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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
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.
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.
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