Takase B, Nagai T, Uehata A, Katushika S, Isojima K, Hakamata N, Ohtomi S, Ota S, Kurita A, Nakamura H
Self Defense Force Central Hospital, Internal Medicine, Tokyo, Japan.
Clin Cardiol. 1997 Mar;20(3):233-8. doi: 10.1002/clc.4960200309.
Prolonged asystole is sometimes an extreme manifestation of neurally mediated syncope.
To investigate the mechanism of head-up tilt testing-induced prolonged (life-threatening) cardiac asystole, we measured temporal changes in frequency domain heart rate variability indices in 25 patients with syncope of undetermined etiology.
Head-up tilt testing (80 degrees) was performed in 25 patients for up to 40 min or until asystole or syncope occurred. Three patients (Group 1; 37 +/- 13 years, 1 man 2 women) had an episode of prolonged cardiac asystole (> or = 10 s) during testing, necessitating cardiopulmonary resuscitation. Syncope, but no asystole, was induced in 10 patients (Group 2; 48 +/- 31 years, 6 men, 4 women), and 12 patients (Group 3; 55 +/- 20 years, 5 men, 7 women) failed to show asystole or syncope during testing. Power spectra of low (0.04-0.15 Hz) and high (0.15-0.40 Hz) frequency, and total (0.01-1.00 Hz) frequency spectra were measured in consecutive 2 min segments throughout the test.
Maximally changed values in heart rate, systolic blood pressure, and heart rate variability indices during testing were compared among the three groups (maximally changed values did not include the values during tilt-induced symptoms). High frequency spectra in Groups 2 and 3, but not in Group 1, decreased during the test. High frequency spectra, low frequency spectra, and total spectra in Group 1 were significantly higher than those in Groups 2 and 3 during testing. In Group 1 patients, findings at test-induced asystole were consistent with exaggerated sympathetic and concurrent persistent parasympathetic activity.
Unusual autonomic responses to orthostatic stress can cause prolonged asystole, and this autonomic nerve dysregulation may relate to asystolic episodes associated with cardiovascular collapse.
长时间心脏停搏有时是神经介导性晕厥的一种极端表现形式。
为研究头高位倾斜试验诱发的长时间（危及生命的）心脏停搏的机制，我们对25例病因不明的晕厥患者的频域心率变异性指标的时间变化进行了测量。
对25例患者进行头高位倾斜试验（80度），持续40分钟或直至出现心脏停搏或晕厥。3例患者（第1组；37±13岁，1男2女）在试验期间出现一次长时间心脏停搏（≥10秒），需要进行心肺复苏。10例患者（第2组；48±31岁，6男4女）诱发了晕厥但未出现心脏停搏，12例患者（第3组；55±20岁，5男7女）在试验期间未出现心脏停搏或晕厥。在整个试验过程中，以连续2分钟的时段测量低频（0.04 - 0.15赫兹）和高频（0.15 - 0.40赫兹）功率谱以及总功率谱（0.01 - 1.00赫兹）。
比较了三组在试验期间心率、收缩压和心率变异性指标的最大变化值（最大变化值不包括倾斜诱发症状期间的值）。第2组和第3组的高频谱在试验期间下降，而第1组未下降。第1组的高频谱、低频谱和总谱在试验期间显著高于第2组和第3组。在第1组患者中，试验诱发心脏停搏时的表现与交感神经亢进及同时存在的持续副交感神经活动一致。
对直立位应激异常的自主神经反应可导致长时间心脏停搏，这种自主神经失调可能与心血管虚脱相关的心脏停搏发作有关。
