Fandino J, Stocker R, Prokop S, Imhof H G
Department of Neurosurgery, University Hospital of Zurich, Switzerland.
Acta Neurochir (Wien). 1999;141(8):825-34. doi: 10.1007/s007010050383.
To correlate the jugular bulb oxygen saturation (SjvO2) and brain tissue oxygen pressure (PbtO2) during carbon dioxide (CO2) and oxygen (O2) reactivity tests in severely head-injured patients.
In nine patients (7 men, 2 women, age: 26 +/- 6.5 years, GCS of 6.5 +/- 2.9), a polarographic microcatheter (Clark-type) was inserted into nonlesioned white matter (frontal lobe). PbtO2 and SjvO2 were monitored simultaneously and cerebral vasoreactivity to CO2 and O2 was tested on days three, five and seven after injury. Simultaneous measurements of vasoreactivity by transcranial Doppler (TCD) were undertaken. A total of twenty-one CO2 and O2 reactivity tests were performed. Critical values of PbtO2 (< 15 mm Hg) during induced hyperventilation could be observed four times in two patients. High PbtO2 values up to 80 mm Hg were observed during hyperoxygenation (FiO2 100%). CO2 vasoreactivity by means of PbtO2 was absent in four tests in which measurements by TCD showed intact responses. A stronger correlation between SjvO2 and PbtO2 during the O2 reactivity tests was observed (r = 0.6, p < 0.001), in comparison to values obtained during the CO2 reactivity tests (r = 0.33, p < 0.001). In addition, there was no statistically significant correlation (r = 0.22, p = 0.26) between CO2 reactivity values measured by TCD (4.5 +/- 5.7%) and PbtO2 (3 +/- 2.8%).
Correlation between SjvO2 and PbtO2 during CO2 reactivity test is low, even if significant differences between normo- and hyperventilation values are present. In comparison to SjvO2, monitoring of PbtO2 might more accurately detect possible focal ischaemic events during rapidly induced hyperventilation in severely head-injured patients. The CO2 vasoreactivity by means of changes in Vm MCA seems to be higher in comparison to changes of PbtO2. These observations lead to the hypothesis that vasoreactivity measured by TCD overestimates the cerebrovascular response to CO2.
在重度颅脑损伤患者的二氧化碳（CO₂）和氧气（O₂）反应性测试期间，将颈静脉球血氧饱和度（SjvO₂）与脑组织氧分压（PbtO₂）进行关联。
在9例患者（7例男性，2例女性，年龄：26±6.5岁，格拉斯哥昏迷量表评分为6.5±2.9）中，将极谱微导管（Clark型）插入未受损的白质（额叶）。同时监测PbtO₂和SjvO₂，并在受伤后第3天、第5天和第7天测试大脑对CO₂和O₂的血管反应性。通过经颅多普勒（TCD）同步测量血管反应性。总共进行了21次CO₂和O₂反应性测试。在2例患者中，诱导过度通气期间PbtO₂的临界值（<15 mmHg）被观察到4次。在高氧状态（吸入氧分数100%）下观察到高达80 mmHg的高PbtO₂值。在4次测试中，通过PbtO₂测得的CO₂血管反应性缺失，而TCD测量显示反应正常。与CO₂反应性测试期间获得的值（r = 0.33，p < 0.001）相比，在O₂反应性测试期间观察到SjvO₂与PbtO₂之间的相关性更强（r = 0.6，p < 0.001）。此外，TCD测得的CO₂反应性值（4.5±5.7%）与PbtO₂（3±2.8%）之间无统计学显著相关性（r = 0.22，p = 0.26）。
即使正常通气值与过度通气值之间存在显著差异，CO₂反应性测试期间SjvO₂与PbtO₂之间的相关性也较低。与SjvO₂相比，监测PbtO₂可能更准确地检测重度颅脑损伤患者快速诱导过度通气期间可能发生的局灶性缺血事件。与PbtO₂的变化相比，通过大脑中动脉平均血流速度（Vm MCA）变化测得的CO₂血管反应性似乎更高。这些观察结果导致这样的假设，即TCD测得的血管反应性高估了脑血管对CO₂的反应。
