Stocchetti Nino, Zanier Elisa Roncati, Nicolini Rita, Faegersten Emelie, Canavesi Katia, Conte Valeria, Gattinoni Luciano
Department of Anesthesia and Critical Care Medicine, Milan University, Italy.
Anesthesiology. 2005 Nov;103(5):957-61. doi: 10.1097/00000542-200511000-00009.
The authors propose that for a moderate reduction of perfusion during progressive irreversible ischemia, oxygen extraction increases to maintain aerobic metabolism, and arteriojugular oxygen difference (AJDo2) increases. Because of reduced carbon dioxide washout, venoarterial difference in carbon dioxide tension (DPco2) increases, with no change in the DPco2/AJDo2 ratio. With further reduction of cerebral perfusion, the aerobic metabolism will begin to decrease, AJDo2 will decrease while DPco2 will continue to increase, and the ratio will increase. When brain infarction develops, the metabolism will be abated, no oxygen will be consumed, and no carbon dioxide will be produced.
The authors studied 12 patients with acute cerebral damage that evolved to brain death and collected intermittent arterial and jugular blood samples.
Four patterns were observed: (1) AJDo2 of 4.1 +/- 0.7 vol%, DPco2 of 6.5 +/- 1.9 mmHg, and a ratio of 1.55 +/- 0.3 with cerebral perfusion pressure of 62.5 +/- 13.4 mmHg; (2) a coupled increase of AJDo2 (5.8 +/- 0.7 vol%) and DPco2 (10.1 +/- 1.0 mmHg) with no change in ratio (1.92 +/- 0.14) and cerebral perfusion pressure (57.9 +/- 5.8 mmHg); (3) AJDo2 of 4.7 +/- 0.4 vol% with an increase in DPco2 (11.8 +/- 1 mmHg) and correspondingly higher ratio (2.7 +/- 0.2); in this phase, cerebral perfusion pressure was 39.7 +/- 10.5 mmHg; (4) immediately before diagnosis of brain death (cerebral perfusion pressure, 17 +/- 10.4 mmHg), there was a decrease of AJDo2 (1.1 +/- 0.1 vol%) and of DPco2 (5.3 +/- 0.6 mmHg) with a further ratio increase (5.1 +/- 0.8).
Until compensatory mechanisms are effective, AJDo2 and DPco2 remain coupled. However, when the brain's ability to compensate for reduced oxygen delivery is exceeded, the ratio of DPco2 to AJDo2 starts to increase.
作者提出，在进行性不可逆性缺血期间，若灌注适度降低，氧摄取会增加以维持有氧代谢，动静脉氧差（AJDo2）增大。由于二氧化碳清除减少，二氧化碳分压的动静脉差值（DPco2）增大，而DPco2/AJDo2比值无变化。随着脑灌注进一步降低，有氧代谢将开始下降，AJDo2会降低而DPco2将继续升高，该比值会增大。当脑梗死发生时，代谢将减弱，不再消耗氧气，也不再产生二氧化碳。
作者研究了12例演变为脑死亡的急性脑损伤患者，并采集了间歇性动脉血和颈静脉血样本。
观察到四种模式：（1）AJDo2为4.1±0.7体积%，DPco2为6.5±1.9 mmHg，比值为1.55±0.3，脑灌注压为62.5±13.4 mmHg；（2）AJDo2（5.8±0.7体积%）和DPco2（10.1±1.0 mmHg）同时升高，比值（1.92±0.14）和脑灌注压（57.9±5.8 mmHg）无变化；（3）AJDo2为4.7±0.4体积%，DPco2升高（11.8±1 mmHg），相应地比值更高（2.7±0.2）；在此阶段，脑灌注压为39.7±10.5 mmHg；（4）在诊断脑死亡前即刻（脑灌注压，17±10.4 mmHg），AJDo2（1.1±0.1体积%）和DPco2（5.3±0.6 mmHg）均降低，比值进一步升高（5.1±0.8）。
在代偿机制有效之前，AJDo2和DPco2保持耦合。然而，当大脑补偿氧输送减少的能力被超过时，DPco2与AJDo2的比值开始升高。
