Correlation between jugular bulb oxygen saturation and partial pressure of brain tissue oxygen during CO2 and O2 reactivity tests in severely head-injured patients.

PURPOSE

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.

METHODS AND RESULTS

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%).

CONCLUSIONS

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.