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Leg crossing, muscle tensing, squatting, and the crash position are effective against vasovagal reactions solely through increases in cardiac output.

Authors :
Krediet, C. T. Paul
De Bruin, Ivar G. J. M.
Ganzeboom, Karin S.
Linzer, Mark
van Lieshout, Johannes J.
Wieling, Wouter
Source :
Journal of Applied Physiology; Nov2005, Vol. 99 Issue 5, p1697-1703, 7p, 1 Diagram, 4 Charts, 3 Graphs
Publication Year :
2005

Abstract

Tensing of lower body muscles without or with leg crossing (LBMT, LCMT), whole body tensing (WBT), squatting, and sitting with the head bent between the knees ("crash position," HBK) are believed to abort vasovagal reactions. The underlying mechanisms are unknown. To study these interventions in patients with a clinical history of vasovagal syncope and a vasovagal reaction during routine tilt table testing, we measured blood pressure (BP) continuously with Finapres and derived heart rate, stroke volume, cardiac output (CO), and total peripheral resistance using Modelflow. In series A (n = 12) we compared LBMT to LCMT. In series B (n = 9), WBT was compared with LCMT. In series C (n = 14) and D (n = 9), we tested squatting and HBK. All maneuvers caused an increase in BP, varying from a systolic rise from 77 ± 8 to 104 ± 18 mmHg (P < 0.05) in series A during LBMT to a rise from 70 ± 10 to 123 ± 9 mmHg (P < 0.05) in series B during LCMT. In each maneuver, the BP increase started within 3-5 s from start of the maneuver. In all maneuvers, there was an increase in CO varying from 54 ± 12% of baseline to 94 ± 21% in WBT to a rise from 65 ± 17% to 110 ± 22% in LCMT in series A. No maneuver caused significant change in total peripheral resistance. We conclude that the mechanism underlying the effects of these maneuvers is exclusively an increase in CO. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
87507587
Volume :
99
Issue :
5
Database :
Complementary Index
Journal :
Journal of Applied Physiology
Publication Type :
Academic Journal
Accession number :
18791995
Full Text :
https://doi.org/10.1152/japplphysiol.01250.2004