Pulmonary Rehabilitation Donner, Claudio; Ambrosino, Nicolino; Goldstein, Roger S
2021, 20200714, 2020, 2020-07-14
eBook
Since publication of the first edition of this book in 2005, there has been growing interest in the role of pulmonary rehabilitation (PR) for the management of chronic respiratory disease, which ...continues to increase as a major cause of global mortality and morbidity. Health providers and healthcare professionals, having become more aware of the improvements in function and quality of life associated with PR, are increasingly including it as an integral part of their approach to disease management. Since the joint European Respiratory Society and American Thoracic Society's 2013 major statements on PR, published guidelines from professional associations around the world have endorsed PR as the prevailing standard of care for those with chronic respiratory conditions.
Summary The main complaint of patients with chronic obstructive pulmonary disease (COPD) is shortness of breath with exercise, that is usually progressive. The principal mechanism that explains this ...symptom is the development of lung hyperinflation (LH) which is defined by an increase of functional residual capacity (FRC) above predicted values. Patients with COPD may develop static LH (sLH) because of destruction of pulmonary parenchyma and loss of elastic recoil. In addition, dynamic LH (dLH) develops when patients with COPD breathe in before achieving a full exhalation and, as a consequence, air is trapped within the lungs with each further breath. Dynamic LH may also occur at rest but it becomes clinically relevant during exercise and exacerbation. Lung hyperinflation may have an impact beyond the lungs and the effects of LH on cardiovascular function have been extensively analysed. The importance of LH makes its identification and measurement crucial. The demonstration of LH in COPD leads to the adoption of strategies to minimise its impact on the daily activities of patients. Several strategies reduce the impact of LH; the use of long-acting bronchodilators has been shown to reduce LH and improve exercise capacity. Non pharmacologic interventions have also been demonstrated to be useful. This article describes the pathophysiology of LH, its impact on the lungs and beyond and reviews the strategies that improve LH in COPD.
Medical management of a chronic obstructive pulmonary disease (COPD) patient must incorporate a broadened and holistic approach to achieve optimal outcomes. This is best achieved with integrated ...care, which is based on the chronic care model of disease management, proactively addressing the patient’s unique medical, social, psychological, and cognitive needs along the trajectory of the disease. While conceptually appealing, integrated care requires not only a different approach to disease management, but considerably more health care resources. One potential way to reduce this burden of care is telemedicine: technology that allows for the bidirectional transfer of important clinical information between the patient and health care providers across distances. This not only makes medical services more accessible; it may also enhance the efficiency of delivery and quality of care. Telemedicine includes distinct, often overlapping interventions, including telecommunication (enhancing lines of communication), telemonitoring (symptom reporting or the transfer of physiological data to health care providers), physical activity monitoring and feedback to the patient and provider, remote decision support systems (identifying “red flags,” such as the onset of an exacerbation), tele-consultation (directing assessment and care from a distance), tele-education (through web-based educational or self-management platforms), tele-coaching, and tele-rehabilitation (providing educational material, exercise training, or even total pulmonary rehabilitation at a distance when standard, center-based rehabilitation is not feasible). While the above components of telemedicine are conceptually appealing, many have had inconsistent results in scientific trials. Interventions with more consistently favorable results include those potentially modifying physical activity, non-invasive ventilator management, and tele-rehabilitation. More inconsistent results in other telemedicine interventions do not necessarily mean they are ineffective; rather, more data on refining the techniques may be necessary. Until more outcome data are available clinicians should resist being caught up in novel technologies simply because they are new.
Nocturnal Cheyne-Stokes respiration (CSR) occurs frequently in patients with chronic heart failure (CHF), and it may be associated with sympathetic activation. The aim of the present study was to ...evaluate whether CSR could affect prognosis in patients with CHF.
Sixty-two CHF patients with left ventricular ejection fraction </=35%, in NYHA class II to III, underwent clinical evaluation, Doppler echocardiography, ergospirometry, phenylephrine test, Holter recording, and a sleep study to evaluate the occurrence of CSR, expressed as percentage of periodic breathing, and apnea/hypopnea index (AHI) (ie, the number of apneas and hypopneas per hour of recording). During a mean follow-up of 28+/-13 months, 15 patients died of cardiac causes. Nonsurvivors were in a higher NYHA functional class than survivors (P<0.001) and had a more depressed left ventricular ejection fraction (P<0.03), a shorter deceleration time of early filling (P<0. 05), larger left and right atria (P<0.05 and P<0.02, respectively) and a lower peak V(O2) (P<0.05). Nonsurvivors also spent a greater percentage of the night in periodic breathing (P<0.01) with a greater AHI (P<0.03) and showed lower values of diurnal baroreflex sensitivity (P<0.05) and of heart rate variability (sdNN: P<0.01). Multivariate analysis revealed the AHI (chi2, 10.4; P<0.01), followed by left atrial area (chi2, 5.7; P<0.01), as the only independent and additional predictors of subsequent cardiac death. Patients at very high risk for fatal outcome could be identified by an AHI >/=30/h and left atria >/=25 cm2.
The AHI is a powerful independent predictor of poor prognosis in clinically stable patients with CHF. The presence of an AHI >/=30/h adds prognostic information compared with other clinical, echocardiographic, and autonomic data and identifies patients at very high risk for subsequent cardiac death.
Abstract
Chronic obstructive pulmonary disease (COPD), one of the leading causes of death worldwide, is substantially influenced by genetic factors. Alpha-1 antitrypsin deficiency demonstrates that ...rare coding variants of large effect can influence COPD susceptibility. To identify additional rare coding variants in patients with severe COPD, we conducted whole exome sequencing analysis in 2543 subjects from two family-based studies (Boston Early-Onset COPD Study and International COPD Genetics Network) and one case-control study (COPDGene). Applying a gene-based segregation test in the family-based data, we identified significant segregation of rare loss of function variants in TBC1D10A and RFPL1 (P-value < 2x10-6), but were unable to find similar variants in the case-control study. In single-variant, gene-based and pathway association analyses, we were unable to find significant findings that replicated or were significant in meta-analysis. However, we found that the top results in the two datasets were in proximity to each other in the protein-protein interaction network (P-value = 0.014), suggesting enrichment of these results for similar biological processes. A network of these association results and their neighbors was significantly enriched in the transforming growth factor beta-receptor binding and cilia-related pathways. Finally, in a more detailed examination of candidate genes, we identified individuals with putative high-risk variants, including patients harboring homozygous mutations in genes associated with cutis laxa and Niemann-Pick Disease Type C. Our results likely reflect heterogeneity of genetic risk for COPD along with limitations of statistical power and functional annotation, and highlight the potential of network analysis to gain insight into genetic association studies.
This report is a summary of a workshop focusing on using telemedicine to facilitate the integrated care of chronic obstructive pulmonary disease (COPD). Twenty-five invited participants from 8 ...countries met for one and one-half days in Stresa, Italy on 7–8 September 2017, to discuss this topic. Participants included physiotherapists, nurses, a nurse practitioner, and physicians. While evidence-based data are always at the center of sound inference and recommendations, at this point in time the science behind telemedicine in COPD remains under-developed; therefore, this document reflects expert opinion and consensus. While telemedicine has great potential to expand and improve the care of our COPD patients, its application is still in its infancy. While studies have demonstrated its effectiveness in some patient-centered outcomes, the results are by no means consistently positive. Whereas this tool may potentially reduce health care costs by moving some medical interventions from centralized locations in to patient's home, its cost-effectiveness has had mixed results and telemonitoring has yet to prove its worth in the COPD population. These discordant results should not be unexpected in view of patient complexity and the heterogeneity of telemedicine. This is reflected in the very limited support offered by the National Health Services to a wider application of telemedicine in the integrated care of COPD patients. However, this situation should challenge us to develop the necessary science to clarify the role of telemedicine in the medical management of our patients, providing a better and definitive scientific basis to this approach.
It is unclear whether airway wall thickening and emphysema make independent contributions to airflow limitation in chronic obstructive pulmonary disease (COPD) and whether these phenotypes cluster ...within families.
To determine whether airway wall thickening and emphysema (1) make independent contributions to the severity of COPD and (2) show independent aggregation in families of individuals with COPD.
Index cases with COPD and their smoking siblings underwent spirometry and were offered high-resolution computed tomography scans of the thorax to assess the severity of airway wall thickening and emphysema.
A total of 3,096 individuals were recruited to the study, of whom 1,159 (519 probands and 640 siblings) had technically adequate high-resolution computed tomography scans without significant non-COPD-related thoracic disease. Airway wall thickness correlated with pack-years smoked (P < or = 0.001) and symptoms of chronic bronchitis (P < 0.001). FEV(1) (expressed as % predicted) was independently associated with airway wall thickness at a lumen perimeter of 10 mm (P = 0.0001) and 20 mm (P = 0.0013) and emphysema at -950 Hounsfield units (P < 0.0001). There was independent familial aggregation of both the emphysema (adjusted odds ratio, 2.1; 95% confidence interval, 1.1-4.0; P < or = 0.02) and airway disease phenotypes (P < 0.0001) of COPD.
