Department of Physiology, The Center for Hypotension, New York Medical College, 19 Bradhurst Ave., Suite 1600S, Hawthorne, NY 10532, USA.
Am J Physiol Heart Circ Physiol. 2009 Dec;297(6):H2084-95. doi: 10.1152/ajpheart.00705.2009. Epub 2009 Oct 9.
Vasovagal syncope may be due to a transient cerebral hypoperfusion that accompanies frequency entrainment between arterial pressure (AP) and cerebral blood flow velocity (CBFV). We hypothesized that cerebral autoregulation fails during fainting; a phase synchronization index (PhSI) between AP and CBFV was used as a nonlinear, nonstationary, time-dependent measurement of cerebral autoregulation. Twelve healthy control subjects and twelve subjects with a history of vasovagal syncope underwent 10-min tilt table testing with the continuous measurement of AP, CBFV, heart rate (HR), end-tidal CO2 (ETCO2), and respiratory frequency. Time intervals were defined to compare physiologically equivalent periods in fainters and control subjects. A PhSI value of 0 corresponds to an absence of phase synchronization and efficient cerebral autoregulation, whereas a PhSI value of 1 corresponds to complete phase synchronization and inefficient cerebral autoregulation. During supine baseline conditions, both control and syncope groups demonstrated similar oscillatory changes in phase, with mean PhSI values of 0.58+/-0.04 and 0.54+/-0.02, respectively. Throughout tilt, control subjects demonstrated similar PhSI values compared with supine conditions. Approximately 2 min before fainting, syncopal subjects demonstrated a sharp decrease in PhSI (0.23+/-0.06), representing efficient cerebral autoregulation. Immediately after this period, PhSI increased sharply, suggesting inefficient cerebral autoregulation, and remained elevated at the time of faint (0.92+/-0.02) and during the early recovery period (0.79+/-0.04) immediately after the return to the supine position. Our data demonstrate rapid, biphasic changes in cerebral autoregulation, which are temporally related to vasovagal syncope. Thus, a sudden period of highly efficient cerebral autoregulation precedes the virtual loss of autoregulation, which continued during and after the faint.
血管迷走性晕厥可能是由于动脉压 (AP) 和脑血流速度 (CBFV) 之间的频率同步引起的短暂性脑灌注不足。我们假设在晕厥期间脑自动调节失败；AP 和 CBFV 之间的相位同步指数 (PhSI) 被用作脑自动调节的非线性、非平稳、时变测量。12 名健康对照者和 12 名有血管迷走性晕厥病史的患者接受了 10 分钟倾斜台测试，连续测量 AP、CBFV、心率 (HR)、呼气末二氧化碳 (ETCO2) 和呼吸频率。定义了时间间隔，以比较晕厥患者和对照组中生理等效的时间段。PhSI 值为 0 对应于相位无同步和有效的脑自动调节，而 PhSI 值为 1 对应于完全相位同步和低效的脑自动调节。在仰卧位基础状态下，对照组和晕厥组的相位均显示出相似的振荡变化，平均 PhSI 值分别为 0.58+/-0.04 和 0.54+/-0.02。在倾斜过程中，对照组的 PhSI 值与仰卧位相似。大约在晕厥前 2 分钟，晕厥组的 PhSI 值急剧下降 (0.23+/-0.06)，代表有效的脑自动调节。在此期间之后，PhSI 值急剧增加，表明脑自动调节效率低下，并且在晕厥时 (0.92+/-0.02) 和返回仰卧位后立即的早期恢复期间 (0.79+/-0.04) 仍保持升高。我们的数据表明，脑自动调节发生快速、双相变化，与血管迷走性晕厥有关。因此，在自动调节功能几乎丧失之前，会出现一段短暂的高效脑自动调节期，并且在晕厥期间和之后，自动调节仍持续。
