A randomized trial of nocturnal oxygen therapy in chronic obstructive pulmonary disease patients. Effect of long-term oxygen therapy on survival in patients with chronic obstructive pulmonary disease with moderate hypoxaemia. Inhaled nitric oxide in term infants with hypoxemic respiratory failure. Training with supplemental oxygen in patients with COPD and hypoxaemia at peak exercise. Oxygen may improve dyspnea and endurance in patients with chronic obstructive pulmonary disease and only mild hypoxemia. Long-term oxygen therapy stops the natural decline of endurance in COPD patients with reversible hypercapnia. Reappraisal of continuous positive airway pressure therapy in acute cardiogenic pulmonary edema. Short-term results and long-term follow-up. Comparison of the acute effects on gas exchange of nasal ventilation and doxapram in exacerbations of chronic obstructive pulmonary disease. Treatment of acute hypoxemic nonhypercapnic respiratory insufficiency with continuous positive airway pressure delivered by a face mask: A randomized controlled trial.
The beneficial effects of nocturnal oxygen therapy (NOT) in chronic obstructive pulmonary disease (COPD) patients with mild-to-moderate daytime hypoxaemia (arterial oxygen tension (Pa,O2) in the range 7.4-9.2 kPa (56-69 mmHg)) and exhibiting sleep-related oxygen desaturation remains controversial. The effectiveness of NOT in that category of COPD patients was studied. The end points included pulmonary haemodynamic effects after 2 yrs of follow-up, survival and requirement for long-term oxygen therapy (LTOT). Seventy-six patients could be randomized, 41 were allocated to NOT and 35 to no NOT (control). The goal of NOT was to achieve an arterial oxygen saturation of >90% throughout the night. All these patients underwent polysomnography to exclude an associated obstructive sleep apnoea syndrome. The two groups exhibited an identical meansD daytime Pa,O2 of 8.4+/-0.4 kPa (63+/-3 mmHg) at baseline. Twenty-two patients (12 in the NOT group and 10 in the control group, p=0.98) required LTOT during the whole follow-up (35+/-14 months). Sixteen patients died, nine in the NOT group and seven in the control group (p=0.84). Forty-six patients were able to undergo pulmonary haemodynamic re-evaluation after 2 yrs, 24 in the NOT and 22 in the control group. In the control group, mean resting pulmonary artery pressure increased from 19.8+/-5.6 to 20.5+6.5 mmHg, which was not different from the change in mean pulmonary artery pressure in the NOT group, from 18.3+/-4.7 to 19.5+/-5.3 mmHg (p= 0.79). Nocturnal oxygen therapy did not modify the evolution of pulmonary haemodynamics and did not allow delay in the prescription of long-term oxygen therapy. No effect of NOT on survival was observed, but the small number of deaths precluded any firm conclusion. These results suggest that the prescription of nocturnal oxygen therapy in isolation is probably not justified in chronic obstructive pulmonary disease patients. To date only two controlled studies have been published on the effects of domiciliary oxygen treatment on survival in patients with chronic obstructive pulmonary disease (COPD) with advanced respiratory failure. The survival in such patients despite oxygen treatment remains poor. The prescription of long term oxygen therapy (LTOT) in less severe disease remains controversial. The aim of this study was to evaluate the rationale for prescribing oxygen to patients with COPD with moderate hypoxaemia.
                One hundred and thirty five patients with COPD, with PaO2 7.4-8.7 kPa (56-65 mmHg) and advanced airflow limitation (mean (SD) forced expiratory volume in one second (FEV1) 0.83 (0.28) 1), were randomly allocated to a control (n = 67) and LTOT (n = 68) group. The patients were followed every three months for at least three years or until death.
                The cumulative survival rate was 88% at one year, 77% at two years, and 66% at three years. No significant differences were found in survival rates between patients treated with LTOT and controls, nor did longer oxygen use (over 15 hours per day) improve survival. Younger age, better spirometric values, and higher body mass index predicted better survival.
                Domiciliary oxygen treatment does not prolong survival in patients with COPD with moderate hypoxaemia. Airway limitation seems to determine survival in this group of patients. To determine whether inhaled nitric oxide (NO) administered during conventional mechanical ventilation could produce improvements in oxygenation and reduce the incidence of meeting extracorporeal membrane oxygenation (ECMO) criteria in infants with hypoxemia.
