Respiratory Failure In Chronic Obstructive Pulmonary Disease Research Articles

Getting It Right in Obstructive Lung Disease.

Chronic hypercapnic respiratory failure in obstructive lung diseases may benefit from nocturnal Home non-invasive ventilation (HNIV). It has been shown that in patients with persistence of hypercapnia after an acute episode of chronic obstructive pulmonary disease (COPD) exacerbation requiring mechanical ventilation, HNIV may improve the risk for new admission and survival. The ability to reach these aims depends on the correct timing of enrolling patients, as well as a correct definition of ventilatory needing and setting of the ventilator. This review tries to define a possible home treatment path of hypercapnic respiratory failure in COPD by analyzing the main studies published in recent years.

High-pressure NIV for acute hypercapnic respiratory failure in COPD: improved survival in a retrospective cohort study

IntroductionUpdated treatment guidelines for acute hypercapnic respiratory failure (AHRF) in chronic obstructive pulmonary disease (COPD) with non-invasive ventilation (NIV) in 2016 recommended a rapid increase in inspiratory positive airway pressure...

Blood biomarkers associated with acute type II respiratory failure in COPD: A meta-analysis.

ObjectiveThis study aims to summarize the risk factors of type II respiratory failure in patients with an acute exacerbation of chronic obstructive pulmonary disease (COPD), to guide clinical treatment in time, and consequently reduce the serious impact of COPD on human health.MethodsFive databases were searched for relevant articles on risk factors of acute exacerbation of COPD combinate with type II respiratory failure. We calculated the standard mean difference (SMD), odds ratio (OR), and their 95% confidence interval (95% CI) utilizing a fixed‐effect model or a random‐effect model according to the level of heterogeneity.ResultsAs of 14 May 2021, 13 articles were included in our meta‐analysis. The results showed that low albumin and uric acid levels were the risk factors for type II respiratory failure in acute exacerbation of COPD patients, and the differences were statistically significant (albumin: SMD = −2.03, 95% CI: −2.81, −1.26; uric acid: SMD = −1.28, 95% CI: −1.41, −1.15). Besides, 10 other systematic markers have been reported to be the risk factors for type II respiratory failure of patients with acute exacerbation of COPD, but only in single study.ConclusionThe meta‐analysis results further confirm that low albumin and uric acid levels are risk factors for type II respiratory failure in acute exacerbation of COPD patients. Additionally, this analysis also summarizes many emerging inflammatory indicators, nutritional indicator, and cardiovascular system indicators to predict the progression of acute exacerbation of COPD to type II respiratory failure but only in single study.

COPD sleep phenotypes: Genesis of respiratory failure in COPD.

The chronic obstructive pulmonary disease (COPD) patients could have respiratory failure during sleep without daytime overt arterial blood gas (ABG) abnormality. We undertook a study first of its kind to attempt in distinguishing the underlying pathophysiological mechanisms. It was a prospective observational study in stable COPD patients. The inclusion criterion was presence of day time PaO2>60 mmHg and PaCO2<45 mmHg. Twenty five out of 110 patients were excluded because of the ABG abnormality. The remaining 85 patients were subjected to overnight pulse oximetry and end-tidal (ET)-CO2 monitoring. The nocturnal oxygen desaturation was defined as per Fletcher's criteria. The nocturnal hypoventilation was defined as per American academy of sleep medicine (AASM) guidelines. Patients having saw-tooth pattern on pulse oximetry and/or snoring were subjected to polysomnography. 38/85(44.8%) patients had nocturnal gas exchange abnormality in absence of daytime respiratory failure and were identified into 3 different phenotypes: obstructive sleep apnoea (OSA), nocturnal hypoventilation and nocturnal oxygen desaturation. The isolated abnormality was seen in 24 patients: 10 patients had OSA, 9 had nocturnal hypoventilation and 5 had nocturnal oxygen desaturation. Overlap of two or more phenotypes was seen in 14 patients. As compared to the nocturnal hypoventilation and desaturation phenotypes, the OSA phenotype had a significantly higher BMI & FEV1. The nocturnal hypoventilation and the desaturation phenotypes did not have significant difference in FEV1 and BMI, but the daytime SpO2 and PaO2 differed significantly. Such parameters could help in identifying the three distinct COPD-sleep phenotypes (OSA, nocturnal hypoventilation and nocturnal oxygen desaturation). A phenotype based nocturnal management may help in delaying the process of overt respiratory failure in COPD.

