Pulmonary Function Testing
Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial in Textbook of Allergy for the Clinician, 2021
Pulmonary function testing helps to differentiate between obstructive and restrictive lung disease. Obstructive lung disease is characterized by obstruction or narrowing of the airways. This is often due to excessive smooth muscle contraction. Examples of obstructive lung disease include asthma, Chronic Obstructive Pulmonary Disease (COPD) and bronchiectasis. Restrictive lung disease is characterized by the inability to fully expand the lungs. This results in decreased lung volume and increased work of breathing. Restrictive lung disease can be due to occupational exposures, medications, neuromuscular disorders or pulmonary fibrosis. Extrinsic diseases can also restrict expansion of the lung. For a comprehensive list of etiologies of restrictive lung disease see Table 16.1 (Johnson et al. 2014).
Exercise training: The role of CPET
Robert B. Schoene, H. Thomas Robertson in Making Sense of Exercise Testing, 2018
Patients with both obstructive and restrictive lung disease have a number of factors that have been described in other chapters that result in a greater work of breathing and dyspnea. Several techniques are used in pulmonary rehabilitation programs to improve respiratory muscle strength and efficiency that decrease dyspnea and the / and /. For instance, resistive training of the respiratory muscles can improve inspiratory muscle strength and endurance and enhance daily function.
Dyspnea in Asthma and Restrictive Lung Disease
Donald A. Mahler, Denis E. O’Donnell in Dyspnea, 2014
Restrictive lung disease is a broad term encompassing several conditions in which lung volumes are reduced. Interstitial lung disease (ILD) is the prototypical restrictive disease. Dyspnea is a common clinical manifestation of ILD. Activity-related dyspnea appears to be the earliest and dominant symptom limiting exercise in the majority of patients afflicted by ILD. This symptom progresses relentlessly with time leading invariably to avoidance of activity with consequent skeletal muscle deconditioning and poor perceived quality of life. Effective management of this symptom awaits a better understanding of its underlying physiology.
Acute chest syndrome in sickle cell anaemia: higher serum levels of interleukin-8 and highly sensitive C-reactive proteins are associated with impaired lung function
Published in Paediatrics and International Child Health, 2018
Samuel Ademola Adegoke, Bankole Peter Kuti, Kehinde Oluyori Omole, Olufemi Samuel Smith, Oyeku Akibu Oyelami, Oluwagbemiga Oyewole Adeodu
A patient was said to have normal lung function when FEV1, FVC and FEV1/FVC were at or above the lower limit of normal (i.e. ≥80% predicted for age, gender and height) [18]. Impaired lung function was further subclassified into those with restrictive lung disease, obstructive lung disease and mixed lung disease. Obstructive lung disease was diagnosed when FEV1 or FEV1/FVC was <80% predicted for age, gender and height, and FVC was normal or increased [18]. Restrictive lung disease was presumed when FVC% predicted for age, gender and height was <80% or FEV1/FVC was >80% with normal FEV1 [18]. Those in whom FEV1 was <80%, FVC <80% and FEV1/FVC <80% predicted for age, gender and height were classified as having mixed impairment [18].
Features of Marfan syndrome not listed in the Ghent nosology – the dark side of the disease
Published in Expert Review of Cardiovascular Therapy, 2019
Yskert von Kodolitsch, Anthony Demolder, Evaldas Girdauskas, Harald Kaemmerer, Katharina Kornhuber, Laura Muino Mosquera, Shaine Morris, Enid Neptune, Reed Pyeritz, Svend Rand-Hendriksen, Alexander Rahman, Nina Riise, Leema Robert, Ingmar Staufenbiel, Katalin Szöcs, Thy Thy Vanem, Stephan J. Linke, Marina Vogler, Anji Yetman, Julie De Backer
The lung manifestations of Marfan syndrome are burdensome and complex [169]. More importantly, they can lead to substantial disability and reduced quality of life. Scoliosis, pectus deformities and respiratory muscle weakness contribute to restrictive lung disease. Parenchymal lung disease, often developmental in origin, leads to upper lobe blebs, pneumothoraces and, especially in the setting of neonatal Marfan syndrome, overt emphysema. Both chest wall deformities and airway wall defects can manifest disorders such as asthma and bronchiectasis. Finally, soft tissue laxity and a predilection for upper airway obstruction confer the high prevalence of sleep-disordered breathing. This spectrum of lung disorders is challenging for care providers who often have to evaluate dyspnea, chest pain and reduced exercise capacity in the context of the known risks of highly morbid and fatal cardiac and aortic disease. Unfortunately, no reliable contemporary (post-Ghent 2010) assessment of lung disease prevalence is available given that screening for pulmonary impairment is inconsistent across centers and mostly symptom- or finding-triggered [170]. However, even small, single-center retrospective studies confirm a high burden of respiratory disease in Marfan syndrome [171].
Indwelling tunneled pleural catheters in patients with hepatic hydrothorax: A single-center analysis for outcomes and complications
Published in Canadian Journal of Respiratory, Critical Care, and Sleep Medicine, 2023
Fatmah F. Alhabeeb, Katia Carle-Talbot, Natalie Rakocevic, Tinghua Zhang, Michael Mitchell, Kayvan Amjadi, Chanel Kwok
Analysis of the chest x-ray scores demonstrate that the majority of patients had a large pleural effusion at the time of insertion, and many failed to completely expand despite the insertion of a catheter. We think that this is likely due to the development of trapped lung, as demonstrated by the radiographic evidence of volume loss, premature cessation of drainage due to pain (1 patient), and residual effusion post-drainage (2 patients with persistent moderate effusion, 1 patient with hydro-pneumothorax). However, given the lack of manometry data, we can use the term “non-expanding lung” instead. This highlights the possibility of developing progressive volume loss and parenchymal stiffening as a result of chronic effusion, even if the underlying etiology is benign. The current fear surrounding pleural interventions in HH may result in unnecessary delays in facilitating lung expansion and may contribute to the development of non-expanding lung. Perhaps earlier intervention with an IPC could prevent the development of this permanent, restrictive lung disease in some patients.
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