Gastric and esophageal intramucosal PCO2 (PiCO2) during endotoxemia: assessment of raw PiCO2 and PCO2 gradients as indicators of hypoperfusion in a canine model of septic shock.

STUDY OBJECTIVES: To validate capnometric recirculating gas tonometry (CRGT) for continuously monitoring gut intramucosal PCO2 (PiCO2) in a septic shock model, and to compare gastric vs esophageal PCO2 vs intramucosal-arterial PCO2 gradients. INTERVENTIONS: CRTG catheters were placed in the stomach and esophagus of six anesthetized dogs. A saline solution filled balloon tonometry (ST) catheter was also placed in the stomach. After equilibration, 3 mg/kg Escherichia coli lipopolysaccharide (LPS) was administered IV. PiCO2 measurements were made at 0, 45, and 90 min post-LPS by ST and continuously by CRGT. RESULTS: Baseline PiCO2 was 41.5+/-1.9 (+/-SE) in the stomach by CRGT, 38.0+/-1.0 by ST, and 43.0+/-4.4 mm Hg in the esophagus (p=not significant). Gastric PiCO2 by CRGT increased to 47.0+/-2.4 mm Hg by 25 min post-LPS (p<0.05), whereas gastric (ST) and esophageal PiCO2 increased significantly by 45 min post-LPS. Good agreement was observed between gastric CRGT and ST measurements (mean bias, 1.3 mm Hg). The PiCO2-PaCO2 gradient increased post-LPS, but was significant only for gastric CRGT measurements 90 min post-LPS infusion. CONCLUSION: CRGT provided continuous gastric PiCO2 measurements that were in close agreement with ST but detected changes earlier than the conventional technique. Continuous esophageal PiCO2 represents a valid alternative for assessing gastric PiCO2.

Relationship between systemic oxygen supply dependency and gastric intramucosal PCO2 during progressive hemorrhage.

BACKGROUND: As systemic oxygen delivery (DO2) is reduced, oxygen consumption (VO2) is maintained until a critical level is reached (DO2crit) below which VO2 becomes supply-dependent and anaerobic metabolism ensues. We examined the relationship between gastric intramucosal PCO2 (PiCO2) and the onset of systemic supply dependency. We also compared PiCO2 to mixed venous and portal venous blood PCO2 (PmvCO2 and PpvCO2) to assess their utility as premonitory indicators of supply dependency. METHODS: Six dogs were subjected to stepwise hemorrhage to effect a progressive decrease in DO2. Inflection points for changes in VO2, PiCO2, PmvCO2, and PpvCO2 versus DO2 were determined. RESULTS: Mean DO2crit was 6.0 +/- 0.7 mL x kg(-1) x min(-1), whereas the DO2 at which inflection points occurred for PiCO2 and PpvCO2 were 13.2 +/- 1.4 and 11.2 +/- 1.5 mL x kg(-1) x min(-1), respectively (p < 0.05 for both). CONCLUSION: Continuous monitoring of PiCO2 using capnometric recirculating gas tonometry can serve as an early indicator of systemic hypoperfusion before the onset of systemic supply dependency.

End-tidal partial pressure of carbon dioxide as a noninvasive indicator of systemic oxygen supply dependency during hemorrhagic shock and resuscitation.

When oxygen delivery (DO2) critically decreases, oxygen consumption (VO2) becomes supply dependent. We examined whether end-tidal PCO2 (PetCO2) would identify supply dependency during shock. Five dogs (Group I) underwent progressive hemorrhage to decrease DO2 until they could no longer maintain a stable blood pressure. Five additional animals (Group II) were bled until VO2 decreased to 70% of baseline, followed by resuscitation. The PetCO2 versus time inflection point was compared with the DO2 at onset of supply dependency (DO2crit). DO2crit for Groups I and II were 6.9 +/- .4 and 8.1 +/- 1.3, respectively (p = NS), and not statistically different from the DO2 values at which PetCO2 decreased (6.6 +/- .7 and 6.3 +/- .7 mL/kg per min, respectively). AT constant minute volume, PetCO2 effectively indicated the onset of supply dependency and rapidly increased during resuscitation, paralleling the changes in VO2 in this model of hemorrhagic shock.