BackgroundIn patients with acute hypercapnic respiratory failure (AHRF) during exacerbations of COPD, mortality can be high despite noninvasive ventilation (NIV). For some, AHRF is terminal and NIV is inappropriate. However there is no definitive method of identifying patients who are unlikely to survive. The aim of this study was to identify factors associated with inpatient mortality from AHRF with respiratory acidosis due to COPD.MethodsCOPD patients presenting with AHRF and who were treated with NIV were studied prospectively. The forced expiratory volume in 1 second (FEV1), World Health Organization performance status (WHO-PS), clinical observations, a composite physiological score (Early Warning Score), routine hematology and biochemistry, and arterial blood gases prior to commencing NIV, were recorded.ResultsIn total, 65 patients were included for study, 29 males and 36 females, with a mean age of 71 ± 10.5 years. Inpatient mortality in the group was 33.8%. Mortality at 30 days and 12 months after admission were 38.5% and 58.5%, respectively. On univariate analysis, the variables associated with inpatient death were: WHO-PS ≥ 3, long-term oxygen therapy, anemia, diastolic blood pressure < 70 mmHg, Early Warning Score ≥ 3, severe acidosis (pH < 7.20), and serum albumin < 35 g/L. On multivariate analysis, only anemia and WHO-PS ≥ 3 were significant. The presence of both predicted 68% of inpatient deaths, with a specificity of 98%.ConclusionWHO-PS ≥ 3 and anemia are prognostic factors in AHRF with respiratory acidosis due to COPD. A combination of the two provides a simple method of identifying patients unlikely to benefit from NIV.

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The effects of posture on lung volume, airway closure, and gas exchange were studied in eight patients with hemidiaphragmatic paralysis. The mean vital capacity in the sitting position was 81% of predicted normal, and in the supine posture fell by a further 19% in right-sided but only 10% in left-sided paralysis. The mean arterial oxygen tension was less than predicted in the sitting posture and fell significantly on lying. Single breath gas transfer factor was normal in all cases whereas the diffusion coefficient was greater than predicted in the sitting posture and rose even further on lying. Closing volume showed no positional change but closing volume as a percentage of vital capacity was higher in the supine position. Regional airways closure was expressed as the relationship expiratory reserve volume minus closing volume. Negative values were found in only two of the subjects in the sitting position but seven had negative values supine, indicating significant airway closure during tidal breathing in this position.

The effects on ventilation of the non-selective beta-blocker propranolol, and the relatively cardioselective beta-blocker, metoprolol, were compared in a randomized single-blind crossover study in 16 patients with asthma, bronchitis and emphysema (American Thoracic Society criteria). Group I had "fixed" airways disease with less than 20% improvement in FEV1 following inhaled salbutamol 5 mg by nebuliser. Group II had "reversible" obstruction, greater than 20% improvement. Bronchodilator therapy was withheld for 24 h with the exception of aerosols which were permitted until 12 h before study. After control observations on each of 2 study days, each patient received cumulative doses of propranolol (maximum 170 mg) and metoprolol (maximum 187.5 mg). Ventilatory function (FEV1, FVC, FEV1%) was assessed at 0, 2, 4, 6 and 8 h. In Group I, 2 patients were unable to complete the study. One patient became dizzy with propranolol 70 mg but tolerated metoprolol 187.5 mg. One patient developed wheeze with propranolol 15 mg but tolerated metoprolol 187.5 mg. Metoprolol was tolerated in all 8 patients with "fixed" disease, although FEV1 was reduced by more than 30% in 1 patient. Three patients in Group II did not complete the study because of wheezing following propranolol 10 mg, metoprolol 37.5 mg; propranolol 17.5 mg, metoprolol 37.5 mg; propranolol 45 mg, tolerated metoprolol 187.5 mg respectively. Wheezing responded in all cases to inhaled isoprenaline. The response to either propranolol or metoprolol was unpredictable in patients with "reversible" disease. When wheezing occurred in this group, it developed following small, potentially subtherapeutic doses of each drug. Although metoprolol was better tolerated, the practical benefit of cardioselectivity in those patients with reversible airways disease was negligible.