Pulmonary Rehabilitation in Intrinsic Restrictive Lung Diseases

Disease/Disorder

Definition

Restrictive lung diseases (RLDs) are a heterogeneous group of disorders characterized by reduced lung volume due to intrinsic parenchymal disease or extrinsic restriction involving the pleura, chest wall, or neuromuscular system. Intrinsic RLDs, most commonly interstitial lung diseases (ILDs) are defined by reduced total lung capacity (TLC), vital capacity, or resting lung volume. Current interpretation standards emphasize defining restriction using the lower limit of normal (LLN; z-score < −1.645) rather than a fixed percent-predicted cutoff (80%), with clinical correlation required. Diffusing capacity is typically reduced and represents the most sensitive physiologic marker of disease severity, but should be interpreted alongside lung volumes, symptoms, imaging, and exercise oxygenation.¹

Despite diverse etiologies, intrinsic RLDs share final common functional impairments: reduced lung compliance, impaired oxygen diffusion, exertional dyspnea, and progressive exercise intolerance.¹

Etiology

Restrictive lung disease can arise from abnormalities affecting the lung parenchyma or from extrapulmonary processes that limit lung expansion. A commonly used framework is the acronym “PAINT,” which categorizes causes of restrictive lung disease into pleural, alveolar, interstitial, neuromuscular, and thoracic cage abnormalities. However, etiologies are more precisely classified according to their pathogenetic mechanism as either intrinsic (pulmonary parenchymal) or extrinsic (extrapulmonary) causes. Intrinsic restrictive lung diseases involve inflammatory or fibrotic processes within the lung tissue, whereas extrinsic causes arise from conditions affecting the chest wall, pleura, obesity, or neuromuscular function that impair normal pulmonary mechanics. In both intrinsic and extrinsic disorders, lung volumes are reduced due to impaired lung expansion.

Intrinsic restrictive lung disease most commonly results from ILDs, a heterogeneous group of disorders characterized by inflammation and fibrosis of the lung interstitium. These conditions can be broadly categorized into idiopathic, exposure-related, autoimmune-associated, granulomatous, and miscellaneous causes.

Idiopathic interstitial pneumonias include several forms of ILD without a clearly identifiable cause. The most common of these is idiopathic pulmonary fibrosis (IPF), which is associated with progressive fibrosis and declining lung function. Other subtypes include nonspecific interstitial pneumonia (NSIP), cryptogenic organizing pneumonia, and acute interstitial pneumonia.

Exposure-related interstitial lung diseases may result from inhalation of environmental or occupational agents. Inorganic dust exposure can lead to disorders such as silicosis, asbestosis, talcosis, pneumoconiosis, berylliosis, hard metal fibrosis, and coal workers’ pneumoconiosis. Organic exposures may cause hypersensitivity pneumonitis, including conditions such as farmer’s lung, bird fancier’s lung, bagassosis, mushroom worker lung, humidifier lung, and hot-tub pneumonitis. Drug- and toxin-induced lung disease may occur with medications including nitrofurantoin, amiodarone, gold compounds, phenytoin, hydralazine, bleomycin, cyclophosphamide, methotrexate, and other chemotherapeutic agents, and restrictive lung disease may also develop following radiation therapy.

Autoimmune disease–associated interstitial lung disease occurs in several connective tissue disorders, including systemic sclerosis, rheumatoid arthritis, ankylosing spondylitis, and inflammatory myopathies.

Granulomatous lung diseases are another important category and include sarcoidosis and hypersensitivity pneumonitis, both of which may result in restrictive ventilatory defects due to chronic interstitial inflammation.

Additional miscellaneous causes of restrictive lung disease include pulmonary vasculitis, pulmonary Langerhans cell histiocytosis (formerly histiocytosis X), and post-viral pneumonitis, including fibrosis following viral infections such as COVID-19.

Environmental and genetic factors also contribute to the development of ILDs. Smoking and air pollution are recognized as risk factors for several interstitial lung diseases, particularly idiopathic pulmonary fibrosis. Genetic susceptibility has also been identified, with variants in the MUC5B promoter gene and genes involved in telomere maintenance associated with an increased risk of fibrotic ILDs, including IPF, hypersensitivity pneumonitis, and rheumatoid arthritis–associated ILD. Familial clustering has also been observed in conditions such as sarcoidosis.²

Epidemiology including risk factors and primary prevention

Estimating the prevalence of restrictive lung diseases is difficult due to the heterogeneity of underlying conditions and variation in clinical presentation. In the United States, intrinsic restrictive lung diseases are estimated to affect 3–6 per 100,000 individuals. Sarcoidosis has a prevalence of approximately 10–40 per 100,000 persons in North America, with higher rates reported in some populations, such as Sweden (about 64 per 100,000).² Rates increase with age and are generally higher in men.

