Cerebrovascular response to carbon dioxide in patients with congestive heart failure

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 Pa_CO2. 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 PET_CO2, 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.