McKinley B A, Butler B D
Department of Anesthesiology, University of Texas-Houston Medical School, Houston 77030, USA.
Crit Care Med. 1999 Sep;27(9):1869-77. doi: 10.1097/00003246-199909000-00027.
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.
Prospective, controlled observational study in an acute experimental preparation.
Physiology laboratory in a university medical school.
Nine mongrel dogs (20 to 35 kg).
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.
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.
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.
使用光纤传感器监测出血、休克及复苏过程中骨骼肌间质内的氧分压(PmO2)、二氧化碳分压(PmCO2)和pH值(pHm),并比较通过胃二氧化碳张力测定法获得的胃黏膜间质内的二氧化碳分压(PrCO2)和pH值(pHi)。
在急性实验制剂中进行的前瞻性对照观察研究。
大学医学院的生理学实验室。
9只杂种犬(20至35千克)。
用戊巴比妥(25毫克/千克静脉注射)诱导麻醉,并在失血性休克后维持(10毫克/小时)。建立机械通气以维持基线动脉血二氧化碳分压(PaCO2)约35托。放置动脉、静脉和肺动脉导管。在右股动脉和静脉周围放置血流探头。将一个带有光纤氧分压、二氧化碳分压和pH传感器的探头(直径0.5毫米)经皮放置在右大腿内收肌中。将胃张力测定导管放置在胃腔内。在收集基线数据后,将平均动脉压(MAP)控制在45至 50毫米汞柱进行控制性出血1小时。然后回输流出的血液。在休克和回输过程中,每隔30分钟收集一次血气、血流动力学和胃张力测定数据,回输后每小时收集一次,共收集4小时。维持正常体温。
MAP达到45毫米汞柱后15分钟内,PmO2迅速从42±13托降至13±9托,30分钟内降至6±4托,回输后恢复至基线水平。pHm在1小时的休克期内从7.23±0.09逐渐降至6.89±0.25,回输后缓慢回升至基线水平。pHi从7.43±0.14降至6.91±0.23,平均在回输后2小时恢复至基线水平。PmCO2从50±12升至113±49托,回输过程中进一步升至124±73托,回输后缓慢恢复至基线水平。PrCO2从35±8升至60±19托,回输后15分钟内恢复至基线水平。在休克和回输过程中,氧输送、混合静脉血氧分压、混合静脉血氧饱和度和PmO2的变化时间过程相似。回输后,平均而言,PmO2超过基线PmO2和混合静脉血氧分压,氧供超过需求,提示存在氧消耗缺陷。平均而言,回输后4小时PmCO2和pHm未恢复至基线值,提示骨骼肌中无氧代谢效应持续存在,时间超过恢复基线MAP、血流速度、氧输送、PrCO2和pHi所需的相对较短时间。
使用光纤传感器在经皮放置的单个小探头中同时监测PmO2、PmCO2和pHm,与传统的全身或胃张力测定变量相比,似乎表明休克的严重程度更高,复苏时间更长。