Ultrasound Shear Wave Elastography for Evaluation of Diaphragm Stiffness in Patients with Stable COPD: A Pilot Trial

Skeletal muscle dysfunction is one of the most common comorbidities in chronic obstructive pulmonary disease (COPD). The occurrence of respiratory failure in COPD is common and leads to the patient's death. The diaphragm is the most important muscle in the respiratory system and plays a key role in the onset of respiratory failure. This study explores the feasibility of ultrasound shear wave elastography (SWE) to measure diaphragmatic stiffness and evaluates its changes in COPD patients. In total, 77 participants (43 patients with stable COPD and 34 healthy controls) were enrolled. All subjects underwent complete diaphragmatic ultrasound SWE measurements and pulmonary function tests. The diaphragmatic stiffness was indicated via diaphragmatic shear wave velocity (SWV) at functional residual capacity (FRC). A trained operator performed the ultrasound SWE examinations of the first 15 healthy controls thrice to assess the reliability of diaphragmatic SWE. A good to excellent reliability was found in diaphragmatic SWV at FRC (ICC = 0.93, 95%CI 0.82-0.98). As compared to the control group, the diaphragmatic SWV at FRC was considerably high in the COPD group (median 2.5 m/s versus 2.1 m/s, P = .008). Diaphragmatic SWV at FRC was linked to forced expiratory volume in one second (r = -0.30, P = .009), forced vital capacity (r = -0.33, P = .003), modified Medical Research Council score (r = 0.30, P = .001), and COPD assessment test score (r = 0.48, P < .001). Ultrasound SWE may be employed as an effective tool for quantitative evaluation of diaphragm stiffness and can help in personalized management of COPD, such as treatment guidance and follow-up monitoring.

NIV for acute respiratory failure in COPD: high in-hospital mortality is determined by patient selection

ABSTRACTIntroduction: Hospital mortality among chronic obstructive pulmonary disease (COPD) patients receiving NIV for acute respiratory failure has shown to be significantly higher in clinical settings than in the randomized trials (RCTs) which clinical guidelines are based on. This may be due to the quality of care of NIV or patient selection. In daily clinical practice, we include patients with terminal pulmonary disease with a do-not-intubate (DNI) or a do-not-resuscitate (DNR) order with a high mortality risk compared to highly selected patients in RCTs. The aim of this study was to determine the role of patient selection for in-hospital mortality among patients receiving NIV for acute respiratory failure of COPD.Methods: We conducted a retrospective study including all patients receiving acute NIV due to acute respiratory failure at the respiratory wards in 2012–2013 at two hospitals in Greater Copenhagen.Results: Overall in-hospital mortality rate was 30%. In patients with a DNI/DNR order, mortality was 59% and in patients with no limitations in treatment 2%. Patients who fulfilled the exclusion criteria of the RCT by Plant et al. had a mortality of 41% compared to 25% in the remaining population.Conclusions: High overall in-hospital mortality reflects that patient selection in clinical practice is very different from RCT. Quality of acute NIV treatment seems acceptable in clinical practice for patients with less severe COPD and no limitations in treatment. Higher mortality in patients with DNI/DNR order may be due to inefficient NIV treatment for these patients with more severe COPD.

Annual decline in arterial blood oxygen predicts development of chronic respiratory failure in COPD with mild hypoxaemia: A 6-year follow-up study.

