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Am J Physiol Heart Circ Physiol (November 15, 2001). doi:10.1152/ajpheart.00554.2001
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Articles in PresS, published online ahead of print November 14, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00554.2001
Submitted on June 25, 2001
Accepted on November 1, 2001

Direct effect of PaCO2 on respiratory sinus arrhythmia in conscious humans

Nobuko Sasano1, Alex E Vesely2, Junichiro Hayano3, Hiroshi Sasano1, Ron B Somogyi2, David Preiss2, Kiyoyuki Miyasaka2, Hirotada Katsuya4, Steve Iscoe5, and Joseph A Fisher2*

1 Anesthesia, University Health Network, University of Toronto, Toronto, Ontario, Canada; Anesthesiology and Resuscitology, Nagoya City University Medical School, Nagoya, Aichi, Japan
2 Anesthesia, University Health Network, University of Toronto, Toronto, Ontario, Canada
3 Third Department of Internal Medicine, Nagoya City University Medical School, Nagoya, Aichi, Japan
4 Anesthesiology and Resuscitology, Nagoya City University Medical School, Nagoya, Aichi, Japan
5 Physiology, Queen's University, Kingston, Ontario, Canada

* To whom correspondence should be addressed. E-mail: joe.fisher{at}utoronto.ca.

Respiratory sinus arrhythmia (RSA) may improve the efficiency of pulmonary gas exchange by matching pulmonary blood flow to lung volume during each respiratory cycle. If so, an increased demand for pulmonary gas exchange may enhance RSA magnitude. We therefore tested the hypothesis that CO2 directly affects RSA in conscious humans even when changes in tidal volume (VT ) and breathing frequency (FB ), which indirectly affect RSA, are prevented. In 7 healthy subjects, we adjusted end-tidal PCO2 (PETCO2 ) to 30, 40 or 50 mmHg in random order at constant VT and FB . The mean amplitude of the high-frequency component of R-R interval variation was used as a quantitative assessment of RSA magnitude. RSA magnitude increased progressively with PETCO2 (P < 0.001). Mean R-R interval did not differ at PETCO2 s of 40 and 50 mmHg but was less at 30 mmHg (P < 0.05). Finally, because VT and FB were constant, these results support our hypothesis that increased CO2 directly increases RSA magnitude, probably via a direct effect on medullary mechanisms generating RSA.




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