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Related Experiment Videos

The heart is not necessarily empty at syncope.

L R Davrath1, R W Gotshall, A Tucker

  • 1Colorado State University, Department of Physiology, Fort Collins 80523, USA.

Aviation, Space, and Environmental Medicine
|April 2, 1999
PubMed
Summary
This summary is machine-generated.

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Post-spaceflight orthostatic intolerance can be triggered by a 28% decrease in left ventricular end-systolic volume (LVESV). This study found that syncope can occur without sympatho-inhibition or bradycardia, challenging previous theories.

Area of Science:

  • Cardiovascular Physiology
  • Aerospace Medicine
  • Autonomic Nervous System Function

Background:

  • The exact mechanisms of post-spaceflight orthostatic intolerance remain unclear.
  • A leading hypothesis suggests syncope is triggered by a hypercontractile left ventricle leading to profound sympatho-inhibition and vagal stimulation.

Purpose of the Study:

  • To test the hypothesis that a reduced left ventricular end-systolic volume (LVESV) during lower body negative pressure (LBNP) triggers syncope.
  • To investigate the role of catecholamine levels in presyncope.

Main Methods:

  • Eight healthy men underwent progressive lower body negative pressure (LBNP) to presyncope.
  • Two-dimensional echocardiography measured left ventricular volumes at each LBNP stage.
  • Plasma catecholamine concentrations were analyzed using high-performance liquid chromatography (HPLC).
Keywords:
NASA Discipline CardiopulmonaryNon-NASA Center

Related Experiment Videos

Main Results:

  • Left ventricular end-systolic volume (LVESV) decreased by 28% at presyncope without cavity obliteration.
  • Norepinephrine levels increased significantly, but no epinephrine surge was observed.
  • Five subjects remained tachycardic at presyncope, while three became bradycardic.

Conclusions:

  • Syncope can be initiated by a 28% reduction in LVESV.
  • Sympatho-inhibition and bradycardia are not necessary for syncope during LBNP.
  • These findings challenge the traditional understanding of orthostatic intolerance mechanisms.