The venous system is the main determinant of hypotension in patients with vasovagal syncope

Abstract

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.

Identical pattern of cerebral hypoperfusion during different types of syncope

“…Consequently, more complete understanding of these interactions in health and disease will require increased cooperation between researchers who conventionally work in separate disciplines. Ultimately, however, we caution the use of the previously described classification system, 6,14,15 because it fails to consider many of complex factors associated with syncope.…”

“…19,20 A fall in systemic vascular resistance in the splanchnic bed might result in translocation of blood to the venous system and a consequential decrease in cardiac output; thereby these responses may interact in an attempt to prevent syncope. Thus, arteriolar dysfunction might underlie, in part, what the earlier authors 6,14,15 have classified as 'venular dysfunction'. Therefore, this method of categorization of syncope should be treated with caution.…”

“…4 The prevalence of OH in the general population is significant (B3%) and recent reports indicate that the incidence of syncope is nearly twice as common in young age groups (o40 years) as in older age groups (460 years). 5 Although the underlying mechanisms are still unknown, some data indicate that OH results from inadequate compensatory responses of the venous system, that is impaired reflex constriction of the venous capacitance beds, [6][7][8] whereas other data suggest an underlying arterial vascular resistance deficit. 9,10 Recently, it has been shown that, at least in young (20-40 years of age) patients with a history of OH, hypotension during routine tilt testing is cardiac output mediated, 11 rather than mediated by a fall in systemic vascular resistance.…”

“…12,13 Because of these differential findings, in part, there have been recent attempts to classify OH into three possible subgroups on the basis of alterations in peripheral resistance and cardiac output at pre-syncope. 6,14,15 These subgroups include (1) defects in the venous system (that is excessive reductions in venous return); (2) defects in the arterial system (that is impaired vasoconstriction); and (3) a combination of the two (that is mixed). In older patients with OH, 14 it has been reported that venular defects affected the majority of patients (54%), compared with arterial (25%) and mixed defects (21%).…”

“…As symptoms and loss of consciousness during syncope are fundamentally due to cerebral hypoperfusion, 3 one limitation of this classification approach 6,14,15 is that it fails to consider the influence of these haemodynamic changes on cerebral perfusion. Moreover, these studies have not quantified the extent to which inappropriate hyperventilation at pre-syncope 17,18 may further exacerbate imminent syncope.…”