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Transient cardiovascular and cerebrovascular responses within the first minute of active standing provide the means to assess autonomic, cardiovascular and cerebrovascular regulation using a real-world everyday stimulus. Traditionally, these responses have been used to detect autonomic dysfunction, and to identify the hemodynamic correlates of patient symptoms and attributable causes of (pre)syncope and falls. This review addresses the physiology of systemic and cerebrovascular adjustment within the first 60 s after active standing. Mechanical factors induced by standing up cause a temporal mismatch between cardiac output and vascular conductance which leads to an initial blood pressure drops with a nadir around 10 s. The arterial baroreflex counteracts these initial blood pressure drops, but needs 2–3 s to be initiated with a maximal effect occurring at 10 s after standing while, in parallel, cerebral autoregulation buffers these changes within 10 s to maintain adequate cerebral perfusion. Interestingly, both the magnitude of the initial drop and these compensatory mechanisms are thought to be quite well-preserved in healthy aging. It is hoped that the present review serves as a reference for future pathophysiological investigations and epidemiological studies. Further experimental research is needed to unravel the causal mechanisms underlying the emergence of symptoms and relationship with aging and adverse outcomes in variants of orthostatic hypotension. [ABSTRACT FROM AUTHOR]

Objectives Continuous noninvasive blood pressure (BP) measurement enables us to observe rapid changes in BP and to study underlying hemodynamic mechanisms. This study aimed to gain insight into the pathophysiological mechanisms underlying short-term orthostatic BP recovery patterns in a real-world clinical setting with (pre)syncope patients. Setting and Participants In a prospective cohort study, the active lying-to-standing test was performed in suspected (pre)syncope patients in the emergency department with continuous noninvasive finger arterial BP measurement. Measures Changes in systolic BP, cardiac output (CO), and systemic vascular resistance (SVR) were studied in normal BP recovery, initial orthostatic hypotension, delayed BP recovery, and sustained orthostatic hypotension. Results In normal recovery (n = 47), ΔBP at nadir was −24 (23) mmHg, with a CO change of +10 (21%) and SVR of −23 (21%). In initial orthostatic hypotension (n = 7) ΔBP at nadir was −49 (17) mmHg and CO and SVR change was −5 (46%) and −29 (58%), respectively. Delayed recovery (n = 12) differed significantly from normal recovery 30 seconds after standing, with a ΔBP of −32 (19) vs 1 (16) mmHg, respectively. Delayed recovery was associated with a significant difference in SVR changes compared to normal recovery, −17 (26%) vs +4 (20%), respectively. There was no difference in CO changes. In sustained orthostatic hypotension (n = 16), ΔBP at 180 seconds after standing was −39 (21) mmHg, with changes in CO of −16 (31%) and SVR of −9 (20%). Conclusions/Implications Hemodynamic patterns following active standing are heterogeneous and differ across orthostatic BP recovery patterns, suggesting that volume status, medication use, and autonomic dysfunction should all be taken into account when evaluating these patients. Moreover, results suggest that a delayed BP recovery is associated with an impaired increase in SVR in a significant proportion of individuals, implying that physicians treating older adults with hypertension should consider the possible negative effect of intensive hypertension treatment on initial orthostatic blood pressure control. [ABSTRACT FROM AUTHOR]