Respiratory.pptVIP

四、对中枢神经系统的影响(Effects on Central Nervous System) PaO2降低和PaCO2升高直接造成中枢神经系统损伤性变化。脑重仅为体重的2%，但脑的耗氧量却为机体总耗氧量的23%，所以脑尤其是大脑皮质对缺氧非常敏感。在急性缺氧时，若PaO2降低至50 mmHg以下时，病人可出现头痛、情绪激动、判断能力降低、运动不协调、神经错乱、甚至惊厥和昏迷。慢性缺氧的病人则可出现易疲劳、嗜睡、注意力不集中及精神抑郁。早期CO2潴留病人也会出现头痛、头昏和嗜睡，到严重阶段会出现谵妄、精神错乱、扑翼样震颤、抽搐和昏迷等中枢神经系统功能障碍，称为“二氧化碳麻醉”（CO2 narcosis）。 呼吸衰竭病人一旦出现脑功能障碍，即可诊断为肺性脑病（pulmonary encephalopathy），主要由缺氧和由于缺氧及CO2潴留造成的酸中毒引起。由于脑脊液缓冲能力比血液弱，而且与血液中HCO3-相比，CO2易通过血脑屏障进入脑脊液，故脑脊液的PCO2可比PaCO2高8 mmHg, 而[HCO3-]两者相似。所以在呼吸衰竭时脑脊液pH降低比血液更严重。缺氧和酸中毒通过影响脑血管和脑细胞功能引起pulmonary encephalopathy，其发生机制是： 1．脑血管受损（Cerebrovascular Injury） 脑血管受损致使脑压增高, 其原因是：① 缺氧和酸中毒使脑血管扩张，脑血流量增多, 脑血管过度扩张,可引起脑水肿；②缺氧和酸中毒损伤脑血管内皮细胞，因管壁通透性增高，出现脑间质水肿；③脑血管内皮受损可引起血管内凝血，加重脑缺氧；④脑压高会压迫脑血管，更加重脑缺氧和酸中毒，因而出现恶性循环，甚至于发生脑疝（hernia of brain）。 2．脑细胞受损（Brain Cell Injury） 脑细胞受损的表现和原因是：①缺氧使ATP生成减少，Na+-K+泵功能障碍，细胞内钠水潴留，脑细胞水肿，脑压增高；②在严重酸中毒时脑细胞生物电活动消失；③酸中毒时脑细胞内抑制性介质γ-氨基丁酸生成增多，导致中枢功能抑制；④酸中毒时细胞膜磷脂酶活性增强，使溶酶体膜通透性增高甚至破裂，进而损伤脑细胞。 A previously healthy 23-year-old male sustained numerous traumatic crush, burn, and smoke inhalation injuries during a landing accident in an airplane. His initial B.P. was 80/50 mmHg, and he was immediately infused with saline at the maximal rate. In the ER he was intubated and had no signs of pneumothorax. His orthopedic injuries and burns were treated. The ventilator was placed on the assist-control mode with the initial settings of inspired O2 concentration at 40%, respiration rate at 12/min, and tidal volume at 900 ml. Arterial blood gas measurements were: pH = 7.47, PCO2 of 33 mmHg, and PO2 of 62 mmHg. Clinical Case 24 hrs. after admission, the patient becomes agitated and his respiration rate increased to 30/min. His minute ventilation also increased from 8.5 l/min to 20 l/min. Airway pressure increased from 18 to 65 cm H2O. Repeat arterial blood gas measurement of PO2 indicated 35 mmHg and chest x-ray now showed diffuse infiltrates in a white out pattern. Clinical Case The diagnosis of ARDS is contingent upon 5 factors