B A McKinley1, B D Butler. 1. Department of Anesthesiology, University of Texas-Houston Medical School, Houston 77030, USA.
Abstract
OBJECTIVES: To monitor PO2, PCO2, and pH in the interstitium of skeletal muscle (PmO2, PmCO2, and pHm) during hemorrhage, shock, and resuscitation using fiber-optic sensors and to compare Pco2 and pH in the interstitium of gastric mucosa (PrCO2 and pHi) obtained using gastric CO2 tonometry. DESIGN: Prospective, controlled observational study in an acute experimental preparation. SETTING: Physiology laboratory in a university medical school. SUBJECTS: Nine mongrel dogs (20 to 35 kg). INTERVENTIONS: Anesthesia was induced with pentobarbital (25 mg/kg iv) and maintained (10 mg/hr) after hemorrhagic shock. Mechanical ventilation was established to maintain baseline PaCO2 approximately 35 torr. Arterial, venous, and pulmonary artery catheters were placed. Blood flow probes were placed around the right femoral artery and vein. A probe (0.5 mm in diameter) with fiber-optic PO2, PCO2, and pH sensors was placed percutaneously in the adductor muscle of the right thigh. A gastric tonometer catheter was placed in the stomach lumen. After baseline data collection, controlled hemorrhage to mean arterial pressure (MAP) of 45 to 50 mm Hg was maintained for 1 hr. Shed blood was then reinfused. Blood gas, hemodynamic, and gastric tonometric data were collected during shock and reinfusion at 30-min intervals and hourly after reinfusion for 4 hrs. Normothermia was maintained. MEASUREMENTS AND MAIN RESULTS: PmO2 decreased rapidly from 42 +/- 13 torr (mean +/- sD) to 13 +/- 9 torr within 15 mins and to 6 +/-4 torr within 30 mins of MAP reaching 45 mm Hg, and it recovered to baseline with reinfusion. pHm decreased gradually from 7.23 +/-0.09 to 6.89 +/- 0.25 during the 1-hr shock period and increased slowly toward baseline after reinfusion. pHi decreased from 7.43 +/- 0.14 to 6.91 +/- 0.23, and on average it returned to baseline 2 hrs after reinfusion. PmCO2 increased from 50 +/- 12 to 113 +/- 49 torr, increased further to 124 +/- 73 torr during reinfusion, and returned slowly toward baseline after reinfusion. PrCO2 increased from 35 +/- 8 to 60 +/- 19 torr and returned to baseline within 15 mins after reinfusion. During shock and reinfusion, oxygen delivery, mixed venous PO2, mixed venous oxygen saturation, and PmO2 responded with similar time courses. After reinfusion, on average, PmO2 exceeded baseline PmO2 and mixed venous PO2, and oxygen availability exceeded demand, suggesting an oxygen consumption defect. On average, PmCO2 and pHm did not return to baseline values 4 hrs after reinfusion, suggesting the persistence of anaerobic metabolic effects in skeletal muscle beyond the relatively short time that is required to reestablish baseline MAP, blood flow rates, oxygen delivery, PrCO2, and pHi. CONCLUSIONS: PmO2, PmCO2, and pHm, monitored simultaneously using fiber-optic sensors in a single, small probe placed percutaneously, appear to indicate greater severity of shock and more prolonged resuscitation than conventional systemic or gastric tonometric variables.
OBJECTIVES: To monitor PO2, PCO2, and pH in the interstitium of skeletal muscle (PmO2, PmCO2, and pHm) during hemorrhage, shock, and resuscitation using fiber-optic sensors and to compare Pco2 and pH in the interstitium of gastric mucosa (PrCO2 and pHi) obtained using gastric CO2 tonometry. DESIGN: Prospective, controlled observational study in an acute experimental preparation. SETTING: Physiology laboratory in a university medical school. SUBJECTS: Nine mongrel dogs (20 to 35 kg). INTERVENTIONS: Anesthesia was induced with pentobarbital (25 mg/kg iv) and maintained (10 mg/hr) after hemorrhagic shock. Mechanical ventilation was established to maintain baseline PaCO2 approximately 35 torr. Arterial, venous, and pulmonary artery catheters were placed. Blood flow probes were placed around the right femoral artery and vein. A probe (0.5 mm in diameter) with fiber-optic PO2, PCO2, and pH sensors was placed percutaneously in the adductor muscle of the right thigh. A gastric tonometer catheter was placed in the stomach lumen. After baseline data collection, controlled hemorrhage to mean arterial pressure (MAP) of 45 to 50 mm Hg was maintained for 1 hr. Shed blood was then reinfused. Blood gas, hemodynamic, and gastric tonometric data were collected during shock and reinfusion at 30-min intervals and hourly after reinfusion for 4 hrs. Normothermia was maintained. MEASUREMENTS AND MAIN RESULTS:PmO2 decreased rapidly from 42 +/- 13 torr (mean +/- sD) to 13 +/- 9 torr within 15 mins and to 6 +/-4 torr within 30 mins of MAP reaching 45 mm Hg, and it recovered to baseline with reinfusion. pHm decreased gradually from 7.23 +/-0.09 to 6.89 +/- 0.25 during the 1-hr shock period and increased slowly toward baseline after reinfusion. pHi decreased from 7.43 +/- 0.14 to 6.91 +/- 0.23, and on average it returned to baseline 2 hrs after reinfusion. PmCO2 increased from 50 +/- 12 to 113 +/- 49 torr, increased further to 124 +/- 73 torr during reinfusion, and returned slowly toward baseline after reinfusion. PrCO2 increased from 35 +/- 8 to 60 +/- 19 torr and returned to baseline within 15 mins after reinfusion. During shock and reinfusion, oxygen delivery, mixed venous PO2, mixed venous oxygen saturation, and PmO2 responded with similar time courses. After reinfusion, on average, PmO2 exceeded baseline PmO2 and mixed venous PO2, and oxygen availability exceeded demand, suggesting an oxygen consumption defect. On average, PmCO2 and pHm did not return to baseline values 4 hrs after reinfusion, suggesting the persistence of anaerobic metabolic effects in skeletal muscle beyond the relatively short time that is required to reestablish baseline MAP, blood flow rates, oxygen delivery, PrCO2, and pHi. CONCLUSIONS:PmO2, PmCO2, and pHm, monitored simultaneously using fiber-optic sensors in a single, small probe placed percutaneously, appear to indicate greater severity of shock and more prolonged resuscitation than conventional systemic or gastric tonometric variables.