|
|
||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Department of Surgery and Anesthesia, Wellington School of Medicine and Health Sciences, Wellington, New Zealand
Submitted 30 July 2006 ; accepted in final form 11 January 2007
Normally, at rest, the amplitude of respiratory sinus arrhythmia (RSA) appears to correlate with cardiac vagal tone. However, recent studies showed that, under stress, RSA dissociates from vagal tone, indicating that separate mechanisms might regulate phasic and tonic vagal activity. This dissociation has been linked to the hypothesis that RSA improves pulmonary gas exchange through preferential distribution of heartbeats in inspiration. We examined the effects of hypercapnia and mild hypoxemia on RSA-vagal dissociation in relation to heartbeat distribution throughout the respiratory cycle in 12 volunteers. We found that hypercapnia, but not hypoxemia, was associated with significant increases in heart rate (HR), tidal volume, and RSA amplitude. The RSA amplitude increase remained statistically significant after adjustment for respiratory rate, tidal volume, and HR. Moreover, the RSA amplitude increase was associated with a paradoxical rise in HR and decrease in low-frequency-to-high-frequency mean amplitude ratio derived from spectral analysis, which is consistent with RSA-vagal dissociation. Although hypercapnia was associated with a significant increase in the percentage of heartbeats during inspiration, this association was largely secondary to increases in the inspiratory period-to-respiratory period ratio, rather than RSA amplitude. Additional model analyses of RSA were consistent with the experimental data. Heartbeat distribution did not change during hypoxemia. These results support the concept of RSA-vagal dissociation during hypercapnia; however, the putative role of RSA in optimizing pulmonary perfusion matching requires further experimental validation.
ventilation-perfusion mismatch; heart rate variability
This article has been cited by other articles:
![]() |
C. Julien, M. J. Parkes, S. Y. C. Tzeng, P. Y. W. Sin, P. N. Ainslie, P. van de Borne, J.-O. Fortrat, M.-A. Custaud, C. Gharib, A. Porta, et al. Comments on Point:Counterpoint: Respiratory sinus arrhythmia is due to a central mechanism vs. respiratory sinus arrhythmia is due to the baroreflex mechanism J Appl Physiol, May 1, 2009; 106(5): 1745 - 1749. [Full Text] [PDF] |
||||
![]() |
Y. C. Tzeng, P. Y. W. Sin, and D. C. Galletly Human sinus arrhythmia: inconsistencies of a teleological hypothesis Am J Physiol Heart Circ Physiol, January 1, 2009; 296(1): H65 - H70. [Abstract] [Full Text] [PDF] |
||||
![]() |
A. Van de Louw, C. Medigue, Y. Papelier, and F. Cottin Breathing cardiovascular variability and baroreflex in mechanically ventilated patients Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2008; 295(6): R1934 - R1940. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |