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Clinical Investigations: COPD |

Effects of Acetazolamide and Furosemide on Ventilation and Cerebral Blood Volume in Normocapnic and Hypercapnic Patients With COPD*

Marjo J. T. van de Ven, MD; Willy N. J. M. Colier, PhD; Marco C. van der Sluijs, BSc; Berend Oeseburg, MD, PhD; Piet Vis, MD, PhD; Hans Folgering, MD, PhD
Author and Funding Information

*From the Department of Pulmonology Dekkerswald (Drs. van de Ven and Folgering) and the Department of Physiology (Drs. Colier, Oeseburg, and Vis and Mr. van der Sluijs), Faculty of Medical Sciences, University Medical Center Nijmegen, The Netherlands.

Correspondence to: Marjo J. T. van de Ven, MD, Department of Pulmonology Dekkerswald, University Medical Center Nijmegen, PO Box 9001, 6560 GB Groesbeek, The Netherlands; e-mail: m_vandeven60@hotmail.com



Chest. 2002;121(2):383-392. doi:10.1378/chest.121.2.383
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Study objectives: Effects of chronic metabolic alkalosis and acidosis and their relation to central chemoregulation may differ between normocapnic and chronic hypercapnic patients with COPD. The relationship between responses of inspired ventilation (Vi), mouth occlusion pressure (P0.1), and cerebral blood volume (CBV), to short-term changes in arterial Pco2 was measured.

Patients and methods: Seventeen patients with chronic hypercapnia and COPD (Paco2 > 6.0 kPa) and 16 normocapnic patients with COPD (Paco2 ≤ 6.0 kPa)[ FEV1 27% predicted] were studied under baseline metabolic conditions and after 1 week of treatment with oral furosemide, 40 mg/d, or acetazolamide, 500 mg/d. Hypercapnia (change in end-tidal carbon dioxide > 1 kPa) was induced by administering adequate amounts of carbon dioxide in the inspired air. CBV was measured using near-infrared spectroscopy.

Results: Compared with baseline metabolic condition, chronic metabolic acidosis and alkalosis did not change ventilatory (ΔVi/ΔPaco2) and cerebrovascular (ΔCBV/ΔPaco2) reactivity. Base excess (BE) decreased by 6.8 ± 1.1 mEq/L and 6.9 ± 1.6 mEq/L, respectively, in the normocapnic and chronic hypercapnic COPD groups during metabolic acidosis, resulting in a not-quite-significant leftward shift of both the ventilatory and cerebrovascular carbon dioxide response curve. BE increased by 2.3 ± 1.2 mEq/L and 1.2 ± 1.3 mEq/L, respectively, during chronic metabolic alkalosis in both COPD groups, without concomitant shift. Poor correlations between ventilatory and cerebrovascular carbon dioxide responsiveness (ΔCBV/ΔPaco2 andΔ Vi/ΔPaco2,Δ CBV/ΔPaco2 andΔ P0.1/ΔPaco2, respectively) were found irrespective of baseline, respiratory condition, and induced metabolic state.

Conclusions: Normocapnic and chronic hypercapnic COPD patients have the same ventilatory and cerebrovascular carbon dioxide responsiveness irrespective of induced metabolic state.

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