Chest

Chest

Volume 122, Issue 2, August 2002, Pages 445-450
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Clinical Investigations
OXYGEN
Cerebral Oxygenation During Exercise in Patients With Terminal Lung Disease

https://doi.org/10.1378/chest.122.2.445Get rights and content

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 (ΔHbO2) and changes in deoxyhemoglobin (ΔHb) 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 ΔHb, while the ΔHbO2 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, ΔHb decreased while ΔHbO2 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.

Section snippets

Materials and Methods

Thirteen patients participated in the study after written informed consent was obtained, as approved by the Ethics Committee of Copenhagen (case No. KF 01–308-98) [Table 1]. The patients had severe pulmonary disease to such an extent that it placed them in New York Heart Association class III-IV. Thus, they presented with such deteriorated lung function (Table 2) that lung transplantation was considered necessary, and five of the patients required long-term O2 therapy.1

The patients were

Results

With an Fio2 of 0.21, the time to exhaustion was 12.5 ± 2.0 min, corresponding to a peak work rate of 26 ± 4 W, and was associated with a perceived exertion (using a visual Borg scale) of 17 (range, 15 to 20).

Before exercise, the Pao2 was low with a further decrease during exercise to reach the lowest value of 44.7 mm Hg (Table 3). The concentration of lactate increased only a little, with the highest level at only 3.8 mmol/L, and the arterial pH remained stable. The Paco2 was not affected at

Discussion

Performed in patients with terminal lung disease, this study demonstrated the following: (1) during exercise the NIRS-determined cerebral hemoglobin concentration increases corresponding to the increase in cerebral perfusion; (2) in normoxia, the cerebral oxygenation decreases as deoxyhemoglobin becomes elevated with an unchanged concentration of oxyhemoglobin; and (3) an elevated Fio2 increases both the Sao2 and the oxygenation of the brain. These results indicate that it is possible to assess

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    Copyright © 2002 The American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.