Risk factors for IPF include older age, male sex, cigarette smoking, metal or wood dust exposure, and genetic susceptibility.³ Approximately 10% of IPF cases are familial, and pathogenic variants in telomere maintenance genes (TERT, TERC, RTEL1, PARN) are associated with earlier onset and more aggressive disease.⁴

Patho-anatomy/physiology

Some ILDs are characterized predominantly by fibro-proliferative disorders, in which repetitive alveolar epithelial injury and fibroblastic proliferation result in fibrosis, whereas others are largely driven by inflammatory disorders in which the pathogenic process changes to a fibro-proliferative pathway under certain conditions. Regardless of the trigger, many factors converge on mechanisms that promote irreversible fibrosis and progressive loss of lung function.³

External factors such as smoking, environmental chemicals, infections, and GERD cause epithelial cell injury and aberrant repair, alveolar macrophage activation, neutrophil recruitment, and oxidative stress in genetically susceptible individuals. Increased extracellular matrix (ECM) turnover leads to the development of fibrosis over time.⁵ The increased lung tissue stiffness further activates and stimulates fibroblasts to drive a self-perpetuating cycle of fibrosis, reducing lung compliance, impairing gas exchange, leading to worsening exertional dyspnea and exercise intolerance.^3,5

Pulmonary fibrosis has been linked to rare pathogenic mutations in telomere maintenance genes and chromosome-protected terminal telomere shortening. Patients with rare telomere-related variants TERT, TERC, PARN, or RTEL1 have varying degrees of pulmonary fibrosis, ranging from IPF to CTD-ILD.⁴

ILDs primarily affect parenchyma but also involve alveolar epithelial and endothelial cells, airways, and pulmonary vasculature. Although histopathologic findings such as fibroblast foci reflect active fibrogenesis and have been associated with disease severity in some ILDs, histopathology alone has limited utility for guiding clinical management and should be interpreted within a multidisciplinary framework. Idiopathic interstitial pneumonias (IIP) is a subgroup of ILD of unknown etiology. IPF is one of the most common forms of IIP and is associated with substantial morbidity and mortality.³

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

Most patients present with dry cough and exertion-induced dyspnea, which typically worsen over time and lead to progressive functional limitation, including dyspnea occurring at rest. Typical features include a restrictive ventilatory defect, reduced diffusing capacity, exertional hypoxemia, and abnormal alveolar-arterial oxygen gradients.⁶

Many fibrosing ILDs follow heterogeneous trajectories, including stable disease, gradual progression, or progressive pulmonary fibrosis despite therapy, and some patients experience acute exacerbations with stepwise functional decline.^3,6,8,9 Referral for lung transplantation should be considered early in the disease course, including at or near the time of diagnosis in those at risk for progression, even if medical therapy is being initiated. Referrals are particularly warranted in patients with worsening symptoms or disease progression despite treatment, physiologic impairment with either FVC <80% predicted or DLCO <40% predicted, or resting or exertional hypoxemia, requiring supplemental oxygen. Lung transplantation remains the definitive therapy for eligible patients with advanced fibrosing ILD.^6,7

Specific secondary or associated conditions and complications

Acute deterioration may be idiopathic or triggered secondary to infections, pneumonia, pulmonary embolism, pneumothorax, or heart failure, and is characterized by rapid worsening respiratory status with new radiographic abnormalities.

Acute exacerbation is defined as an acute, clinically significant respiratory deterioration, characterized by new bilateral ground glass opacities or consolidation superimposed on pre-existing fibrosis, not fully explained by cardiac failure or fluid overload. Histopathology, when available, often demonstrates diffuse alveolar damage superimposed on the underlying fibrotic pattern, supporting an acute lung injury on a background of chronic fibrosis.⁸

Because infection can mimic or precipitate acute deterioration, a thorough evaluation for alternative causes is necessary. Pathogens may be detected in a subset of cases, but many exacerbations remain idiopathic/cryptogenic, and causal significance is often uncertain.^8,9

Essentials of Assessment

History

A careful history of occupation, travel, habits, medications, and exposures should be assessed. Diagnosis of IPF requires the exclusion of known causes of ILDs such as domestic and occupational exposures, connective tissue disease, and drug toxicity.

