Cerebral veno-arterial pCO2 difference as an estimator of uncompensated cerebral hypoperfusion

被引:0
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作者
Rossi, S [1 ]
Colombo, A [1 ]
Magnoni, S [1 ]
Zanier, ER [1 ]
Conte, V [1 ]
Stocchetti, N [1 ]
机构
[1] Osped Maggiore, Policlin IRCCS, Dept Anesthesia & Intens Care, Pad Beretta Ovest, I-20122 Milan, Italy
关键词
ischemia; hypoperfusion; veno-arterial difference in pCO(2);
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中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The aim of the present study was to assess the veno-arterial difference in pCO2 (DeltapCO2) as an indicator of ischemia compared to the arteriovenous O2 difference (AVDO2). Staircase cerebral blood flow (CBF) reductions were obtained in seven domestic pigs by inducing intracranial hypertension: CBF 100%, 50-60% of baseline, 20-30% of baseline. ICP, MAP, CPP and CBF (Laser-Doppler method) were continuously recorded. The superior sagittal sinus was punctured to determine AVDO2 and DeltapCO2. AVDO2 was 5.9 (+/- 1.78, range 3.3-7.4), 7.01 (+/- 1.31, range 5-8.9) and 8.17 ( +/- 1.51, range 6.0-11.3) ml/100 ml in the three CBF steps (p = 0.001). CBF impairment was accompanied by the following increases in DeltapCO2: from 10 (+/- 4, range 4-15) mmHg to 14.5 ( +/- 4.11, range 10-27) mmHg, and to 31.2 ( +/- 9.0, range 17-39) mmHg (p < 0.001). When CBF declines DeltaVDO2 increases, indicating greater extraction of O2 to satisfy the aerobic metabolism. However, this mechanism can no longer compensate once a critical CBF threshold is reached. DeltapCO2 rises slowly during moderate CBF reduction because of defective washout; the rise is impressive during marked CBF impairment when anaerobic metabolism takes place with proton buffering in CO2 and H2O. Therefore, when the brain's ability to compensate for low blood flow is exceeded, CO2 production outweighs O2 extraction.
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页码:201 / 204
页数:4
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