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Published ahead of print on March 5, 2003, doi:10.1164/rccm.200208-793OC

Am. J. Respir. Crit. Care Med., Volume 167, Number 11, June 2003, 1534-1539

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Submitted on August 6, 2002
Accepted on February 28, 2003

Influence of Cheyne-Stokes Respiration on Cardiovascular Oscillations in Heart Failure

Richard S. T. Leung1, John S Floras2, Geraldo Lorenzi-Filho3, Fiona Rankin4, Peter Picton5, and T. Douglas Bradley1*

1 Medicine, Toronto General Hospital/ University Health Network, Toronto, ON, Canada; Sleep and Cardiovascular Physiology Research Laboratories, Mount Sinai Hospital, Toronto, ON, Canada; Centre for Sleep Medicine and Circadian Biology, University of Toronto, Toronto, ON, Canada, 2 Medicine, Mount Sinai Hospital, Toronto, ON, Canada; Sleep and Cardiovascular Physiology Research Laboratories, Mount Sinai Hospital, Toronto, ON, Canada, 3 Medicine, Toronto General Hospital/ University Health Network, Toronto, ON, Canada; Sleep and Cardiovascular Physiology Research Laboratories, Mount Sinai Hospital, Toronto, ON, Canada, 4 Sleep and Cardiovascular Physiology Research Laboratories, Mount Sinai Hospital, Toronto, ON, Canada, 5 Medicine, Toronto General Hospital/ University Health Network, Toronto, ON, Canada

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

In patients with congestive heart failure, Cheyne-Stokes respiration is accompanied by oscillations in blood pressure and heart rate at very low frequency. It is not known whether these cardiovascular oscillations are primarily related to oscillations in ventilation or oxyhemoglobin saturation. We hypothesized that abolition of the ventilatory oscillations of Cheyne-Stokes respiration by CO2 inhalation would eliminate accompanying oscillations in blood pressure and heart rate, but that elimination of hypoxic dips by supplemental O2 would not. We studied 10 subjects with heart failure and Cheyne-Stokes respiration during sleep using frequency spectral analysis. During Cheyne-Stokes respiration, heart rate and blood pressure oscillated in association with respiratory oscillations at very low frequency. Inhalation of CO2 abolished Cheyne-Stokes respiration and associated oscillations in both blood pressure and heart rate. In contrast, inhalation of O2 sufficient to eliminate hypoxic dips had no significant effect on Cheyne-Stokes respiration, blood pressure (n=6) or heart rate (n=5). We conclude that ventilatory oscillations during Cheyne-Stokes respiration rather than oscillations in oxygenation per se powerfully induce heart rate and blood pressure oscillations. Cheyne-Stokes respiration is therefore one of the mechanisms that contributes to the very low frequency oscillations in heart rate and blood pressure observed in patients with heart failure.
Key words: central sleep apnea, heart rate variability, blood pressure variability




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