                Prospective, randomized, controlled trial. Enrolled infants were assigned to conventional treatment with or without adjunctive inhaled NO. Control infants meeting failure criteria (partial pressure of arterial oxygen (PaO2)<80 mm Hg (10.7 kPa)) were allowed to cross over. Caregivers were not masked to group assignment.
                Neonatal intensive care units at the University of Alabama Hospital and the Children's Hospital of Alabama, October 1993 to May 1994.
                Newborn infants, both term and near-term, with PaO2 less than 100 mm Hg (13.3 kPa) who were receiving mechanical ventilation with 100% oxygen. Exclusion criteria included major congenital anomalies, diaphragmatic hernia, profound asphyxia, and significant bleeding.
                Inhaled NO was initiated in the NO group at a dose of 20 to 40 ppm and advanced stepwise to 80 ppm if PaO2 remained less than 100 mm Hg (13.3 kPa).
                Primary outcome variables were treatment failure and meeting of ECMO criteria before crossover. Improvement in oxygenation and ultimate use of ECMO or high-frequency oscillatory ventilation were secondary outcome variables.
                Seventeen neonates with hypoxemia were enrolled; 16 had echocardiographic evidence of pulmonary hypertension, and eight had extrapulmonary shunting. At 1 hour of treatment, two infants in the NO group responded with increases in PaO2 of more than 100 mm Hg (13.3 kPa); after crossover, two had increases in PaO2 of more than 10 mm Hg (1.3 kPa) and one control infant had an increase in PaO2 of more than 10 mm Hg (1.3 kPa). All control infants met failure criteria and crossed over to receive NO; two had increases in PaO2 of more than 10 mm Hg (1.3 kPa) with NO treatment. Despite initial responses, all subjects in both groups eventually met failure criteria. There were no differences between groups in primary outcome variables.
                Although inhaled NO produced a transient improvement in oxygenation in some infants, it did not reduce the incidence of meeting ECMO criteria in this population. Supplemental oxygen has acute beneficial effects on exercise performance in patients with chronic obstructive pulmonary disease (COPD). The purpose of this study was to investigate whether oxygen-supplemented training enhances the effects of training while breathing room air in patients with severe COPD. A randomized controlled trial was performed in 24 patients with severe COPD who developed hypoxaemia during incremental cycle exercise (arterial oxygen saturation (Sa,O2) <90% at peak exercise). All patients participated in an in-patient pulmonary rehabilitation programme of 10 weeks duration. They were assigned either to general exercise training while breathing room air (GET/RA group: forced expiratory volume in one second (FEV1) 38% of predicted; arterial oxygen tension (Pa,O2) 10.5 kPa at rest; Pa,O2 7.3 kPa at peak exercise), or to GET while breathing supplemental oxygen (GET/O2 group: FEV1 29% pred; Pa,O2 10.2 kPa at rest; Pa,O2 7.2 kPa at peak exercise). Sa,O2 was not allowed to fall below 90% during the training. The effects on exercise performance while breathing air and oxygen, and on quality of life were compared. Maximum workload (Wmax) significantly increased in the GET/RA group (mean (SD) 17 (15) W, p<0.01), but not in the GET/O2 group (7 (25) W). Six minute walking distance (6MWD), stair-climbing, weight-lifting exercise (all while breathing room air) and quality of life significantly increased in both groups. Acute administration of oxygen improved exercise performance before and after training. Training significantly increased Wmax, peak carbon dioxide production (V'CO2) and 6MWD while breathing oxygen in both groups. Differences between groups were not significant. Pulmonary rehabilitation improved exercise performance and quality of life in both groups. Supplementation of oxygen during the training did not add to the effects of training on room air. Oxygen (O2) has been reported to improve exercise tolerance in some patients with chronic obstructive pulmonary disease (COPD) despite only mild resting hypoxemia (PaO2 greater than 60 mm Hg). To confirm these prior studies and evaluate potential mechanisms of benefit, we measured dyspnea scores by numeric rating scale during cycle ergometry endurance testing and correlated the severity of dyspnea with right ventricular systolic pressure (RVSP) measured by Doppler echocardiography during a separate supine incremental exercise test. Both sets of exercise were performed according to a randomized double-blind crossover