Chronic respiratory failure (CRF) with hypoxaemia is an important pathophysiology in patients with chronic obstructive pulmonary disease (COPD), and existing mild hypoxaemia may be a sign of future CRF development. However, little is known about the trajectory of partial arterial pressure of oxygen (PaO2 ) decline in patients with COPD. We assessed decline in PaO2 and the impact of short-term reductions in PaO2 to predict future decline in PaO2 . A total of 172 outpatients with COPD from a prospective cohort study were enrolled. Pulmonary function tests and arterial blood gas (ABG) analyses were conducted at baseline and 1 year after enrolment and changes in PaO2 (ΔPaO2 ) and other parameters were calculated. Survival and incidence of CRF (as assessed by prescription of long-term home oxygen therapy) were monitored for 6 years. A total of 164 patients completed the observation period and 101 patients had mild hypoxaemia (PaO2 < 80 Torr) at baseline. No patients with normal PaO2 (≥80 Torr) developed CRF, and 10 patients with mild hypoxaemia developed CRF in 6 years. Baseline airflow limitation and diffusion capacity were significantly associated with development of CRF. Receiver-operating characteristic curve analysis showed that ΔPaO2 of -3.05 Torr/year is a useful cut-off value to predict development of CRF in 6 years (hazard ratio (HR): 12.6, 95% CI: 3.48-58.73, P < 0.0001). Patients with COPD and mild hypoxaemia may benefit from repeat ABG after 1 year. Although PaO2 trajectories widely varied, significant annual changes in PaO2 of at least -3.0 Torr/year were predictive of CRF development.

Severe hypoalbuminemia is a strong independent risk factor for acute respiratory failure in COPD: a nationwide cohort study.

BackgroundAcute respiratory failure (ARF) is a life-threatening event, which is frequently associated with the severe exacerbations of chronic obstructive pulmonary disease (COPD). Hypoalbuminemia is associated with increased mortality in patients with COPD. However, to date, little is known regarding whether or not hypoalbuminemia is a risk factor for developing ARF in COPD.MethodsWe conducted a retrospective cohort study using data from the National Health Insurance system of Taiwan. A total of 42,732 newly diagnosed COPD patients (age ≥40 years) from 1997 to 2011 were enrolled. Among them, 1,861 (4.36%) patients who had received albumin supplementation were defined as hypoalbuminemia, and 40,871 (95.6%) patients who had not received albumin supplementation were defined as no hypoalbuminemia.ResultsOf 42,732 newly diagnosed COPD patients, 5,248 patients (12.3%) developed ARF during the 6 years follow-up period. Patients with hypoalbuminemia were older, predominantly male, had more comorbidities, and required more steroid treatment and blood transfusions than patients without hypoalbuminemia. In a multivariable Cox regression analysis model, being elderly was the strongest independent risk factor for ARF (adjusted hazard ratio [HR]: 4.63, P<0.001), followed by hypoalbuminemia (adjusted HR: 2.87, P<0.001). However, as the annual average dose of albumin supplementation was higher than 13.8 g per year, the risk for ARF was the highest (adjusted HR: 11.13, 95% CI: 10.35–11.98, P<0.001).ConclusionHypoalbuminemia is a strong risk factor for ARF in patients with COPD. Therefore, further prospective studies are required to verify whether or not albumin supplementation or nutritional support may help to reduce the risk of ARF in patients with COPD.

Oxygen therapy in acute exacerbations of chronic obstructive pulmonary disease.

Acute exacerbations of chronic obstructive pulmonary disease (COPD) are important events in the history of this debilitating lung condition. Associated health care utilization and morbidity are high, and many patients require supplemental oxygen or ventilatory support. The last 2 decades have seen a substantial increase in our understanding of the best way to manage the respiratory failure suffered by many patients during this high-risk period. This review article examines the evidence underlying supplemental oxygen therapy during exacerbations of COPD. We first discuss the epidemiology and pathophysiology of respiratory failure in COPD during exacerbations. The rationale and evidence underlying oxygen therapy, including the risks when administered inappropriately, are then discussed, along with further strategies for ventilatory support. We also review current recommendations for best practice, including methods for improving oxygen provision in the future.

