Am. J. Respir. Crit. Care Med., Vol 155, No. 2, Feb 1997, 530-535.
Factors contributing to relief of exertional breathlessness during hyperoxia in chronic airflow limitation
DE O'Donnell, DJ Bain and KA Webb
Department of Medicine, Queen's University, Kingston, Ontario, Canada.
The mechanisms of exertional dyspnea relief in response to supplemental
oxygen (O2) in chronic airflow limitation (CAL) are not precisely known and
are likely multifactorial. To explore factors contributing to the relief of
dyspnea after oxygen administration, 11 patients with severe CAL (FEV1.0 =
39 +/- 3% predicted, mean +/- SEM) and mild hypoxemia (resting PaO2 = 74
+/- 2 mm Hg) breathed room air (RA) and 60% O2 during exercise at
approximately 50% of their maximal incremental exercise capacity.
Breathlessness ratings (Borg scale), endurance time, respiratory drive
(change in mouth occlusion pressure over the first 0.1 s of inspiration,
P0.1), ventilation (VE), breathing pattern, operational lung volumes, gas
exchange, and metabolic parameters were compared during RA and 60% O2. PaO2
at exercise cessation during RA and 60% O2 was 65 +/- 3 mm Hg and 226 +/-
12 mm Hg, respectively (p < 0.001). With 60% O2, the mean of individual
Borg/time slopes fell significantly (p < 0.05) by 23 +/- 12% and was
associated with a 35 +/- 11% increase (p < 0.01) in endurance time (r =
-0.64, p < 0.05). During 60% O2, slopes of P0.1 and lactate over time
also fell significantly (p < 0.05), whereas delta PaCO2/time did not
change significantly. At a standardized time near end-exercise, Borg, VE,
and P0.1 changed during 60% O2 by -0.8 +/- 0.3 (p < 0.05), -4.1 +/- 2.0
L/min (p = 0.07), and - 1.3 +/- 0.5 cm H2O/s (p < 0.05), respectively.
Slopes of Borg/VE, Borg/lactate, and VE/lactate were essentially
superimposable during tests on RA and O2: Borg, lactate, and VE all fell
proportionally during hyperoxia. In patients with CAL and mild exercise
hypoxemia, relief of exertional breathlessness during hyperoxia is
explained by reduced ventilatory demand in association with reduced blood
lactate levels.
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Copyright © 1997 American Thoracic Society
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