Medications (e.g., amiodarone, methotrexate, nitrofurantoin, bleomycin, and immune checkpoint inhibitors) can cause drug-induced ILD and should be reviewed in any suspected ILD evaluation.^3,10

Physical examination

Rapid shallow breathing, use of accessory respiratory muscles, and tachypnea may denote respiratory insufficiency. Distinguishing features include bibasilar “Velcro” crackles on auscultation of the lungs and digital clubbing. Cyanosis, when present, suggests advanced disease. Loud P2 and right ventricular heaves which are findings of pulmonary hypertension may present in later stages (Cor Pulmonale).³

Laboratory studies

Routine laboratory assessments often fail to reveal positive findings. Although there is no specific role of serology in diagnosing IPF, serologic testing should be performed to diagnose CTD.

In sarcoidosis, biomarkers such as angiotensin-converting enzyme (ACE) and soluble interleukin-2 receptor may support disease activity but lack sufficient specificity to establish diagnosis in isolation.^3,11

Imaging

High-resolution computed tomography (HRCT) is central to the diagnosis and classification of ILD. A usual interstitial pneumonia (UIP) pattern—defined by basal and subpleural-predominant reticulation, traction bronchiectasis, and honeycombing with minimal ground-glass opacity is sufficient to diagnose IPF without tissue sampling.³

Alternative HRCT patterns suggest other ILDs, including upper-lobe or peri lymphatic nodules with mediastinal lymphadenopathy in sarcoidosis, ground-glass opacities with mosaic attenuation in hypersensitivity pneumonitis, and diffuse ground-glass or organizing pneumonia patterns in drug-induced ILD. The extent of fibrotic abnormalities, such as honeycombing and traction bronchiectasis—correlates with physiologic impairment and prognosis.^3,11

Supplemental assessment tools

In the absence of the typical findings on HRCT, tissue sampling may be considered. In appropriate patients and experienced centers, transbronchial lung cryobiopsy is an accepted diagnostic option, while surgical lung biopsy is reserved for selected cases when less invasive approaches are nondiagnostic and results are likely to change management.¹²

Diffusing capacity is commonly reduced in fibrosing ILD and is a sensitive marker for respiratory function. A DLCO <40% predicted generally reflects advanced disease and worse outcomes. Ventilatory and gas exchange abnormalities are the main factors that limit exercise capacity. Cardiac dysfunction, particularly in the setting of pulmonary hypertension, may further contribute to the deficits as well.^1,6

There are data that suggest that the accuracy of diagnosis is improved by integrating clinical, radiologic, and pathologic data when available. Sequential pulmonary functional test (PFT) findings are essential to monitor the course and determine the efficacy of treatment in ILD.^1,6

Another assessment tool is the 6-minute walk test, with shorter distance and exertional desaturation indicating more severe disease and poorer outcomes.⁶

Early predictions of outcomes

PFTs and exercise-induced hypoxemia can aid in defining the prognosis of the disease. Lower baseline FVC and DLCO, as well as ≥10% relative decline in FVC over 12 months, are associated with increased mortality and disease progression. Exercise-induced oxygen desaturation during the 6-minute walk test is also a strong predictor of worse outcomes and mortality.^3,6

Composite scoring systems have been developed to predict mortality in patients with progressive fibrosing ILDs. One of the most widely used is the GAP (gender, age, physiology) model, which was developed to predict mortality in patients with IPF based on gender, age, FVC % predicted and DLCO % predicted. Since then, it has been demonstrated that this model can also predict mortality in patients with RA-ILD, SSc-ILD, unclassifiable ILD, and a mixed cohort.^3,6

Blood biomarkers have also been investigated as predictors of disease progression in patients with fibrosing ILDs. Elevated levels of KL-6 and surfactant protein-D (SP-D) have been associated with more rapid disease progression and worse outcomes in IPF and connective tissue disease-associated ILD.^4,6

