Julu P O O, Cooper V L, Hansen S, Hainsworth R
Institute for Cardiovascular Research, University of Leeds, UK.
J Physiol. 2003 May 15;549(Pt 1):299-311. doi: 10.1113/jphysiol.2002.036715. Epub 2003 Apr 4.
To study cardiovascular control in the period leading to vasovagal syncope we monitored beat-to-beat blood pressure, heart rate (HR) and forearm blood flow in 14 patients with posturally related syncope, from supine through to tilt-induced pre-syncope. Signals of arterial blood pressure (BP) from a Finapres photoplethysmograph and an electrocardiograph (ECG) were fed into a NeuroScope system for continuous analysis. Non-invasive indices of cardiac vagal tone (CVT) and cardiac sensitivity to baroreflex (CSB) were derived on a beat-to-beat basis from these data. Brachial vascular resistance (VR) was assessed intermittently from brachial blood flow velocity (Doppler ultrasound) divided by mean arterial pressure (MAP). Patients underwent a progressive orthostatic stress test, which continued to pre-syncope and consisted of 20 min head-up tilt (HUT) at 60 deg, 10 min combined HUT and lower body suction (LBNP) at -20 mmHg followed by LBNP at -40 mmHg. Pre-syncope was defined as a fall in BP to below 80 mmHg systolic accompanied by symptoms. Baseline supine values were: MAP (means +/- S.E.M.) 84.9 +/- 3.2 mmHg; HR, 63.9 +/- 3.2 beats min-1; CVT, 10.8 +/- 2.6 (arbitrary units) and CSB, 8.2 +/- 1.6 ms mmHg-1. HUT alone provoked pre-syncope in 30 % of the patients whilst the remaining 70 % required LBNP. The cardiovascular responses leading to pre-syncope can be described in four phases. Phase 1, full compensation: where VR increased by 70.9 +/- 0.9 %, MAP was 89.2 +/- 3.8 mmHg and HR was 74.8 +/- 3.2 beats min-1 but CVT decreased to 3.5 +/- 0.5 units and CSB to 2.7 +/- 0.4 ms mmHg-1. Phase 2, tachycardia: a progressive increase in heart rate peaking at 104.2 +/- 5.1 beats min-1. Phase 3, instability: characterised by oscillations in BP and also often in HR; CVT and CSB also decreased to their lowest levels. Phase 4, pre-syncope: characterised by sudden decreases in arterial blood pressure and heart rate associated with intensification of the symptoms of pre-syncope. This study has given a clearer picture of the cardiovascular events leading up to pre-syncope. However, the mechanisms behind what causes a fully compensated system suddenly to become unstable remain unknown.
为研究血管迷走性晕厥发作前期的心血管控制情况，我们对14例体位性相关晕厥患者从仰卧位到倾斜诱发晕厥前期进行逐搏血压、心率（HR）和前臂血流监测。来自Finapres光电容积描记仪和心电图（ECG）的动脉血压（BP）信号输入NeuroScope系统进行连续分析。基于这些数据逐搏得出心脏迷走神经张力（CVT）和心脏压力反射敏感性（CSB）的无创指标。通过肱动脉血流速度（多普勒超声）除以平均动脉压（MAP）间歇性评估肱血管阻力（VR）。患者接受渐进性直立应激试验，试验持续至晕厥前期，包括60°头高位倾斜（HUT）20分钟、-20 mmHg下HUT与下体负压（LBNP）联合10分钟，随后-40 mmHg下LBNP。晕厥前期定义为收缩压降至80 mmHg以下并伴有症状。仰卧位基线值为：MAP（均值±标准误）84.9±3.2 mmHg；HR，63.9±3.2次/分钟；CVT，10.8±2.6（任意单位），CSB，8.2±1.6 ms/mmHg。仅HUT诱发30%的患者出现晕厥前期，其余70%的患者需要LBNP。导致晕厥前期的心血管反应可分为四个阶段。第1阶段，完全代偿：VR增加70.9±0.9%，MAP为89.2±3.8 mmHg，HR为74.8±3.2次/分钟，但CVT降至3.5±0.5单位，CSB降至2.7±0.4 ms/mmHg。第2阶段，心动过速：心率逐渐增加，峰值为104.2±5.1次/分钟。第3阶段，不稳定期：其特征为血压波动，常伴有心率波动；CVT和CSB也降至最低水平。第4阶段，晕厥前期：其特征为动脉血压和心率突然下降，伴有晕厥前期症状加重。本研究更清晰地描绘了导致晕厥前期的心血管事件。然而，导致完全代偿系统突然变得不稳定的背后机制仍不清楚。