Predictors for PaO2 and Hypoxemic Respiratory Failure in COPD–A Three-Year Follow-up

Background: Knowledge about predictors for developing hypoxemia in the course of chronic obstructive pulmonary disease (COPD) progression is limited. The objective of the present study was to investigate predictors for overall PaO2, for a potential change in PaO2 over time, and for first occurrence of hypoxemia. Methods: 419 patients aged 40–76 years with COPD GOLD stages II-IV underwent clinical and pulmonary function measurements, including repeated arterial blood gases over three years. Airway obstruction, lung hyperinflation, markers of systemic inflammation and cardiovascular health, exacerbation frequency, smoking habits, and body composition were tested as possible predictors of PaO2 and first episode of hypoxemia. Results: In multivariate adjusted longitudinal analyses, forced expiratory volume in 1 second, total lung capacity and functional residual capacity (all in% predicted), resting heart rate and fat mass index were all associated with overall PaO2 (all P < 0.005). We found no change in PaO2 over time (ρ = 0.33), nor did we find evidence that any of the tested variables predicted change in PaO2 over time. In multivariate adjusted survival analyses, functional residual capacity and resting heart rate were predictors of episodic hypoxemia (both ρ < 0.005). Conclusions: This longitudinal study identified pulmonary, cardiac and metabolic risk factors for overall PaO2 and episodic hypoxemia, but detected no change in PaO2 over time.

Chronic obstructive pulmonary disease (COPD) patients with osteoporotic vertebral compression fractures (OVCFs): improvement of pulmonary function after percutaneous vertebroplasty (VTP).

To investigate the changes of respiratory function in patients affected by chronic obstructive pulmonary disease (COPD) with single dorsal osteoporotic vertebral compression fractures (OVCFs) treated with vertebroplasty (VTP). Forty-five patients affected by COPD and single dorsal OVCF underwent VTP (29 men, 16 women; mean age 71.4 years, range 65-77 years). Inclusion criteria were magnetic resonance findings of bone marrow oedema, without intracanal bone fragments and refractory pain to medical treatment for at least 3 months. Osteoporosis was assessed by bone densitometry. Spirometry was performed before and after treatment. A significant VAS-score decrease was observed 1 week after VTP, with a subsequent decrease over time; vital capacity (VC) and forced vital capacity (FVC) improved over time, reaching a plateau at 3 months. Forced expiratory volume at 1 s (FEV1) did not significantly differ between the pre-VTP values and follow-up values. A significant correlation was observed between VAS-score values and VC, and VAS-score values and FVC. No significant correlation was observed between VAS-score values and FEV1 values. VTP improves restrictive ventilatory impairment in patients with moderate and severe COPD affected by single thoracic OVCFs. We recommend this treatment in the management of these patients. • Osteoporosis is a major comorbidity in chronic obstructive pulmonary disease (COPD) patients. • Pain due to osteoporotic vertebral compression fractures worsens respiratory failure in COPD. • Vertebroplasty improves ventilatory impairment in COPD patients with osteoporotic vertebral compression fractures.

