镇痛镇静对急诊重症蛛网膜下腔出血患者脑氧代谢的影响

Effect of Analgesia and Sedation on Cerebral Metabolism in Patients with Severe Subarachnoid Hemorrhage

目的:研究镇痛镇静对急诊重症蛛网膜下腔出血患者脑氧代谢的影响。方法:选取80例在我院就诊的急诊重症蛛网膜下腔出血患者,所有患者在常规治疗基础上根据患者疼痛情况,镇痛剂选用舒芬太尼,镇静剂选用咪达唑仑治疗。对患者镇痛镇静治疗前、镇痛镇静后2h、镇痛镇静结束后1h、3h、6h的颈动脉、颈静脉及中心静脉血氧饱和度、脑氧代谢指标进行比较。结果:所有患者镇痛镇静前后颈动脉血氧饱和度无明显改变,依次为0.88±0.19、0.80±0.15、0.82±0.12、0.84±0.15、0.85±0.15。颈静脉和中心静脉血氧饱和度在镇痛镇静前偏低(0.48±0.07;0.50±0.05),镇痛镇静后2h恢复正常(0.65±0.11;0.69±0.13),在镇痛镇静结束后1h(0.58±0.090.61±0.10;)、3h(0.51±0.08;0.56±0.10)及6h(0.49±0.03;0.52±0.07)逐渐下降,接近于镇痛镇静前水平。所有患者镇痛镇静前后Ca O_2无明显改变(P>0.05)。Cjv O_2在镇痛镇静后均显著高于镇痛镇静前(P<0.05),Da-jv O_2和CERO_2镇痛镇静后均显著低于镇痛镇静前(P<0.05)。结论:镇痛镇静可降低急诊重症蛛网膜下腔出血患者的脑氧代谢。

Objective： To study the effect of analgesia and sedation on cerebral metabolism in patients with severe subarachnoid hemorrhage. Methods： 80 patients with severe subarachnoid hemorrhage were given sufentanil and midazolam in treatment. After sedation and analgesia, 1h, 6h, carotid and jugular venous oxygen saturation, central venous oxygen saturation and cerebral oxygen metabolism indexes were compared before and after sedation and analgesia in 2h, 3h, and after analgesia. Results： All patients before and after sedation carotid arterial oxygen saturation did not change significantly, were 0.88 ± 0.19, 0.80 ± 0.15,0.82 ± 0.12,0.84 ± 0.15, 0.85 ± 0.15. Jugular vein and central venous oxygen saturation before sedation is low （0.48 ± 0.07; 0.50 ± 0.05）, 2h back to normal after sedation （0.65 ± 0.11; 0.69 ± 0.13）, at the end of lh after sedation （0.58 ± 0.090.61 ± 0.10）, 3h （0.51 ± 0.08; 0.56 ± 0.10） and 6h （0.49 ± 0.03; 0.52 ± 0.07） decreased, close to the level before sedation. There was no significant change in CaO2 before and after sedation in all patients （P〉0.05）.The CjvO2 after analgesic and sedative were significantly higher than before analgesic and sedative （P〈0. 05）, CERO2 and Da-jvO2 after analgesic and sedative were significantly lower than before analgesic and sedative （P〈0.05）. Conclusion： Analgesia and sedation could reduce the cerebral oxygen metabolism in patients with severe subarachnoid hemorrhage.