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Related Experiment Video

Updated: May 24, 2026

Tilt Testing with Combined Lower Body Negative Pressure: a "Gold Standard" for Measuring Orthostatic Tolerance
14:09

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Published on: March 21, 2013

MSNA during prolonged post-faint hypotension.

J Rozenberg1, W Wieling, I K Schon

  • 1Department of Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. Josien.Rozenberg@student.uva.nl

Clinical Autonomic Research : Official Journal of the Clinical Autonomic Research Society
|March 15, 2012
PubMed
Summary
This summary is machine-generated.

Prolonged post-faint hypotension (PPFH) is not caused by vasodilation or sympathetic withdrawal. Delayed cardiac output recovery, potentially due to increased vagal outflow, is the likely mechanism for this condition.

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Area of Science:

  • Cardiovascular Physiology
  • Autonomic Nervous System Function
  • Syncope Pathophysiology

Background:

  • Delayed hemodynamic recovery after syncope, termed prolonged post-faint hypotension (PPFH), is increasingly recognized.
  • The underlying mechanisms, particularly regarding sympathetic nervous system activity and peripheral vasodilation, remain unclear.
  • Previous studies suggest a vagal mechanism, but direct evidence from muscle sympathetic nerve activity (MSNA) is lacking.

Purpose of the Study:

  • To investigate the role of muscle sympathetic nerve activity (MSNA) and hemodynamic changes in prolonged post-faint hypotension (PPFH).
  • To compare patients with PPFH to those with normal recovery (NR) after tilt-back following syncope.
  • To determine if exaggerated vasodilation or sympathetic withdrawal contributes to PPFH.

Main Methods:

  • Retrospective analysis of continuous blood pressure (BP) and MSNA recordings during tilt-induced syncope.
  • Patients were tilted head-up and administered glyceryl trinitrate (GTN) if needed, then returned to the horizontal position.
  • PPFH was defined as systolic BP <85 mmHg for at least 2 minutes post-tilt-back; hemodynamic and MSNA parameters were analyzed at various time points.

Main Results:

  • Both PPFH and NR groups showed decreased mean arterial pressure (MAP) post-recovery, but MAP and heart rate (HR) were lower in the PPFH group.
  • Cardiac output (CO) remained below baseline in early recovery only in the PPFH group, while total peripheral resistance (TPR) was similar in both groups.
  • Muscle sympathetic nerve activity (MSNA) tended to remain elevated above baseline in both groups during recovery, not showing withdrawal.

Conclusions:

  • Prolonged post-faint hypotension (PPFH) is not mediated by exaggerated peripheral vasodilation or sympathetic withdrawal.
  • Delayed recovery of cardiac output, likely influenced by increased vagal outflow, is a more probable cause of PPFH.
  • These findings highlight the complex autonomic regulation following syncope and identify potential targets for future research.