal muscle. Intestinal and renal VA K+ increased, while muscular VA K+ decreased. Arterial lactate and H+ increased considerably, whereas arterial BE decreased.
  
  
  CONCLUSIONS
  With progressive hemorrhage, renal blood flow, but not intestinal and skeletal muscle blood flow, was reduced more than cardiac output. Supply dependent oxygen metabolism (VO2) and organ acidosis occurred simultaneously in the three organs, despite differences in blood flow reductions. Organ ischemia coincided with a pronounced change in arterial lactate and systemic acid base parameters.
authors.affiliation: Department of Anesthesiology, Rikshospitalet, University of Oslo, Norway.
authors.forename: G
authors.initials: G
authors.lastname: Kvarstein
authors.forename: P
authors.initials: P
authors.lastname: Mirtaheri
authors.forename: T I
authors.initials: TI
authors.lastname: Tønnessen
mesh_terms: D000136:Acid-Base Equilibrium / Q000502:physiology; D000138:Acidosis / Q000503:physiopathology; D000693:Anaerobiosis / Q000502:physiology; D000818:Animals; D001784:Blood Gas Analysis; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D004567:Electrodes, Implanted; D004594:Electrophysiology; D005260:Female; D006339:Heart Rate / Q000502:physiology; D007422:Intestines / Q000098:blood supply; D007511:Ischemia / Q000175:diagnosis* / Q000209:etiology*; D008297:Male; D018482:Muscle, Skeletal / Q000098:blood supply; D010101:Oxygen Consumption / Q000502:physiology; D012039:Regional Blood Flow / Q000502:physiology; D012079:Renal Circulation / Q000502:physiology; D012771:Shock, Hemorrhagic / Q000150:complications*; D013552:Swine