通气程度对颅脑损伤患者脑氧供需平衡的影响(英文)

Effect of hyperventilation on cerebral oxygen supply-demand balance in patients with traumatic brain injury

背景不适当的过度通气可能诱使脑血管收缩,导致脑低灌流和氧供需失衡。目的探讨过度通气对严重颅脑伤患者颈内静脉球血氧饱和度、脑动静脉氧含量差和脑静动脉血乳酸差的影响。设计病例分析。单位汕头大学医学院第一附属医院麻醉科。对象选择汕头大学医学院第一附属医院2002-01/07收治的严重颅脑损伤急诊手术患者16例进行观察。方法颅脑损伤手术患者全身麻醉后,调节呼吸频率使二氧化碳分压达30m m Hg并维持15m in,然后提高呼吸频率使二氧化碳分压达到25m m H g亦维持15m in,再降低呼吸频率以使二氧化碳分压恢复至30m m Hg同样维持15min,改变吸入氧浓度以使血氧分压稳定在100～150m m Hg,并于上述二氧化碳分压改变并维持15m in后,分别采集动脉和颈内静脉球血液进行血气分析。调高吸入氧浓度将血氧分压增至200～250m m H g,再重复上述通气调节依此将二氧化碳分压改变为30→25→30m m H g,测定颈内静脉球血氧饱和度、脑动静脉氧含量差及脑静动脉血乳酸差。主要观察指标血氧分压和二氧化碳分压变化对颈内静脉球血氧饱和度、脑动静脉氧含量差和脑静动脉血乳酸差的影响。结果16例患者符合标准并完成数据采集。当动脉血氧分压为100～150m m H g及200～250m m H g,动脉血二氧化碳分压从30m m H g降至25m m H g时,可使颈内静脉球血氧饱和度明显降低、脑动静脉氧含量差明显升高,但血氧分压200～250m m H g与血氧分压100～150m m H g相比,颈内静脉球血氧饱和度的绝对值均明显较高,脑动静脉氧含量差绝对值明显较低。与基础值相比,血氧分压100～150m m H g、二氧化碳分压30mm H g及25m m Hg和血氧分压200～250m m H g、二氧化碳分压25m m H g时,脑静动脉血乳酸差均明显升高。结论较高动脉血氧水平(血氧分压200～250m m H g)和中度过度通气(二氧化碳分压30m m H g)对脑氧供需平衡无明显影响。

BACKGROUND： Inadequate hyperventilation may trigger cerebmvascular contraction and lead to lowered cerebral perfusion and oxygen supply-demand imbalance. OBJECTIVE： To investigate the influence of hyperventilation on oxygen saturation in the internal jugular vein, difference in oxygen and lactic acid contents between the cerebral arteries and veins in patients with serious traumatic brain injury. DESIGN： Case analysis. SETTING： Department of Anesthesiology, First Hospital Affiliated to Shantou University. PARTICIPANTS： Sixteen patients who received emergency operations in the First Hospital Affiliated to Shantou University between January and July 2002. METHODS： Patients with traumatic brain injury underwent operation under general anesthesia, and the PaCO： was maintained at 30 mm Hg for 15 minutes by regulating the respiration rate, followed by decrease to 25 mm Hg, maintained for 15 minutes before restoration to 30 mm Hg for 15 minutes. The fractional concentration of inspired oxygen was adjusted to maintain blood PaO2 at around 100-150 mm Hg, and the blood sample was collected from the artery and internal jugular vein 15 minutes after adjustment of PaCO2 for blood gas analysis. The Pa02 was then increased to 200-250 mm Hg by increasing the fractional concentration of inspired oxygen, and the PaCO2 was adjusted from 30 to 25 and then back to 30 mm Hg in the described manner, and the oxygen saturation in the internal jugular vein, difference in oxygen and lactic acid contents between the arteries and the veins were measured. MAIN OUTCOME MEASURES： Influence of blood PaO2 and PaCO2 on oxygen saturation in the internal jugular vein, difference in oxygen and lactic acid contents between the arteries and the veins. RESULTS： Sixteen patients met the diagnostic criteria and completed data collection. The arterial PaCO2 decreased from 30 to 25 mm Hg when arterial blood oxygen pressure increased from 100-150 to 200- 250 mm Hg, which leads to obvious decrease of oxygen saturation in the internal jugular vein and obvious increased difference in oxygen content between the cerebral artery and vein. However the absolute value of oxygen saturation in the internal jugular vein was obviously higher at PaO2 of 200-250 mm Hg than that at PaO2 of 100-150 mm Hg, while the absolute value of cerebral arteriovenous difference of brain oxygen content was obviously lower. Compared to the basal level, the arteriovenous lactic acid difference was obviously increased at PaO2 of 100-150 mm Hg, PaCO2 of 30 and 25 mm Hg, and at PaO2 of 200-250 mm Hg and PaCO2 of 25 mm Hg. CONCLUSION： Relatively higher PaO2 （200-250 mm Hg） and mild hyperventilation （PaCO2 of 30 mm Hg） has no obvious effect on brain oxygen supply-demand balance.