Mangin P, Krieger J, Kurtz D
J Neurol Sci. 1982 Nov-Dec;57(1):67-82. doi: 10.1016/0022-510x(82)90111-3.
To assess the incidence of posthyperventilation apnea (PHA), breathing patterns after active voluntary hyperventilation were determined during EEG recording by means of: (1) a thermocouple in 1060 patients; (2) a pneumotachograph coupled with a capnograph in 100 further patients. All the patients were randomly chosen. PHA of 12.6 +/- 0.48 occurred in only 18% of awake subjects and was not related to the magnitude of the lowering of end-tidal FECO2 during the test. PHA frequency increased when sleep followed hyperventilation and in patients with clinical or EEG evidence of cerebral pathology and seemed to be age-related. This study supports the hypothesis that in man a central neural mechanism closely linked to vigilance and connected with active breathing supplies sufficient neural facilitation to prevent the apnea consequent on the decrease in chemical humoral stimulation. Posthyperventilation sleep reduces this neural facilitation, allowing the lack of chemical stimulation to induce apnea. The high incidence of PHA reported in some studies might be due to a decrease in vigilance which was not detected by the usual behavioral or electroencephalographic tests.
为评估过度通气后呼吸暂停(PHA)的发生率,在脑电图记录期间,通过以下方式确定主动自愿过度通气后的呼吸模式:(1)对1060例患者使用热电偶;(2)对另外100例患者使用与二氧化碳分析仪联用的呼吸流速描记器。所有患者均为随机选取。12.6±0.48秒的PHA仅出现在18%的清醒受试者中,且与测试期间呼气末二氧化碳分压降低的幅度无关。过度通气后紧接着睡眠以及有脑部病变临床或脑电图证据的患者中,PHA频率增加,且似乎与年龄相关。本研究支持以下假说:在人类中,一种与警觉性密切相关且与主动呼吸相连的中枢神经机制提供了足够的神经促进作用,以防止化学性体液刺激减少导致的呼吸暂停。过度通气后睡眠会减少这种神经促进作用,使化学刺激缺乏从而诱发呼吸暂停。一些研究中报道的PHA高发生率可能是由于未通过常规行为或脑电图测试检测到的警觉性降低所致。