title: Cerebrovascular response to carbon dioxide in patients with congestive heart failure.
abstract: BACKGROUND
  Cerebrovascular reactivity to CO(2) 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 Pa(CO(2)). However, there are no studies relating cerebral circulation abnormality to the presence or absence of central sleep apnea in patients with heart failure.
  
  
  OBJECTIVE
  To determine whether patients with congestive heart failure and central sleep apnea have an attenuated cerebrovascular responsibility to CO(2).
  
  
  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 CO(2), 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.
  
  
  RESULTS
  The overall cerebrovascular reactivity to CO(2) (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).
  
  
  CONCLUSIONS
  Patients with central sleep apnea have a diminished cerebrovascular response to PET(CO(2)), especially to hypocapnia. The compromised cerebrovascular reactivity to CO(2) might affect stability of the breathing pattern by causing ventilatory overshooting during hypercapnia and undershooting during hypocapnia.
authors.affiliation: Department of Medicine, University of Wisconsin, Madison, 53705, USA. axie@facstaff.wisc.edu
authors.forename: Ailiang
authors.initials: A
authors.lastname: Xie
authors.forename: James B
authors.initials: JB
authors.lastname: Skatrud
authors.forename: Rami
authors.initials: R
authors.lastname: Khayat
authors.forename: Jerome A
authors.initials: JA
authors.lastname: Dempsey
authors.forename: Barbara
authors.initials: B
authors.lastname: Morgan
authors.forename: Douglas
authors.initials: D
authors.lastname: Russell
mesh_terms: D000368:Aged; D001783:Blood Flow Velocity; D002245:Carbon Dioxide / Q000008:administration & dosage*; D016022:Case-Control Studies; D002560:Cerebrovascular Circulation; D006333:Heart Failure / Q000150:complications / Q000503:physiopathology*; D006801:Humans; D006935:Hypercapnia; D016857:Hypocapnia; D008297:Male; D008875:Middle Aged; D020182:Sleep Apnea, Central / Q000150:complications / Q000503:physiopathology*; D017585:Ultrasonography, Doppler, Transcranial
chemical_list: D002245:Carbon Dioxide