Interpretation of Pulmonary Function Tests (Pfts)
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Lung Function Studies in Diagnostics and Follow-Up of Pulmonary Sarcoidosis
Lung Function Studies in Diagnostics and Follow-up of Pulmonary Sarcoidosis By INGELA BRÅDVIK Lund 1994 From the Department of Lung Medicine and the Department of Clinical Physiology University of Lund, Sweden Lung Function Studies in Diagnostics and Follow-up of Pulmonary Sarcoidosis Ingela Brådvik Lund 1994 Organization Document name LUND UNIVERSITY DOCTORAL DISSERTATION Department of Lung Medicine Date of issue University Hospital 94 06 09 S-22I 85 Lund CODEN: ISRN LUMEDW/MELL- - 1007- - SE Authorfj) Sponsoring organization Ingela Brådvik The Swedish Heart Lung Foundation Title and subtitle Lung function studies in diagnostics and follow-up of pulmonary sarcoidosis Abstract In 66 patients the relationship between lung volumes and lung mechanics in pulmonary sarcoidosis was investigated Lung volumes, static lung mechanics, lung resistance, dynamic lung mechanics and arterial blood gases at rest and during exercise were obtained. Fifteen functionally compromised patients received steroids during one year. They were re-investigated during the treatment and at a follow-up after an average of 7 years. In another 41 patients with newly diagnosed sarcoidosis, the kinetics of the lung clearance of ^9mTc-DTPA measured over 180 minutes was explored, and compared to kinetics in healthy smokers. The relationship between lung clearance and lung volumes, lung mechanics, arterial blood gases and disease activity assessed with serum angiotensin-converting enzyme and "'Ga scintigraphy was studied. Reduced lung volumes and compliance, increased resistance and decreased arterial oxygen tension were common. Vital i capacity (VC), and changes of VC at follow-up, corresponded to the slope of the static elastic pressure/volume curve, . and to the variation of it. -
Effect of an Indwelling Pleural Catheter Vs Talc Pleurodesis On
This supplement contains the following items: 1. Original protocol, final protocol, summary of changes. 2. Original statistical analysis plan. There were no further changes to the original statistical analysis plan. Downloaded From: https://jamanetwork.com/ on 10/02/2021 The Australasian Malignant Pleural Effusion Trial (AMPLE) A Multicentre Randomized Study Comparing Indwelling Pleural Catheter vs Talc Pleurodesis in Patients with Malignant Pleural Effusions Ethics Registration number 2012-005 Protocol version number 1.0 Protocol date 10/01/2012 Authorised by: Name: Prof YC Gary Lee Role: Chief Investigator Signature: Date: 10/01/2012 Downloaded From: https://jamanetwork.com/ on 10/02/2021 General Information This document describes the Western Australian Randomised Malignant Effusion trial for the purpose of submission for review by the relevant human research and ethics committees. It provides information about procedures for entering patients into the trial and this protocol should not be used as a guide for the treatment of other patients; every care was taken in its drafting, but corrections or amendments may be necessary. Questions or problems relating to this study should be referred to the Chief Investigator or Trial Coordinator. Compliance The trial will be conducted in compliance with this protocol, the National Statement on Ethical Conduct in Human Research, data protection laws and other guidelines as appropriate. It will be registered with the Australia and New Zealand Clinical Trials Registry, once ethical approval is secured. -
Bronchodilators Accelerate the Dynamics of Muscle O2 Delivery
Chronic obstructive pulmonary disease Bronchodilators accelerate the dynamics of muscle Thorax: first published as 10.1136/thx.2009.120857 on 13 July 2010. Downloaded from O2 delivery and utilisation during exercise in COPD Danilo C Berton,1 Priscila B Barbosa,1 Luciana S Takara,1 Gaspar R Chiappa,1 Ana Cristina B Siqueira,1 Daniela M Bravo,1 Leonardo F Ferreira,2 J Alberto Neder1 See Editorial, p 573 ABSTRACT (QT), suggesting an important role for the central Background Expiratory flow limitation and lung cardiovascular adjustments in setting the limits of < Supplementary methods are hyperinflation promote cardiocirculatory perturbations increase in peripheral QO at the onset of exercise. published online only. To view 2 these files please visit the that might impair O2 delivery to locomotor muscles in Further experimental evidence for this contention