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(Chest. 2002;122:445-450.)
© 2002 American College of Chest Physicians

Cerebral Oxygenation During Exercise in Patients With Terminal Lung Disease*

Gabrielle Jensen, MD; Henning Bay Nielsen, MD; Kojiro Ide, PhD; Per Lav Madsen, MD; Lars Bo Svendsen, MD; Ulrik Gerner Svendsen, MD, PhD and Niels Henry Secher, MD, PhD

* From the Department of Anesthesia (Drs. Jensen, Nielsen, Ide, Madsen, L.B. Svendsen, and Secher), Copenhagen Muscle Research Center, Copenhagen, Denmark; and the Pulmonary Clinic (Dr. U.G. Svendsen), The Heart Center, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark.

Correspondence to: Henning Bay Nielsen, MD, Department of Anesthesia 2041, Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen Ø, Denmark; e-mail: h.bay{at}dadlnet.dk

Study objectives: In patients with terminal lung disease who were exercising, we assessed whether improved arterial O2 saturation with an increased fraction of inspired oxygen (FIO2) affects cerebral oxygenation.

Design: Randomized, crossover.

Patients and methods: The cerebral changes in oxyhemoglobin ({Delta}HbO2) and changes in deoxyhemoglobin ({Delta}Hb) levels were evaluated using near-infrared spectrophotometry and the middle cerebral artery (MCA) mean velocity (Vmean) was determined by transcranial Doppler ultrasonography in 13 patients with terminal lung disease (New York Heart Association class III-IV). Patients were allocated to an FIO2 of either 0.21 or 0.35 during incremental exercise with 15 min between trials.

Results: Peak exercise intensity (mean [± SE], 26 ± 4 W) reduced the arterial O2 pressure (at rest, 64 ± 3 mm Hg; during exercise, 56 ± 3 mm Hg) and the arterial oxygen saturation (SaO2) [at rest, 92 ± 2%; 87 ± 2%; p < 0.05], while the arterial CO2 pressure was not significantly affected. The MCA Vmean increased from 49 ± 5 to 63 ± 7 cm/s (p < 0.05) as did the {Delta}Hb, while the {Delta}HbO2 remained unaffected by exercise. With an elevated FIO2, the SaO2 level (at rest, 95.8 ± 0.7%; during exercise, 96.0 ± 1.0%) and arterial O2 pressure (at rest, 102 ± 11 mm Hg; during exercise, 100 ± 8 mm Hg) were not significantly affected by exercise, and the levels of blood oxygenation remained higher than the values established at normoxia (p < 0.05). The MCA Vmean increased to a level similar to that achieved during control exercise (ie, to 70 ± 11 cm/s). In contrast to control exercise, {Delta}Hb decreased while {Delta}HbO2 increased during exercise with 35% O2 (p < 0.05).

Conclusion: An O2-enriched atmosphere enabled patients with terminal lung disease to maintain arterial O2 saturation during exercise. An exercise-induced increase in cerebral perfusion was not affected by hyperoxia, whereby the enhanced availability of oxygenated hemoglobin increases cerebral oxygenation. The clinical implication of the study is that during physical activity patients with terminal lung disease are recommended to use an elevated FIO2 to protect cerebral oxygenation.

Key Words: acidosis • arterial oxygen saturation • cycling • hyperoxia • lactate






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