Non-invasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma

Asthma is a chronic respiratory condition causing inflammation and changes to the airways. Care of people with asthma includes routine and urgent management across primary and tertiary care; however, due to sub-optimal long-term care and delays in obtaining help during acute exacerbations, the mortality and morbidity related to asthma is still a major health concern. There is reason to believe that non-invasive positive pressure ventilation (NPPV) could be beneficial to patients with severe acute asthma; however, the evidence surrounding the efficacy of NPPV is unclear, despite its common use in clinical practice. To determine the efficacy of NPPV in adults with severe acute asthma in comparison to usual medical care with respect to mortality, tracheal intubation, changes in blood gases and hospital length of stay. We carried out a search in the Cochrane Airways Group Specialised Register of trials (July 2012). Following this, the bibliographies of included studies and review articles were searched for additional studies (July 2012). We included randomised controlled trials of adults with severe acute asthma as the primary reason for presentation to the emergency department or for admission to hospital. Asthma diagnosis was defined by internationally accepted criteria. Studies were included if the intervention was usual medical care for the management of severe acute asthma plus NPPV applied through a nasal or facemask compared to usual medical care alone. Studies including patients with features of chronic obstructive pulmonary disease (COPD) were excluded unless data were provided separately for patients with asthma in studies recruiting both COPD and asthmatic patients. A combination of two review authors independently assessed trial quality and extracted data. Study authors were contacted for additional information where required. All data were analysed using RevMan 5.1. For continuous variables, a mean difference and 95% confidence interval were used and for dichotomous variables, risk ratio with 95% confidence interval were calculated. We identified six trials for inclusion. Five studies on 206 participants contributed data, while one study was available in abstract form only and was not fully incorporated into this review. For the primary outcome of endotracheal intubation there were two studies that contributed data: two intubations were needed in 45 participants on NPPV and no intubations in 41 control patients (risk ratio 4.48; 95% CI 0.23 to 89.13). There were no deaths in either of these studies. Length of hospital stay was reported in two studies, though meta-analysis was not possible. Hospitalisation was reported in one small study, in which there were three admissions out of 17 on NPPV and 10 admissions out of 16 in control patients (RR 0.28, 95% CI 0.09, 0.84). This review of studies has highlighted the paucity of data that exist to support the use of NPPV in patients in status asthmaticus. As such this course of treatment remains controversial despite its continued use in current clinical practice. Larger, prospective randomised controlled trials of rigorous methodological design are needed to determine the role of NPPV in patients with asthma.

High pressure versus high intensity noninvasive ventilation in stable hypercapnic chronic obstructive pulmonary disease: a randomized crossover trial

BackgroundHigh-intensity (high-pressure and high backup rate) noninvasive ventilation has recently been advocated for the management of stable hypercapnic chronic obstructive pulmonary disease (COPD). However, the relative contributions of high inspiratory pressure and high backup rate to ventilator adherence and physiological outcome have not been investigated.MethodsPatients with stable hypercapnic COPD (daytime PaCO2 > 6 kPa) and nocturnal hypoventilation were enrolled. Patients were randomly allocated to high-pressure and high backup rate (high-intensity) and high-pressure and low backup rate (high-pressure) for a 6-week period. At the end of the first treatment period, patients were switched to the alternative treatment. The primary outcome measure was mean nightly ventilator usage.ResultsTwelve patients were recruited, with seven completing the 12-week trial protocol. The mean patient age was 71 ± 8 years, with a forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) of 50% ± 13% and FEV1 of 32% ± 12%. The baseline PaCO2 and PaO2 were 8.6 ± 1.7 kPa and 7.3 ± 1.4 kPa, respectively. There was no significant difference demonstrated in mean nightly ventilator usage between the high-intensity and high-pressure groups (difference of 4 minutes; 95% confidence interval −45 to 53; P = 0.9). Furthermore, there were no differences in any of the secondary endpoints, with the exception of the respiratory domain of the Severe Respiratory Insufficiency questionnaire, which was lower in the high-intensity arm than in the high-pressure arm (57 ± 11 versus 69 ± 16; P < 0.05).ConclusionThere was no additional benefit, in terms of night-time ventilator adherence or any of the other measured parameters, demonstrated by addition of a high backup rate to high-pressure noninvasive ventilation. These data suggest that it is the high-pressure component of the high-intensity noninvasive ventilation approach that plays the important therapeutic role in the management of hypercapnic respiratory failure in COPD patients.

Explained variance for blood gases in a population with COPD

Variation of blood gas levels in chronic obstructive pulmonary disease (COPD) patients has not been extensively reported and there is limited knowledge about predictors of chronic respiratory failure in COPD patients. The aim of this study was to identify predictors of hypoxemia, hypercapnia and increased alveolar-arterial oxygen difference in COPD patients. We hypothesized that prediction of arterial blood gases will be improved in multivariate models including measurements of lung function, anthropometry and systemic inflammation. A cross-sectional sample of 382 Norwegian COPD patients, age 40-76, Global Initiative for Chronic Obstructive Lung Disease stage II-IV, with a smoking history of at least 10 pack-years, underwent extensive measurements, including medical examination, arterial blood gases, systemic inflammatory markers, spirometry, plethysmography, respiratory impedance and bioelectrical impedance. Possible predictors of arterial oxygen (PaO(2)), arterial carbon dioxide (PaCO(2)) and alveolar-arterial oxygen difference (AaO(2)) were analyzed with both bivariate and multiple regression methods. We found that various lung function measurements were significantly associated with PaO2, PaCO(2) and AaO(2). In addition, heart rate and Fat Mass Index were predictors of PaO(2) and AaO(2), while heart failure and current smoking status were associated with PaCO(2). The explained variance (R(2)) in the final multivariate regression models was 0.14-0.20. With a wide assortment of possible clinical predictors, we could explain 14-20% of the variation in blood gas measurements in COPD patients.