journal online (http://thorax.bmj. patients with chronic obstructive pulmonary disease was obtained in a subsequent study in which com). (COPD). The hypothesis that decreases in lung hyperinflation a strategy aimed to reduce the resistive work of 1Pulmonary Function and Clinical after the inhalation of bronchodilators would improve breathing and dynamic hyperinflation (heliox) Exercise Physiology Unit skeletal muscle oxygenation during exercise was tested. simultaneously accelerated the dynamics of QTand (SEFICE), Division of Respiratory 5 Methods Twelve non- or mildly hypoxaemic males QO2 in patients with moderate to severe COPD. Diseases, Department of (forced expiratory volume in 1 s (FEV1)¼38.5612.9% -
Maximum Expiratory Flow Rates in Induced Bronchoconstriction in Man
Maximum expiratory flow rates in induced bronchoconstriction in man A. Bouhuys, … , B. M. Kim, A. Zapletal J Clin Invest. 1969;48(6):1159-1168. https://doi.org/10.1172/JCI106073. Research Article We evaluated changes of maximum expiratory flow-volume (MEFV) curves and of partial expiratory flow-volume (PEFV) curves caused by bronchoconstrictor drugs and dust, and compared these to the reverse changes induced by a bronchodilator drug in previously bronchoconstricted subjects. Measurements of maximum flow at constant lung inflation (i.e. liters thoracic gas volume) showed larger changes, both after constriction and after dilation, than measurements of peak expiratory flow rate, 1 sec forced expiratory volume and the slope of the effort-independent portion of MEFV curves. Changes of flow rates on PEFV curves (made after inspiration to mid-vital capacity) were usually larger than those of flow rates on MEFV curves (made after inspiration to total lung capacity). The decreased maximum flow rates after constrictor agents are not caused by changes in lung static recoil force and are attributed to narrowing of small airways, i.e., airways which are uncompressed during forced expirations. Changes of maximum expiratory flow rates at constant lung inflation (e.g. 60% of the control total lung capacity) provide an objective and sensitive measurement of changes in airway caliber which remains valid if total lung capacity is altered during treatment. Find the latest version: https://jci.me/106073/pdf Maximum Expiratory Flow Rates in Induced Bronchoconstriction in Man A. Bouiuys, V. R. HuNTr, B. M. Kim, and A. ZAPLETAL From the John B. Pierce Foundation Laboratory and the Yale University School of Medicine, New Haven, Connecticut 06510 A B S T R A C T We evaluated changes of maximum ex- rates are best studied as a function of lung volume. -
The Pulmonary Manifestations of Left Heart Failure*
The Pulmonary Manifestations of Left Heart Failure* Brian K. Gehlbach, MD; and Eugene Geppert, MD Determining whether a patient’s symptoms are the result of heart or lung disease requires an understanding of the influence of pulmonary venous hypertension on lung function. Herein, we describe the effects of acute and chronic elevations of pulmonary venous pressure on the mechanical and gas-exchanging properties of the lung. The mechanisms responsible for various symptoms of congestive heart failure are described, and the significance of sleep-disordered breathing in patients with heart disease is considered. While the initial clinical evaluation of patients with dyspnea is imprecise, measurement of B-type natriuretic peptide levels may prove useful in this setting. (CHEST 2004; 125:669–682) Key words: Cheyne-Stokes respiration; congestive heart failure; differential diagnosis; dyspnea; pulmonary edema; respiratory function tests; sleep apnea syndromes Abbreviations: CHF ϭ congestive heart failure; CSR-CSA ϭ Cheyne-Stokes respiration with central sleep apnea; CPAP ϭ continuous positive airway pressure; Dlco ϭ diffusing capacity of the lung for carbon monoxide; DM ϭ membrane conductance; FRC ϭ functional residual capacity; OSA ϭ obstructive sleep apnea; TLC ϭ total lung ϭ ˙ ˙ ϭ capacity; VC capillary volume; Ve/Vco2 ventilatory equivalent for carbon dioxide early 5 million Americans have congestive heart For a detailed review of the pathophysiology of N failure (CHF), with 400,000 new cases diag- high-pressure pulmonary edema, the reader is re- nosed each year.1 Unfortunately, despite the consid- ferred to several excellent recent reviews.2–4 erable progress that has been made in understanding the pathophysiology of pulmonary edema, the pul- monary complications of this condition continue to The Pathophysiology of Pulmonary challenge the bedside clinician. -
