Aims In patients with vasovagal syncope (VVS), a neural reflex appears the main determinant of hypotension leading to loss of consciousness; whether hypotension is mainly due to involvement of the arterial system or the venous system remains a debated issue. The aim of the present study was to assess which of these two systems is responsible for the fall in blood pressure (BP) in patients with VVS; to this end, a haemodynamic study was carried out not only before and during loss of consciousness but also during the recovery phase. Methods and results Beat-to-beat recordings of heart rate (HR), BP (volume-clamp method) and stroke volume (SV) (modelflow method), cardiac output (CO), and total peripheral resistance (TPR) were made at rest, during unmedicated tilt testing (TT) and recovery from loss of consciousness in 18 patients with a history of syncope (age 45 + 23 years) and positive response to TT. Blood pressure showed a significant fall during prodromal symptoms and a further fall at the beginning of loss of consciousness, together with a fall in SV, CO, and HR, and a slight, but significant, increase in TPR. At the beginning of recovery, BP showed a significant increase and a further increase 5 min later, together with an increase in SV, CO, and HR without significant changes in TPR. Conclusion These results suggest that in VVS the fall in BP is mainly caused by reduced venous return to the heart. The arterial system does not appear to be the main determinant of the fall of BP; however, the system appears unable to make the appropriate compensatory changes.

The hemodynamics of induced atrial fibrillation (AF) was investigated in 15 patients (ages 58 +/- 11 years) with paroxysmal AF presenting without organic heart disease or hypertension. A hemodynamic study was performed both during sinus rhythm and after the induction of AF. The mean heart rate increased from 73 +/- 11 to 128 +/- 18 beats/min (P < 0.001) after AF. Systolic and mean aortic pressures did not significantly change, and diastolic aortic pressure increased (78 +/- 11 vs 89 +/- 12 mmHg, P < 0.01). Left ventricular end-diastolic pressure decreased during AF (9 +/- 3 vs 6 +/- 2.6 mmHg, P < 0.005), whereas mean pulmonary wedge pressure increased (8 +/- 2 vs 12 +/- 4 mmHg, P < 0.001). Systolic pulmonary arterial pressure did not show significant variations, and there was a slight but statistically significant increase in the diastolic and mean pulmonary arterial pressures (P < 0.01). The right ventricular end-diastolic pressure decreased during AF (5.6 +/- 2 vs 3.8 +/- 2 mmHg, P < 0.01), whereas mean right atrial pressure showed a trend toward an increase. Stroke volume markedly decreased (P < 0.001) while the cardiac index did not significantly change. Systemic vascular resistance, pulmonary arteriolar resistance, and the arteriovenous O2 difference showed no significant variations after the induction of AF. These results suggest that in subjects without organic heart disease, paroxysmal AF is well tolerated hemodynamically, and the rise in the atrial pressures during AF is not related to an increase in the ventricular end-diastolic pressure.

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