AJP - Heart Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Heart Circ Physiol 295: H372-H381, 2008. First published May 23, 2008; doi:10.1152/ajpheart.00101.2008
0363-6135/08 $8.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
295/1/H372    most recent
00101.2008v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Taneja, I.
Right arrow Articles by Stewart, J. M.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Taneja, I.
Right arrow Articles by Stewart, J. M.

Increased vasoconstriction predisposes to hyperpnea and postural faint

Indu Taneja,1,2,3 Marvin S. Medow,1,4 June L. Glover,1 Neeraj K. Raghunath,1 and Julian M. Stewart1,2,4

1Department of Pediatrics, 2Department of Medicine, 3Department of Pharmacology, and 4Department of Physiology, New York Medical College, Valhalla, New York

Submitted 30 January 2008 ; accepted in final form 15 May 2008

Our prior studies indicated that postural fainting relates to splanchnic hypervolemia and thoracic hypovolemia during orthostasis. We hypothesized that thoracic hypovolemia causes excessive sympathetic activation, increased respiratory tidal volume, and fainting involving the pulmonary stretch reflex. We studied 18 patients 13–21 yr old, 11 who fainted within 10 min of upright tilt (fainters) and 7 healthy control subjects. We measured continuous blood pressure and heart rate, respiration by inductance plethysmography, end-tidal carbon dioxide (ETCO2) by capnography, and regional blood flows and blood volumes using impedance plethysmography, and we calculated arterial resistance with patients supine and during 70° upright tilt. Splanchnic resistance decreased until faint in fainters (44 ± 8 to 21 ± 2 mmHg·l–1·min–1) but increased in control subjects (47 ± 5 to 53 ± 4 mmHg·l–1·min–1). Percent change in splanchnic blood volume increased (7.5 ± 1.0 vs. 3.0 ± 11.5%, P < 0.05) after the onset of tilt. Upright tilt initially significantly increased thoracic, pelvic, and leg resistance in fainters, which subsequently decreased until faint. In fainters but not control subjects, normalized tidal volume (1 ± 0.1 to 2.6 ± 0.2, P < 0.05) and normalized minute ventilation increased throughout tilt (1 ± 0.2 to 2.1 ± 0.5, P < 0.05), whereas respiratory rate decreased (19 ± 1 to 15 ± 1 breaths/min, P < 0.05). Maximum tidal volume occurred just before fainting. The increase in minute ventilation was inversely proportionate to the decrease in ETCO2. Our data suggest that excessive splanchnic pooling and thoracic hypovolemia result in increased peripheral resistance and hyperpnea in simple postural faint. Hyperpnea and pulmonary stretch may contribute to the sympathoinhibition that occurs at the time of faint.

splanchnic resistance; total peripheral resistance; minute ventilation; regional blood flow



Address for reprint requests and other correspondence: I. Taneja, The Center for Pediatric Hypotension, Suite 3050N, 19 Bradhurst Ave., New York Medical College, Hawthorne, NY 10532 (e-mail: indu_taneja{at}nymc.edu)







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2008 by the American Physiological Society.