Genetic factors have also been linked to prognosis in fibrosing ILD. Variants in telomere maintenance genes and shortened telomere length are associated with more aggressive disease and poorer survival across fibrosing ILDs. In IPF, the MUC5B promoter variant (rs35705950) has been associated with improved survival, whereas variants in genes such as TOLLIP have been linked to worse outcomes.^4,6

Environmental

A significant increase in risk is noted with exposure to metal dust (brass, lead, steel), wood dust (pine), farming, raising birds, hairdressing, stone cutting/polishing, and exposure to livestock/vegetable dust.⁶

Medical management

Management generally includes a combination of supportive care, use of selected medications (pirfenidone, nintedanib), consideration of participation in clinical trials, referral for lung transplantation evaluation when appropriate, and identification and treatment of comorbidities. Supportive care may include supplemental oxygen, pulmonary rehabilitation, vaccination, and palliative care.^3,6

Professional issues

End of life issues and care are important discussion points that need to be addressed by the clinician.

Rehabilitation Management and Treatments

Functional assessment and necessity of rehabilitation in ILD

Interstitial Lung Diseases comprise a heterogeneous group of disorders characterized by inflammation and/or fibrosis of the lung parenchyma and vasculature which leads to structural and mechanical pulmonary system alterations. This mainly causes pathological reduction of pulmonary and cardiovascular functions. Patients gradually develop exertional dyspnea which limits their exercise tolerance and endurance deteriorates to the extent that performing activities of daily living becomes difficult. As lung function declines, patients commonly develop limitations in functional capacity, exacerbated by secondary impairments such as cardiovascular strain, peripheral muscle deconditioning, and psychological distress. Pharmacologic therapies can slow disease progression but do not reverse established fibrosis or cure the disease; therefore, non-pharmacologic interventions are integral to management. Pulmonary rehabilitation incorporates tailored exercise training, education, and symptom management, and is recommended by contemporary guidelines for ILD to improve exercise capacity, dyspnea, and health-related quality of life (HRQL).^13,14,15,16

Mechanism of reduced exercise capacity in ILD

Reduced exercise capacity in ILD is multifactorial, resulting from combined ventilatory, gas-exchange, circulatory, and peripheral muscle limitations. Impaired gas exchange, due to destruction of the pulmonary capillary bed, leads to a ventilation-perfusion mismatch and oxygen diffusion limitations. Pulmonary vascular involvement and reduced cardiac output may further impair oxygen delivery in advanced disease. Peripheral muscle dysfunction from chronic physical deconditioning can play a role. Chronic corticosteroid exposure may also lead to drug-induced myopathy.^16,20

Available or current treatment guidelines

Pulmonary rehabilitation (PR) is an evidence-based, multidisciplinary, comprehensive intervention involving a program of structured exercise, self-management education and psychosocial support. The 2023 ATS clinical practice guideline provides a strong recommendation for PR in adults with chronic respiratory disease, including ILD, based on moderate-certainty evidence for improvements in exercise capacity and health-related quality of life. Current guidelines recognize that it can be delivered through multiple settings, including outpatient center-based programs (the most established model), as well as inpatient, home-based, community-based, and telerehabilitation approaches. Traditionally, PR programs are center-based and shown positive outcomes across a broad range of ILD subtypes.^13,14,16,17 Systematic review evidence in ILD demonstrates consistent, clinically meaningful improvements in functional exercise capacity (e.g., 6-minute walk distance), dyspnea, and HRQL following PR, although benefits may attenuate without maintenance activity.^15,16

A typical pulmonary rehabilitation team consists of physicians, nurses, respiratory therapists, physical therapists, social workers, dieticians. Exercise training is the central component of PR and includes a combination of aerobic/endurance training and progressive resistance or functional strength training. Aerobic exercise most commonly involves walking and stationary cycling, performed either continuously or in intervals based on symptom tolerance and oxygenation, while resistance training targets major upper- and lower-limb muscle groups to address peripheral muscle weakness and deconditioning. Exercise intensity is individualized and guided by symptoms, functional testing, and oxygen saturation rather than fixed workload targets. PR has been shown to be safe for patients with ILD, including those with advanced disease and those requiring supplemental oxygen, and disease severity alone should not preclude referral. The primary goal of PR in ILD is improvement in functional capacity and reduction of activity-limiting dyspnea through enhanced conditioning and peripheral muscle efficiency rather than modification of underlying fibrotic lung pathology.^14,15,16

