Vasovagal syncope (VVS) and classical orthostatic hypotension (cOH) are very common causes of syncope and orthostatic intolerance. VVS causes syncope at least once in one third of all people and cOH occurs with or without syncope in 25-30% of the elderly.

              Both can be evoked with a 'tilt test' (TT). Applying continuous non-invasive blood pressure recordings and analysis software ('Modelflow') yield estimates of the three determinants of Mean Arterial Pressure (MAP), i.e., heart rate (HR), stroke volume (SV) and total peripheral resistance (TPR).       

              VVS is most often triggered by pain, fear ('emotional VVS') or just standing ('orthostatic VVS'); TT studies of the latter type of VVS showed that the first abnormality is a gradual decrease of SV, explained through by gradual venous pooling in the splanchnic and probably muscle venous beds. This causes a moderate decrease of MAP, which, if not countered by sitting or lying, can in turn evoke a sudden calamitous decrease of HR causing an ever faster decrease of MAP, ending in syncope. It is unclear how and why standing occasionally causes venous pooling that sets the VVS cascade in motion, functioning normally on other occasions.

              cOH is by definition triggered by standing. The best understood mechanism is autonomic damage causing a triple defect. First, a failure of TPR to increase when upright causes an 'arterial leak'; second, a simultaneous decrease of SV again suggests venous pooling, presumably because of deficient venous vasoconstriction; third, a failure of HR to increase can cause very low upright MAP. The contribution of low SV, i.e., venous pooling to cOH is probably underestimated.

              In VVS as well as cOH, the role of the venous system is implied by alterations on the arterial side of the circulation. Understanding the pathophysiology of VVS and cOH could benefit from tools that measure fluid distribution over venous beds and assess venous vasoconstriction.