慢性肺心病并发呼衰对脑循环及其代谢的改变

本文对慢性肺心病急性发作期并发呼吸衰竭的28例测定结果:(1)脑血流量及其与心排量比数均随缺O_2与CO_2潴留的程度而明显增加;(2)颈内静脉血PaO_2随动脉血PaO_2的减低而下降;(3)在脑内的O_2传递、O_2耗量及O_2摄取量虽在呼衰时均减低,但与缺O_2及CO_2潴留的程度无相关;(4)乳酸与丙酮酸含量均增加,但与缺O_2的严重程度无关。我们认为呼衰时脑血流量的增加从而使脑组织对缺O_2的改变得以代偿,与本组患者PaO_2下降很少达4kPa以下的严重程度也有关。

CEREBRAL BLOOD FLOW AND OXYGEN METABOLISM IN RESPIRATORY FAILURE

Cerebral blood flow (CBF) and cardiac output (CO)were measured and blood samples were drawn from radial artery and internal jugular vein for determining pH,PO2 and PCO2. Lactate and pyruvate were determined from internal jugular venous blood in 28 patients with respiratory failure. The results were as follows: (l)CBF and CBF/CO ratio increased significantly with the severity of hypoxemia and hypercapnia during respiratory failure. (2) PO2 of internal jugular venous blood (PviO2) and P(a -vi)O2 decreased with the decline of PaO2. (3)There was no correlation between O2 delivery of consumption,and O2 extract rate and the severity of hypoxemia and hypercapnia, although they decreased. (4)The lactate and lactate/pyryvate ratio increased,which was not related to the severity of hypoxemia. We belived that CBF was increased during respiratory failure,but there was no significant change in oxygen metabolism, owing to the response to hypoxia diminished as CBF increased. Besides the response to hypoxia was perhaps limited as the majority of these patients were not severe enough as their PaO2 did not decrease under 4 kPa.