Lipsitz L A, Hayano J, Sakata S, Okada A, Morin R J
Hebrew Rehabilitation Center for Aged Research and Training Institute, Department of Medicine, Harvard Medical School, Boston, Mass 02131, USA.
Circulation. 1998 Sep 8;98(10):977-83. doi: 10.1161/01.cir.98.10.977.
The dynamic autonomic processes leading to vasovagal syncope are poorly understood.
We used complex demodulation to continuously assess changes in respiration, R-R interval, and arterial pressure (blood pressure) variability during 60 degree head-up tilt in 25 healthy subjects with tilt-induced vasovagal syncope and 25 age-matched nonsyncopal control subjects. Coherence and transfer function analyses were used to examine the relation between respiration and R-R interval variability before syncope. Baseline blood pressure, R-R, and ventilation were similar between syncope subjects and control subjects. Syncope subjects experienced an increase in tidal volume and decrease in BP beginning 3 minutes before impending syncope (systolic blood pressure <80 mm Hg) necessitated termination of tilt. Approximately 90 seconds before syncope there was a sudden prolongation of R-R interval and increase in amplitude of high and low frequency R-R interval variability, indicating an abrupt enhancement of vagal tone. The increase in respiratory amplitude between 180 and 90 seconds before syncope was not accompanied by changes in R-R interval or R-R variability, suggesting a dissociation between respiration and the respiratory sinus arrhythmia. The coherence analysis showed fewer syncope subjects with coherence between respiratory and R-R interval variabilities and lower transfer magnitudes in syncope subjects compared with control subjects. Nonsyncopal subjects had no change in respiratory, R-R interval, or blood pressure dynamics during matched time periods before the time of syncope.
Vasovagal syncope is preceded by a period of hyperpnea and cardiorespiratory decoupling followed by an abrupt increase in cardiovagal tone. Respiratory pumping without inspiratory cardiac slowing may partially counteract preload reduction until sudden bradycardia precipitates syncope.
导致血管迷走性晕厥的动态自主神经过程尚不清楚。
我们使用复解调技术，持续评估25名倾斜诱发血管迷走性晕厥的健康受试者和25名年龄匹配的非晕厥对照受试者在60度头高位倾斜过程中呼吸、R-R间期和动脉压（血压）变异性的变化。采用相干分析和传递函数分析来研究晕厥前呼吸与R-R间期变异性之间的关系。晕厥受试者和对照受试者的基线血压、R-R间期和通气情况相似。晕厥受试者在即将发生晕厥（收缩压<80 mmHg）导致倾斜终止前3分钟开始出现潮气量增加和血压下降。在晕厥前约90秒，R-R间期突然延长，高频和低频R-R间期变异性幅度增加，表明迷走神经张力突然增强。晕厥前180至90秒呼吸幅度增加，但未伴有R-R间期或R-R变异性变化，提示呼吸与呼吸性窦性心律不齐之间存在分离。相干分析显示，与对照受试者相比，晕厥受试者中呼吸与R-R间期变异性之间具有相干性的较少，且传递幅度较低。在晕厥时间前的匹配时间段内，非晕厥受试者的呼吸、R-R间期或血压动态无变化。
血管迷走性晕厥之前有一段呼吸急促和心肺解耦期，随后是心迷走神经张力突然增加。无吸气性心率减慢的呼吸泵血可能部分抵消前负荷降低，直到突然心动过缓引发晕厥。
