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Tilt Testing with Combined Lower Body Negative Pressure: a "Gold Standard" for Measuring Orthostatic Tolerance
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Increased vasoconstriction predisposes to hyperpnea and postural faint.

Indu Taneja1, Marvin S Medow, June L Glover

  • 1Department of Pediatrics, New York Medical College, Hawthorne, NY 10532, USA. indu_taneja@nymc.edu

American Journal of Physiology. Heart and Circulatory Physiology
|May 27, 2008
PubMed
Summary

Simple postural fainting involves excessive blood pooling in the abdomen (splanchnic hypervolemia) and reduced blood in the chest (thoracic hypovolemia). This leads to increased breathing (hyperpnea) and may trigger fainting via the pulmonary stretch reflex.

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Area of Science:

  • Cardiovascular Physiology
  • Autonomic Nervous System Function
  • Respiratory Physiology

Background:

  • Previous research links postural fainting to splanchnic hypervolemia and thoracic hypovolemia during orthostasis.
  • A hypothesis suggests thoracic hypovolemia drives sympathetic overactivation, increased tidal volume, and fainting through the pulmonary stretch reflex.

Purpose of the Study:

  • To investigate the physiological mechanisms underlying simple postural fainting.
  • To determine the role of thoracic hypovolemia, sympathetic activation, and respiratory changes in the fainting response.

Main Methods:

  • Studied 18 young individuals (11 fainters, 7 controls) undergoing 70-degree upright tilt.
  • Measured continuous blood pressure, heart rate, respiration (inductance plethysmography), end-tidal CO2 (capnography), and regional blood volumes/flows (impedance plethysmography).
  • Calculated arterial resistance and splanchnic blood volume changes.

Main Results:

  • Fainters exhibited decreased splanchnic resistance and increased splanchnic blood volume during tilt, unlike controls.
  • Fainters showed increased normalized tidal volume and minute ventilation, with decreased respiratory rate, preceding faint.
  • End-tidal CO2 decreased proportionally to the increase in minute ventilation in fainters.

Conclusions:

  • Excessive splanchnic pooling and thoracic hypovolemia contribute to increased peripheral resistance and hyperpnea in simple postural faint.
  • Hyperpnea and pulmonary stretch reflexes may play a role in the sympathoinhibition observed during fainting.
  • Findings elucidate the complex interplay of cardiovascular and respiratory systems in orthostatic intolerance.