Cardiovascular regulation in the period preceding vasovagal syncope in conscious humans

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.