title: Increases in both buccal and sublingual partial pressure of carbon dioxide reflect decreases of tissue blood flows in a porcine model during hemorrhagic shock.
abstract: BACKGROUND
  Earlier studies had demonstrated that gastric partial pressure of carbon dioxide (PCO2) of the gastric wall is an early indication of perfusion failure. Because hypercarbia is a general phenomenon of perfusion failure, this study investigated whether sublingual and buccal mucosal tissue PCO2 also serve as a sensitive indicator of systemic blood flow during hemorrhagic shock.
  
  
  RESULTS
  Hemorrhagic shock was induced in five male domestic pigs. Buccal and sublingual PCO2 increased from 60 to 129 mm Hg (p < 0.01) in parallel with average decreases in cardiac output to 44% (from 6.1 to 2.8 L/minute; p < 0.01), and mean arterial pressure to 47% (from 115 to 57 mm Hg; p < 0.01), over the 2-hour interval of shock. According to colored microspheres used for measurements, buccal mucosal flow decreased to 35% (from 6.3 to 2.2 mL/minute/100 g; p < 0.01) in close parallel with sublingual blood flow, which decreased to 34% (from 7.2 to 2.5 mL/minute/100 g; p < 0.01). Liver flow decreased to 56% (from 152 to 85 mL/minute/100 g;p < 0.01), and renal flow to 47% (from 272 to 128 mL/minute/100 g;p < 0.01) of baseline values. The procedure yielded to overall comparable volume exchanges in different animals. After reinfusion of shed blood, buccal PCO2, like sublingual PCO2, was restored to approximately baseline values (respectively, from 56 to 71 mm Hg and from 60 to 71 mm Hg; p = not significant), together with arterial pressure, cardiac output, and end-tidal CO2 (EtCO2) (respectively, from 115 to 115 mm Hg, from 6.1 to 6.3 L/minute, and from 35 to 39 mm Hg; p = not significant), but there was delayed reversal of lactic acidosis (from 0.7 to 2.5 mmol/L;p < 0.01). In five unbled control animals, no significant changes were observed over the same interval.
  
  
  CONCLUSIONS
  The current study extends the rationale for noninvasive measurements to both buccal and sublingual mucosa for diagnosis and quantitation of hemorrhagic shock severity.
authors.affiliation: Institute of Critical Care Medicine, Rancho Mirage, California, USA.
authors.forename: Tommaso
authors.initials: T
authors.lastname: Pellis
authors.forename: Max Harry
authors.initials: MH
authors.lastname: Weil
authors.forename: Wanchun
authors.initials: W
authors.lastname: Tang
authors.forename: Shijie
authors.initials: S
authors.lastname: Sun
authors.forename: Peter
authors.initials: P
authors.lastname: Csapozi
authors.forename: Carlos
authors.initials: C
authors.lastname: Castillo
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002245:Carbon Dioxide / Q000378:metabolism*; D002302:Cardiac Output; D002610:Cheek / Q000502:physiology; D004195:Disease Models, Animal; D007668:Kidney / Q000098:blood supply; D019344:Lactic Acid / Q000097:blood; D008099:Liver / Q000098:blood supply; D008297:Male; D009061:Mouth Mucosa / Q000378:metabolism*; D010313:Partial Pressure; D012039:Regional Blood Flow; D012771:Shock, Hemorrhagic / Q000378:metabolism*; D013552:Swine
chemical_list: D002245:Carbon Dioxide; D019344:Lactic Acid