Ventilatory and cerebrovascular responses in normocapnic and hypercapnic COPD patients

This study investigated the hypothesis that hypercapnia in some chronic obs tructive pulmonary disease (COPD) patients may be related to a high cerebro vascular response to carbon dioxide (CO2). The relationship between responses of ventilation and of cerebral blood vol ume (CBV) to acute changes in carbon dioxide tension in arterial blood (Pa, co,) was measured in 17 chronic hypercapnic (Pa,CO2 > 6.0 kPa) and 16 normo capnic (Pa,CO2 less than or equal to 6.0 kPa) COPD patients, who were match ed for degree of airway obstruction (forced expiratory volume in one second 27% predicted). Results were compared with 15 age-matched healthy subjects . CBV was measered using near infrared spectroscopy during normo- and hyper capnia and related to inspired minute ventilation (V 'I) and mouth occlusio n pressure (P0.1). Hypercapnia (end-tidal pressure of carbon dioxide (Delta PET,CO2) > 1 kPa) was induced by giving adequate amounts Of CO2 in the ins pired air. During normocapnia, CBV (mL.100 g(-1)) was 2.41 +/- 0.66 and 2.90 +/- 0.60 (mean +/- SD) in the normocapnic and chronic hypercapnic patients, respecti vely, which was significantly lower compared to healthy subjects (3.53 +/- 0.77). All slopes Of CO2 responsiveness (Delta CBV/Delta Pa,CO2, DeltaV 'I/ Delta Pa,CO2, Delta P0.1/Delta Pa,CO2) were significantly lower in both COP D groups relative to healthy subjects, but were not significantly different between the COPD groups. A poor but positive correlation between ventilato ry and cerebrovascular CO2 responsiveness (Delta CBV/Delta Pa,CO2 and Delta V 'I/Delta Pa,CO2) was found in COPD patients and healthy subjects. The findings do not support the hypothesis of abnormal cerebrovascular resp onses to carbon dioxide in hypercapnic chronic obstructive pulmonary diseas e patients.