Oxygen for hypoxemic patients with chronic lung disease?
ACP J Club. 1992 May-June;116:71. doi:10.7326/ACPJC-1992-116-3-071
Swinburn CR, Mould H, Stone TN, Corris PA, Gibson GJ. Symptomatic benefit of supplemental oxygen in hypoxemic patients with chronic lung disease. Am Rev Respir Dis. 1991 May;143:913-5.
To evaluate symptomatic response to supplemental oxygen in hypoxemic patients with chronic lung disease.
Randomized, double-blind, placebo-controlled crossover trial.
Hospital department of respiratory medicine.
10 inpatients with interstitial lung disease (ILD) and 12 with chronic obstructive airways disease (COAD) who were severely disabled and breathless at rest and claimed benefit from supplemental oxygen. Baseline characteristics for the ILD and COAD groups included mean age, 56 and 60 years; proportion of men, 60% and 58%; forced expiratory volume in 1 s (FEV1), 1.5 L and 0.7 L; and partial pressure of CO2 in arterial blood (PaCO2), 35 mm Hg and 47 mm Hg, respectively.
While comfortably seated, patients received 28% oxygen or air each for 2 periods of 10 min, with a 5-min washout period in between, in a randomly determined sequence, through the same face mask at the same source flow rate. A 10-minute run was considered acceptable if the arterial oxygen saturation (SaO2) measured with an ear oximeter remained stable during the last 5 minutes. Ventilation was measured noninvasively in 9 patients with ILD and 10 patients with COAD using 2 pairs of magnetometers.
Main outcome measures
Mean values were calculated from the 2 periods for SaO2, ventilation (VE), average tidal volume (VT, respiratory rate, and severity of breathlessness scored on a 100-mm visual analog scale. Patients were asked at the end of each period if the gas helped their breathing.
Both groups had higher mean SaO2 values while breathing oxygen (95% vs. 86% and 93% vs. 85%, respectively, P < 0.01 for each comparison). In both groups patients reported a benefit more often with oxygen than with air (P < 0.05 for each comparison). 13 of 22 patients gave concordant positive responses after breathing oxygen to the question about their breathing being helped, whereas 6 of 22 patients gave concordant positive responses after air. Concordant negative responses were given by 7 patients after air, but by none of the patients after oxygen. Visual analog scale scores were lower (indicating less breathlessness) in both groups after O2 (P < 0.05). VT andVE values were lower after O2 for the COAD group only (P < 0.01).
Supplemental oxygen reduced symptoms of breathlessness in hospitalized, hypoxemic patients with chronic lung disease.
Source of funding: Not stated.
Address for article reprint: Dr. G.J. Gibson, Department of Respiratory Medicine, Freeman Hospital, Newcastle upon Tyne, NE7 7DN, United Kingdom.
During the acute exacerbation of chronic lung disease (CLD), correction of hypoxemia is one of the mainstays of therapy (1). Frequently, oxygen therapy is administered in inadequate amounts for fear of inducing hypercarbia and respiratory acidosis. The hypercarbia is often modest if therapy is titrated to just achieve a SaO2 of 90% (1). Nevertheless, it is often difficult to distinguish specific symptomatic benefits from oxygen therapy in the setting where multiple treatment modalities are used.
This study describes a subset of inpatients with severe CLD and hypoxemia and breathlessness at rest. The findings of the study support the suggestion that a decrease in breathlessness with oxygen administration is a specific response to O2. However, the patients were preselected according to previous responses to O2, and the sample size was small.
Factors postulated to influence dyspnea include chemical drive to breathe and mechanical coupling of the breathing pattern with respiratory loads and drive. Objective measurement of dyspnea is inherently limited, but the current methods are reasonable. The decrease in VT with O2 in the subset of patients with COAD and hypercarbia has been previously described (2). This finding and the symptomatic relief with O2 may be caused by relief of hypoxic bronchoconstriction because there is no clear decrease in the drive to breathe in these patients (2). The respiratory pattern in patients with end-stage ILD is largely determined by the substantial elastic load on the respiratory system, which may be unable to further respond to the additional chemical hypoxemic stimulus. This lack of response may then cause dyspnea with no change in respiratory pattern.
Kenneth W. Presberg, MD
Medical College of Wisconsin Milwaukee, Wisconsin