protocol in which patients breathed compressed air or 40% O2. We studied 12 patients with severe COPD (FEV1 0.89 +/- 0.09 L [mean +/- SEM], FEV1/FVC 37 +/- 2%, DLCO 9.8 +/- 1.5 ml/min/mm Hg[47% of predicted], PaO2 71 +/- 2.6 mm Hg). With endurance testing on compressed air, PaO2 did not change significantly in the group as whole (postexercise PaO2 63 +/- 5.1 mm Hg, p = NS), but did fall to less than 55 mm Hg in four patients from this group. Duration of exercise increased on 40% O2 from 10.3 +/- 1.6 to 14.2 +/- 1.5 min (p = 0.005), and the rise in dyspnea scores was delayed. Oxygen delayed the rise in RVSP with incremental exercise in all patients and lowered the mean RVSP at maximum exercise from 71 +/- 8 to 64 +/- 7 mm Hg (p less than 0.03). Improvement in duration of exercise correlated with decrease in dyspnea (r2 = 0.66, p = 0.001) but not with decreases in heart rate, minute ventilation, or RVSP.(ABSTRACT TRUNCATED AT 250 WORDS) Respiratory muscle weakness is one of the most important causes of hypercapnia in patients with COPD. There is evidence that stable hypercapnic patients will benefit from long-term oxygen therapy (LTOT).
                The prognostic role of reversible hypercapnia in COPD is still unclear. Early implementation of LTOT in these patients may influence endurance time and mortality.
                In this pilot study, we investigated 28 patients (26 males, 49-74 years) with COPD, advanced airflow limitation [forced expiratory volume in 1 s (percentage of predicted value) 40.8 +/- 10.2] and mild hypoxaemia (pO(2) 66.5 +/- 6.3 mm Hg). All patients had developed a moderate reversible hypercapnia during an acute exacerbation or during exercise testing (peak pCO(2) 48.0 +/- 2.5 mm Hg). Patients were allocated randomly to a control group (n = 14) or an LTOT group (n = 14). The two groups were well matched in terms of physiological data. Lung function, endurance time (cycle ergometer), dyspnoea score, blood gases and LTOT compliance were measured at baseline and every 6 months over a period of 3 years.
                Endurance time increased from 6.4 +/- 2.7 min at baseline to 7.1 +/- 2.7 min after 1 year in the LTOT group and decreased from 6.1 +/- 3.0 to 4.9 +/- 3.8 min in the controls (p < 0.05). After 1 year, the end-exercise dyspnoea score was significantly lower in the LTOT group (4.5 +/- 1.5) than in the controls (5.7 +/- 1.9).
                COPD patients with reversible hypercapnia and mild hypoxaemia benefit from LTOT in terms of endurance time and a reduction of exertional dyspnoea after 1 year.
                Copyright 2004 S. Karger AG, Basel To investigate whether serial incremental continuous positive airway pressure (CPAP) has any short-term or long-term advantages over face-mask oxygen therapy by way of intrapulmonary shunt reduction, 100 patients admitted to the coronary care unit for the treatment of acute cardiogenic pulmonary edema were studied. All patients received Swan-Ganz catheterization. Hemodynamic and pulmonary function parameters were recorded over the next 6 h, and the patients were followed until hospital discharge. All survivors received regular follow-up at 1-month intervals in the outpatient clinic. During the first-stage investigation period (3 h) PaO2 in the CPAP group showed a significant increase, whereas the intrapulmonary shunt and alveolar-arterial oxygen tension gradient (P[A-a]O2) was significantly reduced (p < 0.005). The CPAP group had significantly lower rate-pressure product and higher stroke volume index compared with the control group. The therapeutic failure rate over 6 h was 24% in the CPAP group and 50% in the control group (p < 0.01). The CPAP group had a significantly lower incidence of tracheal intubation and ventilator therapy than the control group; however, there was no significant difference in short-term mortality and hospital stay between the two groups. In conclusion, although study size was not large enough to demonstrate a difference in mortality, CPAP therapy resulted in physiologic cardiovascular and pulmonary function improvement and significantly reduced the need for intubation; however, it did not decrease mortality in patients with acute cardiogenic pulmonary edema, and a much larger study is needed to investigate this possibility. Nasal intermittent positive pressure ventilation (NIPPV) is useful in exacerbations of chronic obstructive pulmonary disease (COPD) complicated by ventilatory failure. The effects of NIPPV were compared with those of the respiratory stimulant doxapram on gas exchange in patients with COPD and acute ventilatory failure.