Airway wall thickening and emphysema make independent contributions to airflow obstruction in COPD. These phenotypes show independent aggregation within families of individuals with COPD, suggesting that different genetic factors influence these disease processes.
Although large surveys have documented the favourable safety profile of β2-adrenoceptor agonists (β2-agonists) and, above all, that of the long-acting agents, the presence in the literature of ...reports of adverse cardiovascular events in patients with obstructive airway disease must induce physicians to consider this eventuality. The coexistence of β1- and β2-adrenoceptors in the heart clearly indicates that β2-agonists do have some effect on the heart, even when they are highly selective. It should also be taken into account that the β2-agonists utilised in clinical practice have differing selectivities and potencies. β2-agonist use has, in effect, been associated with an increased risk of myocardial infarction, congestive heart failure, cardiac arrest and sudden cardiac death. Moreover, patients who have either asthma or chronic obstructive pulmonary disease may be at increased risk of cardiovascular complications because these diseases amplify the impact of these agents on the heart and, unfortunately, are a confounding factor when the impact of β2-agonists on the heart is evaluated. Whatever the case may be, this effect is of particular concern for those patients with underlying cardiac conditions. Therefore, β2-agonists must always be used with caution in patients with cardiopathies because these agents may precipitate the concomitant cardiac disease.
Chronic obstructive pulmonary disease (COPD) susceptibility is in part related to genetic variants. Most genetic studies have been focused on genome-wide common variants without a specific focus on ...coding variants, but common and rare coding variants may also affect COPD susceptibility.
To identify coding variants associated with COPD.
We tested nonsynonymous, splice, and stop variants derived from the Illumina HumanExome array for association with COPD in five study populations enriched for COPD. We evaluated single variants with a minor allele frequency greater than 0.5% using logistic regression. Results were combined using a fixed effects meta-analysis. We replicated novel single-variant associations in three additional COPD cohorts.
We included 6,004 control subjects and 6,161 COPD cases across five cohorts for analysis. Our top result was rs16969968 (P = 1.7 × 10(-14)) in CHRNA5, a locus previously associated with COPD susceptibility and nicotine dependence. Additional top results were found in AGER, MMP3, and SERPINA1. A nonsynonymous variant, rs181206, in IL27 (P = 4.7 × 10(-6)) was just below the level of exome-wide significance but attained exome-wide significance (P = 5.7 × 10(-8)) when combined with results from other cohorts. Gene expression datasets revealed an association of rs181206 and the surrounding locus with expression of multiple genes; several were differentially expressed in COPD lung tissue, including TUFM.
In an exome array analysis of COPD, we identified nonsynonymous variants at previously described loci and a novel exome-wide significant variant in IL27. This variant is at a locus previously described in genome-wide associations with diabetes, inflammatory bowel disease, and obesity and appears to affect genes potentially related to COPD pathogenesis.
Reactive nitrogen species, formed via the reaction of nitric oxide (NO) with superoxide anion and via (myelo)peroxidase-dependent oxidation of NO
2
−, have potent proinflammatory and oxidizing ...actions. Reactive nitrogen species formation and nitrosative stress are potentially involved in chronic obstructive pulmonary disease (COPD) pathogenesis.
To investigate the expression of markers of nitrosative stress, including nitrotyrosine (NT), inducible NO synthase (iNOS), endothelial NO synthase (eNOS), myeloperoxidase (MPO), and xanthine oxidase (XO) in bronchial biopsies and bronchoalveolar lavage from patients with mild to severe stable COPD compared with control groups (smokers with normal lung function and nonsmokers).
The expression of NT, iNOS, eNOS, MPO and XO in the bronchial mucosa and bronchoalveolar lavage of patients was measured by using immunohistochemistry, Western blotting, and ELISA and correlated with the inflammatory cell profile.
Patients with severe COPD in stable phase had higher numbers of NT
+ and MPO
+ cells in their bronchial submucosa compared with mild/moderate COPD, smokers with normal lung function, and nonsmokers (
P < .01). iNOS
+ and eNOS
+ but not XO
+ cells were significantly increased in smokers with COPD or normal lung function compared with nonsmokers (
P < .05 and
P < .01, respectively). In patients with COPD, the number of MPO
+ cells was significantly correlated with the number of neutrophils (
r = +0.61;
P < .0025) in the bronchial submucosa. Furthermore, the number of NT
+ and MPO
+ cells was negatively correlated with postbronchodilator FEV
1.
These data suggest that nitrosative stress, mainly mediated by MPO and neutrophilic inflammation, may contribute to the pathogenesis of severe COPD.
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