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Published ahead of print on May 18, 2005, doi:10.1164/rccm.200406-807OC
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American Journal of Respiratory and Critical Care Medicine Vol 172. pp. 371-378, (2005)
© 2005 American Thoracic Society
doi: 10.1164/rccm.200406-807OC

Original Article

Cerebrovascular Response to Carbon Dioxide in Patients with Congestive Heart Failure

Ailiang Xie, James B. Skatrud, Rami Khayat, Jerome A. Dempsey, Barbara Morgan and Douglas Russell

Departments of Medicine, Orthopedics and Rehabilitation, and Population Health Sciences, University of Wisconsin; and the William S. Middleton Memorial Veterans Hospital, Madison, Wisconsin

Correspondence and requests for reprints should be addressed to Ailiang Xie, M.D., Ph.D., Pulmonary Physiology Laboratory, William S. Middleton Veterans Hospital, 2500 Overlook Terrace, Madison, WI 53705. E-mail: axie{at}facstaff.wisc.edu

Rationale: Cerebrovascular reactivity to CO2 provides an important counterregulatory mechanism that serves to minimize the change in H+ at the central chemoreceptor, thereby stabilizing the breathing pattern in the face of perturbations in PaCO2. However, there are no studies relating cerebral circulation abnormality to the presence or absence of central sleep apnea in patients with heart failure. Objectives: To determine whether patients with congestive heart failure and central sleep apnea have an attenuated cerebrovascular responsibility to CO2. Methods: Cerebral blood flow velocity in the middle cerebral artery was measured in patients with stable congestive heart failure with (n = 9) and without (n = 8) central sleep apnea using transcranial ultrasound during eucapnia (room air), hypercapnia (inspired CO2, 3 and 5%), and hypocapnia (voluntary hyperventilation). In addition, eight subjects with apnea and nine without apnea performed a 20-second breath-hold to investigate the dynamic cerebrovascular response to apnea. Measurements and Main Results: The overall cerebrovascular reactivity to CO2 (hyper- and hypocapnia) was lower in patients with apnea than in the control group (1.8 ± 0.2 vs. 2.5 ± 0.2%/mm Hg, p < 0.05), mainly due to the prominent reduction of cerebrovascular reactivity to hypocapnia (1.2 ± 0.3 vs. 2.2 ± 0.1%/mm Hg, p < 0.05). Similarly, brain blood flow demonstrated a smaller surge after a 20-second breath-hold (peak velocity, 119 ± 4 vs. 141 ± 8% of baseline, p < 0.05). Conclusion: Patients with central sleep apnea have a diminished cerebrovascular response to PETCO2, especially to hypocapnia. The compromised cerebrovascular reacticity to CO2 might affect stability of the breathing pattern by causing ventilatory overshooting during hypercapnia and undershooting during hypocapnia.

Key Words: central sleep apnea • cerebral blood flow • hypercapnia • hypocapnia




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