                Patients admitted with acute exacerbations of COPD and type 2 respiratory failure (Pao2 < 8 kPa and PaCO2 > 6.7 kPa) who did not improve with conventional treatment were randomised to receive either NIPPV or intravenous doxapram. Blood gas tensions were monitored for four hours.
                In nine patients who received NIPPV the arterial PaO2 improved from a mean (SE) of 5.9 (0.4) kPa to a maximum of 8.1 (0.6) kPa which was maintained at four hours. Eight patients who received doxapram had a similar baseline Pao2 of 5.6 (0.4) kPa which rose to a maximum of 7.3 (0.5) kPa but this was not maintained at four hours. The improvement in Pao2 in patients on NIPPV was accompanied by a fall in Paco2 but, in contrast, in those who received doxapram there was no improvement in Paco2.
                NIPPV may be more effective than doxapram in the management of acute ventilatory failure complicating COPD. Continuous positive airway pressure (CPAP) is widely used in the belief that it may reduce the need for intubation and mechanical ventilation in patients with acute hypoxemic respiratory insufficiency.
                To compare the physiologic effects and the clinical efficacy of CPAP vs standard oxygen therapy in patients with acute hypoxemic, nonhypercapnic respiratory insufficiency.
                Randomized, concealed, and unblinded trial of 123 consecutive adult patients who were admitted to 6 intensive care units between September 1997 and January 1999 with a PaO(2)/FIO(2) ratio of 300 mm Hg or less due to bilateral pulmonary edema (n = 102 with acute lung injury and n = 21 with cardiac disease).
                Patients were randomly assigned to receive oxygen therapy alone (n = 61) or oxygen therapy plus CPAP (n = 62).
                Improvement in PaO(2)/FIO(2) ratio, rate of endotracheal intubation at any time during the study, adverse events, length of hospital stay, mortality, and duration of ventilatory assistance, compared between the CPAP and standard treatment groups.
                Among the CPAP vs standard therapy groups, respectively, causes of respiratory failure (pneumonia, 54% and 55%), presence of cardiac disease (33% and 35%), severity at admission, and hypoxemia (median [5th-95th percentile] PaO(2)/FIO(2) ratio, 140 [59-288] mm Hg vs 148 [62-283] mm Hg; P =.43) were similarly distributed. After 1 hour of treatment, subjective responses to treatment (P<.001) and median (5th-95th percentile) PaO(2)/FIO(2) ratios were greater with CPAP (203 [45-431] mm Hg vs 151 [73-482] mm Hg; P =.02). No further difference in respiratory indices was observed between the groups. Treatment with CPAP failed to reduce the endotracheal intubation rate (21 [34%] vs 24 [39%] in the standard therapy group; P =.53), hospital mortality (19 [31%] vs 18 [30%]; P =.89), or median (5th-95th percentile) intensive care unit length of stay (6.5 [1-57] days vs 6.0 [1-36] days; P =.43). A higher number of adverse events occurred with CPAP treatment (18 vs 6; P =.01).
                In this study, despite early physiologic improvement, CPAP neither reduced the need for intubation nor improved outcomes in patients with acute hypoxemic, nonhypercapnic respiratory insufficiency primarily due to acute lung injury. JAMA. 2000;284:2352-2360.
Long-term home oxygen therapy improved survival in a selected group of COPD patients with severe hypoxaemia (arterial PaO2 less than 55 mm Hg (8.0 kPa)). Home oxygen therapy did not appear to improve survival in patients with mild to moderate hypoxaemia or in those with only arterial desaturation at night.