Kanemoto Y, Kamada K, Sasaoka Y, Nishimura A, Sakitani H
Department of Neurosurgery, Nara Prefectural Critical Care Medical Center.
No Shinkei Geka. 1995 Jul;23(7):575-9.
This report describes the clinical course of patients with sudden cardiorespiratory arrest (CRA) due to subarachnoid hemorrhage (SAH). We have seen fifteen patients of SAH that presented initially as CRA. All of them were diagnosed as SAH by CT scan. The patients were divided into two groups; one group (early DOA group) included 11 patients, who had been recognized as CRA within 60 minutes from the onset of SAH, the other group (late DOA group) consisted of 4 patients, who developed CRA more than 60 minutes after the initial onset. The major mechanism leading to delayed CRA in the late DOA group appeared to have been from brain stem herniation, but another mechanism appeared to be involved in sudden CRA in the early DOA group. Sixty percent of our patients with CRA due to SAH had a low serum potassium concentration, though hypokalemia was observed in only 4 out of 100 patients with CRA due to diseases other than SAH. These facts suggest that sympathetic hyperstimulation might result not only from stress but also from a disorder of the central autonomic nervous system. We speculate that the mechanism leading to early CRA after SAH appears to result from a disorder of the central autonomic nerve system.
本报告描述了因蛛网膜下腔出血（SAH）导致的心搏呼吸骤停（CRA）患者的临床病程。我们共收治了15例最初表现为CRA的SAH患者。所有患者均通过CT扫描确诊为SAH。患者被分为两组；一组（早期死亡组）包括11例患者，他们在SAH发病后60分钟内被诊断为CRA，另一组（晚期死亡组）由4例患者组成，他们在初始发病60分钟后出现CRA。晚期死亡组导致延迟CRA的主要机制似乎是脑干疝，但早期死亡组突发CRA似乎还涉及另一种机制。我们因SAH导致CRA的患者中有60%血清钾浓度较低，而在因SAH以外疾病导致CRA的100例患者中，只有4例出现低钾血症。这些事实表明，交感神经过度刺激可能不仅源于应激，还源于中枢自主神经系统紊乱。我们推测，SAH后导致早期CRA的机制似乎是中枢自主神经系统紊乱所致。