Limitations of pulmonary rehabilitation

While PR improves exercise capacity, symptoms, and health-related quality of life in patients with ILD, there is insufficient evidence that it improves long-term survival.^15,16 Benefits may be smaller in advanced ILD and are generally more modest than those seen in COPD, though disease severity alone should not preclude referral.^14,16 Recent ILD-focused reviews and syntheses support home-based and hybrid PR models as effective options to expand access and improve participation while maintaining clinically meaningful functional gains.^16,17 Ongoing research and multidisciplinary collaboration are needed to optimize program design and patient-centered care.^14,16,17

Patient & family education

In addition to exercise training, education is a core component of PR and aims to improve self-management, coping skills, and long-term health behaviors in patients with ILD. Education focuses on helping patients adapt to changes in physical function and symptom burden and take an active role in their care. A comprehensive PR education program typically includes management of breathlessness, cough, and fatigue; strategies to address anxiety and depression; principles of oxygen therapy; health maintenance in ILD (including vaccination, nutrition, exercise, and recognition of disease exacerbations); and strategies to maintain physical activity after completion of PR. Education should be individualized and may also include medication management, comorbidity management, and access to community and caregiver support resources.^13,14,16

Current guidance emphasizes the importance of early, patient-centered discussions about disease course, prognosis, and advance care planning, tailored to patient preferences and revisited over time. Integrating these discussions into PR supports shared decision-making, aligns rehabilitation goals with patient values, and promotes a holistic, multidisciplinary approach to ILD care.^14,18

Emerging/unique interventions

ILD-specific patient-reported outcome measures, particularly King’s Brief Interstitial Lung Disease (K-BILD), are increasingly used to assess health-related quality of life and treatment response, offering improved sensitivity to ILD-specific symptoms compared with generic respiratory questionnaires.¹⁹ Functional assessment has also expanded to include simple, low-burden performance tests that capture peripheral muscle dysfunction and mobility limitations. These measures are commonly paired with traditional field tests such as 6MWT to monitor functional change over time and to support exercise prescription within PR.^14,16 Measures such as the 5-repetition sit-to-stand (5-STS) and timed up-and-go (TUG) have demonstrated reliability and validity in ILD populations and are increasingly incorporated into pulmonary rehabilitation and clinical monitoring, especially for patients unable to perform maximal exercise testing.¹⁶ Cardiopulmonary exercise testing (CPET) provides important information concerning exertional dyspnea and mechanisms of exercise limitation as a comprehensive assessment of the physiological changes in the respiratory, cardiovascular and musculoskeletal systems during exercise, which may be also useful for exercise prescription.²⁰

Translation into practice: Practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

Pulmonary rehabilitation remains underutilized in ILD despite strong guideline support, largely due to limited program availability, low referral rates, and access barriers such as transportation, scheduling constraints, and patient misconceptions about exercise safety. Exercise training within PR improves exercise capacity, dyspnea, and health-related quality of life, but benefits may diminish over time without maintenance, highlighting the need for ongoing physical activity support after program completion. To address access gaps, home-based, hybrid, and telerehabilitation models are recommended as practical strategies to expand PR delivery and promote patient-centered care.^14,17

Cutting Edge/Emerging and Unique Concepts and Practice

Despite advances in pharmacotherapy, IPF and ILDs remain associated with substantial morbidity and mortality, and current treatments primarily aim to slow disease progression rather than reverse established fibrosis. Contemporary guideline-based management emphasizes early diagnosis, antifibrotic therapy for IPF, and supportive care (including PR and oxygen when indicated) across the disease course.^3,14

In CTD-ILD, evolving evidence has clarified that methotrexate is not a major cause of chronic fibrotic lung disease in rheumatoid arthritis and should not be routinely avoided, shifting prior clinical practice. Antifibrotic therapy with nintedanib is now recommended for patients with progressive fibrosing ILD, including CTD-ILD, based on demonstrated efficacy in reducing lung function decline. In addition, targeted immunomodulatory therapies, such as anti–interleukin-6 agents in systemic sclerosis–associated ILD, represent an emerging treatment strategy. Ongoing research includes identifying noninvasive biomarkers and imaging-based predictors of disease progression to allow earlier intervention before irreversible lung damage occurs.³