Below What FEV 1 Should Arterial Blood be Routinely Taken to Detect Chronic Respiratory Failure in COPD?

Introduction To diagnose and assess chronic respiratory failure in stable chronic obstructive pulmonary disease (COPD) the measurement of arterial blood gases (ABG) is required. It has been suggested that ABG could be determined for this purpose when FEV 1 ranges between 50% and 30% predicted, but these thresholds are not evidence-based. Objective To identify the post-bronchodilator (BD) FEV 1 and arterial oxygen saturation (SaO 2) values that provide the best sensitivity, specificity, and likelihood ratio (LR) for the diagnosis of hypoxaemic and/or hypercapnic chronic respiratory failures in stable COPD. Methods A total of 150 patients were included (39 with PaO 2 < 60 mm Hg [8 kPa], 14 of them with a PaCO 2 ≥ 50 mm Hg [6.7 kPa]). The best post-BD FEV 1 and SaO 2 cut-off points to predict chronic respiratory failure were selected using the PC and the Receiver Operating Characteristics (ROC) curves. Results A post-BD FEV 1 equal to 36% and an SaO 2 of 90% were the best predictive values for hypoxaemic respiratory failure and a post-BD FEV 1 equal to 33% for the hypercapnic variant. An FEV 1 ≥ 45% ruled out hypoxaemic respiratory failure. Conclusion A post-BD FEV 1 of 36% is the best cut-off point to adequately predict both hypoxaemic and hypercapnic respiratory failure in the patient with stable COPD. For its part, an SaO 2 of 90% is the best value for isolated hypoxaemic failure. These values could be considered for future clinical recommendations/guidelines for COPD.

Functional Haplotypes in the Promoter Region of Transcription FactorNrf2in Chronic Obstructive Pulmonary Disease

Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) protects against oxidative stress which is important in the pathogenesis of chronic obstructive pulmonary disease (COPD). Three single nucleotide polymorphisms and 1 triplet repeat polymorphism are found in the promoter region of theNrf2gene. Molecular haplotyping of theNrf2promoter region was performed using DNA obtained from the peripheral blood of 69 COPD patients. The luciferase activities ofNrf2promoter constructs containing all possible combinations of the 4 polymorphisms were determined and found to differ among the 16 haplotypes.The haplotypes isolated from the subjects were divided into 3 groups (L: low; M: medium; H: high) on the basis of luciferase activities. The proportions of subjects belonging to global initiative for chronic obstructive lung disease stage 3 or 4 decreased from the group with the LL haplotype to that with the HH haplotype. Presence of the LH or MM haplotype (hazard ratio, 3.36; 95% confidence interval, 1.16–9.69), gender (0.13; 0.02–0.67), and post-bronchodilator FEV1value of predicted (0.95; 0.91–0.99) are significant predictors of respiratory failure development.The haplotype of theNrf2gene promoter affects its activity, and is associated with the severity and the development of respiratory failure in COPD.

Functional haplotypes in the promoter region of transcription factor Nrf2 in chronic obstructive pulmonary disease.

Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) protects against oxidative stress which is important in the pathogenesis of chronic obstructive pulmonary disease (COPD). Three single nucleotide polymorphisms and 1 triplet repeat polymorphism are found in the promoter region of the Nrf2 gene. Molecular haplotyping of the Nrf2 promoter region was performed using DNA obtained from the peripheral blood of 69 COPD patients. The luciferase activities of Nrf2 promoter constructs containing all possible combinations of the 4 polymorphisms were determined and found to differ among the 16 haplotypes.The haplotypes isolated from the subjects were divided into 3 groups (L: low; M: medium; H: high) on the basis of luciferase activities. The proportions of subjects belonging to global initiative for chronic obstructive lung disease stage 3 or 4 decreased from the group with the LL haplotype to that with the HH haplotype. Presence of the LH or MM haplotype (hazard ratio, 3.36; 95% confidence interval, 1.16–9.69), gender (0.13; 0.02–0.67), and post-bronchodilator FEV1 value of predicted (0.95; 0.91–0.99) are significant predictors of respiratory failure development.The haplotype of the Nrf2 gene promoter affects its activity, and is associated with the severity and the development of respiratory failure in COPD.

Management of COPD

Chronic obstructive pulmonary disease (COPD) remains a major cause of morbidity and mortality in the UK and worldwide. The association of COPD with the term 'irreversible airways disease' has led many doctors to the mistaken conclusion that it is 'untreatable'. Overcoming negative expectations is the first step in effective management. Acute respiratory failure in COPD is described in Respiratory Failure; this contribution focuses on the care of relatively stable patients who present to the out-patient department or general practitioner's surgery, or who have recently recovered from an acute exacerbation.

Management of acute respiratory failure in chronic obstructive pulmonary disease.

Acute respiratory failure in the setting of preexisting chronic obstructive pulmonary disease (COPD) is a common reason for hospitalization and results in the consumption of a substantial amount of health care resources. In recent years, new therapies have been proposed, and new information about older therapies has become available. Noninvasive ventilation is finding an important place as a means of avoiding tracheal intubation. The role of bacterial infection as a frequent precipitant to acute respiratory failure in COPD remains poorly defined and presumptive antibiotic therapy remains controversial. Vasodilators of the pulmonary circulation have received much attention but so far have been disappointing in this situation. The role of several other traditional therapies, such as mucolytics and methods of secretion removal, have also been challenged in recent years. In this review we focus or recent advances in the assessment and management of acute respiratory failure in the setting of pre-existing COPD.

Reversible hypercapnia in chronic obstructive pulmonary disease: A distinct pattern of respiratory failure with a favorable prognosis

Hypercapnia is regarded as a poor prognostic indicator in chronic obstructive pulmonary disease (COPD), but many patients hospitalized with hypercapnia associated with an acute exacerbation of COPD revert to normocapnia during recovery. We wished to determine if this reversible hypercapnia represents a distinct pattern of respiratory failure in COPD, or simply a stage in the progression to chronic hypercapnia. We therefore compared the long-term clinical progression and survival of COPD patients with reversible hypercapnic respiratory failure (defined as type 2.1) to those with normocapnic (PaCO2 < 50 mm Hg; type 1) and also to those patients with chronic hypercapnic (PaCO2 > 50 mm Hg) respiratory failure (defined as type 2.2). We prospectively followed for 5 years a cohort of 85 patients who had been admitted as emergencies during a 1-year period to the respiratory unit of a University teaching hospital with an exacerbation of COPD complicated by respiratory failure (PaO2 < 60 mm Hg). The main long-term outcome measures were survival and blood gas changes. Sixty-eight (80%) patients survived the initial admission, and 17 (27%) survived 5 years. PaCO2 rose substantially more during exacerbations in type 2.1 patients (mean 15.8 mm Hg), compared with type 2.2 (mean 6.8 mm Hg) and type 1 patients (mean 1.5 mm Hg). We analyzed 149 subsequent admissions among the survivors over the following 5 years. Type 2.1 patients had a better 5-year survival (28%) than type 2.2 (11% survival; P < 0.05), and similar to type 1 patients (33% 5-year survival). Only 24% of reversible hypercapnic patients developed chronic hypercapnia during long-term followup. The data support reversible hypercapnia being a distinct manifestation of respiratory failure in COPD, with a similar prognosis to that of normocapnic respiratory failure.