title: Skeletal muscle acidosis correlates with the severity of blood volume loss during shock and resuscitation.
abstract: BACKGROUND
  Continuous assessment of tissue perfusion and oxygen utilization may allow for early recognition and correction of hemorrhagic shock. We hypothesized that continuously monitoring skeletal muscle (SM) PO2, PCO2, and pH during shock would provide an easily accessible method for assessing the severity of blood loss and the efficacy of resuscitation.
  
  
  METHODS
  Thirteen anesthetized pigs (25-35 kg) underwent laparotomy and femoral vessel cannulation. Multiparameter fiberoptic sensors were placed in the deltoid (SM) and femoral artery. Ventilation was maintained at a PaCO2 of 40-45 mm Hg. Total blood volume (TBV) was measured using an Evans blue dye technique. Animals were bled for 15 minutes, maintained at a mean arterial pressure (MAP) of 40 mm Hg for 1 hour, resuscitated (shed blood + 2 times shed volume in normal saline) and observed for 1 hour. Four animals served as controls (sham hemorrhage). Blood and tissue samples were taken at each time point.
  
  
  RESULTS
  Blood loss ranged from 28.5-56% of TBV. SM pH and SM PO2 levels fell rapidly with shock. SM PO2 returned to normal with resuscitation; however, SM pH did not return to baseline. SM PCO2 significantly rose with shock, but returned to baseline promptly with resuscitation. There was a significant correlation between SM pH and blood volume loss at end shock (r2 = 0.73, p < 0.001) and recovery (r2 = 0.84, p < 0.001). Animals (n = 2) whose SM pH did not recover to 7.2 were found to have ongoing blood loss from biopsy sites and persistent tissue hypercarbia despite normal MAP.
  
  
  CONCLUSIONS
  Continuous multiparameter monitoring of SM provides a minimally invasive method for assessing severity of shock and efficacy of resuscitation. Both PCO2 and PO2 levels change rapidly with shock and resuscitation. SM pH is directly proportional to lost blood volume. Persistent SM acidosis (pH < 7.2) and elevated PCO2 levels suggest incomplete resuscitation despite normalized hemodynamics.
authors.affiliation: Harvard Center for Minimally Invasive Surgery, Brigham and Women's Hospital, Boston, Massachusetts, USA.
authors.forename: C
authors.initials: C
authors.lastname: Sims
authors.forename: P
authors.initials: P
authors.lastname: Seigne
authors.forename: M
authors.initials: M
authors.lastname: Menconi
authors.forename: J
authors.initials: J
authors.lastname: Monarca
authors.forename: C
authors.initials: C
authors.lastname: Barlow
authors.forename: J
authors.initials: J
authors.lastname: Pettit
authors.forename: J C
authors.initials: JC
authors.lastname: Puyana
mesh_terms: D000140:Acidosis, Lactic / Q000503:physiopathology*; D000818:Animals; D001810:Blood Volume; D004195:Disease Models, Animal; D005440:Fluid Therapy; D006863:Hydrogen-Ion Concentration; D008297:Male; D008991:Monitoring, Physiologic / Q000379:methods; D018482:Muscle, Skeletal / Q000503:physiopathology; D012720:Severity of Illness Index; D012769:Shock / Q000503:physiopathology* / Q000628:therapy*; D013552:Swine