Gaps in the Evidence-Based Knowledge

Participation in pulmonary rehabilitation remains low, pointing to important gaps in implementation and access, including referral practices, funding models, and how services are delivered. Expanding evidence for home-based and hybrid PR models highlights an opportunity to improve access, but implementation barriers such as technology, staffing, reimbursement, and standardization of protocols remain.^14,16,17

Additional research is needed to develop and evaluate policy- and system-level strategies that improve referral, uptake, and long-term participation in PR. In pharmacologic management, although antifibrotic therapies are now standard of care for IPF and progressive pulmonary fibrosis, no current treatment improves survival or reverses established fibrosis, highlighting the ongoing need for therapies that more meaningfully alter disease course. Across ILD subtypes, significant knowledge gaps persist in identifying early predictors of disease progression, treatment response, and patient-centered outcomes, which continue to limit timely intervention and truly personalized care.³

References

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4. Borie R, Kannengiesser C, Nathan N, et al. Pulmonary fibrosis associated with telomere-related gene variants. Respirology. 2021.
5. Shao T, Shi X, Yang S, et al. Interstitial Lung Disease in Connective Tissue Disease: A Common Lesion With Heterogeneous Mechanisms and Treatment Considerations. Front Immunol. 2021;12:2092. doi:10.3389/FIMMU.2021.684699/BIBTEX
6. Wijsenbeek M, Cottin V. Spectrum of fibrotic lung diseases. N Engl J Med. 2020;383(10):958–968. doi:10.1056/NEJMra2005230
7. Weill D, Benden C, Corris PA, et al. A consensus document for the selection of lung transplant candidates: 2021 update from the International Society for Heart and Lung Transplantation. J Heart Lung Transplant. 2021;40(11):1349–1379. doi:10.1016/j.healun.2021.07.005
8. Egashira R, Jacob J, Kokosi M, et al. Acute exacerbation of fibrotic interstitial lung disease beyond idiopathic pulmonary fibrosis. Eur Respir J. 2023;61(5):2300459. doi:10.1183/13993003.00459-2023
9. Luo X, Lian X, Wang J, et al. Acute exacerbation of idiopathic pulmonary fibrosis: a narrative review. J Thorac Dis. 2024;16(1):165–179. doi:10.21037/jtd-23-1229
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12. Korevaar DA, Colella S, Fally M, et al. European Respiratory Society guidelines on transbronchial lung cryobiopsy in the diagnosis of interstitial lung diseases. Eur Respir J. 2022;60(5):2200425. doi:10.1183/13993003.00425-2022
13. Holland AE, Cox NS, Houchen-Wolloff L, et al. Defining modern pulmonary rehabilitation. An official American Thoracic Society Workshop Report. American Journal of Respiratory and Critical Care Medicine. 2021;203(12):e7–e18.
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14. Rochester CL, Alison JA, Carlin B, et al. Pulmonary rehabilitation for adults with chronic respiratory disease: ATS clinical practice guideline. Am J Respir Crit Care Med. 2023;208(4):e7–e26. doi:10.1164/rccm.202306-1066ST
15. Reina-Gutiérrez S, Torres-Costoso A, et al. Effectiveness of pulmonary rehabilitation in interstitial lung disease, including coronavirus diseases: a systematic review and meta-analysis. 2021.
16. Guler SA, et al. Pulmonary rehabilitation in interstitial lung disease. Chest. 2025.
17. Bongiovanni G, et al. Home-based rehabilitation in interstitial lung disease: systematic review. ERJ Open Res. 2025.
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Original Version of the Topic

Farha S. Ikramuddin, MD MBBS. Pulmonary rehabilitation in intrinsic restrictive lung diseases. 9/20/2014

Previous Revision(s) of the Topic

Rajashree Srinivasan, MD, MBBS, Veronica Reyor, DO. Pulmonary rehabilitation in intrinsic restrictive lung diseases. 9/27/2020

Rajashree Srinivasan, MD, MBBS, Saylee Dhamdhere, MD, Nikhil Gopal, MBBS, Pulmonary Rehabilitation in Intrinsic Restrictive Lung Diseases. 5/25/2023

Author Disclosures

Saylee Dhamdhere, MD
Nothing to Disclose

Eunyeop Kim, MD
Nothing to Disclose

Rajashree Srinivasan, MD, MBBS
Nothing to Disclose