Bronchiolitis After Lung Transplantation Lymphoid Tissue In
The Role of Intrapulmonary De Novo Lymphoid Tissue in Obliterative Bronchiolitis after Lung Transplantation This information is current as Masaaki Sato, Shin Hirayama, David M. Hwang, Humberto of September 25, 2021. Lara-Guerra, Dirk Wagnetz, Thomas K. Waddell, Mingyao Liu and Shaf Keshavjee J Immunol 2009; 182:7307-7316; ; doi: 10.4049/jimmunol.0803606 http://www.jimmunol.org/content/182/11/7307 Downloaded from References This article cites 46 articles, 4 of which you can access for free at: http://www.jimmunol.org/content/182/11/7307.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 25, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2009 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology The Role of Intrapulmonary De Novo Lymphoid Tissue in Obliterative Bronchiolitis after Lung Transplantation1 Masaaki Sato,* Shin Hirayama,* David M. Hwang,*† Humberto Lara-Guerra,* Dirk Wagnetz,* Thomas K. Waddell,* Mingyao Liu,* and Shaf Keshavjee2* Chronic rejection after lung transplantation is manifested as obliterative bronchiolitis (OB). -
Effect of Heliox Breathing on Flow Limitation in Chronic Heart Failure Patients
Eur Respir J 2009; 33: 1367–1373 DOI: 10.1183/09031936.00117508 CopyrightßERS Journals Ltd 2009 Effect of heliox breathing on flow limitation in chronic heart failure patients M. Pecchiari*, T. Anagnostakos#, E. D’Angelo*, C. Roussos#, S. Nanas# and A. Koutsoukou# ABSTRACT: Patients with chronic heart failure (CHF) exhibit orthopnoea and tidal expiratory flow AFFILIATIONS limitation in the supine position. It is not known whether the flow-limiting segment occurs in the *Istituto di Fisiologia Umana I, Universita` degli Studi di Milano, peripheral or central part of the tracheobronchial tree. The location of the flow-limiting segment Milan, Italy, and can be inferred from the effects of heliox (80% helium/20% oxygen) administration. If maximal #Dept of Critical Care and Pulmonary expiratory flow increases with this low-density mixture, the choke point should be located in the Services, Evangelismos General central airways, where the wave-speed mechanism dominates. If the choke point were located in Hospital, Medical School, University of Athens, Athens, Greece. the peripheral airways, where maximal flow is limited by a viscous mechanism, heliox should have no effect on flow limitation and dynamic hyperinflation. CORRESPONDENCE Tidal expiratory flow limitation, dynamic hyperinflation and breathing pattern were assessed in M. Pecchiari 14 stable CHF patients during air and heliox breathing at rest in the sitting and supine position. Istituto di Fisiologia Umana I via L. Mangiagalli 32 No patient was flow-limited in the sitting position. In the supine posture, eight patients exhibited 20133 Milan tidal expiratory flow limitation on air. Heliox had no effect on flow limitation and dynamic Italy hyperinflation and only minor effects on the breathing pattern. -
Air Trapping on Computed Tomography: Regional Versus Diffuse
EDITORIAL | SMOKING Air trapping on computed tomography: regional versus diffuse Firdaus A. Mohamed Hoesein and Pim A. de Jong Affiliation: Dept of Radiology, University Medical Center Utrecht, Utrecht, The Netherlands. Correspondence: Firdaus A. Mohamed Hoesein, University Medical Center Utrecht, Department of Radiology, Heidelberglaan 100, PO box 855000, 3508 GA, Utrecht, The Netherlands. E-mail: [email protected] @ERSpublications Future studies on the distribution of air trapping in the lungs of COPD patients are needed http://ow.ly/86hc304JiIK Cite this article as: Mohamed Hoesein FA, de Jong PA. Air trapping on computed tomography: regional versus diffuse. Eur Respir J 2017; 49: 1601791 [https://doi.org/10.1183/13993003.01791-2016]. Chronic obstructive pulmonary disease (COPD) is diagnosed and classified by spirometry, assessing the presence of airflow obstruction and extent of forced expiratory flow deterioration. Spirometry, however, is unsuitable for characterising and quantifying the underlying pulmonary pathology of COPD, including alveolar destruction (emphysema) and airway remodelling (large- and small-airway disease). Accurate diagnosis of the pulmonary pathologies underlying COPD is seen as an important step towards better understanding its biology and “personalised” treatment. Computed tomography (CT) of the lungs provides an excellent opportunity to assess COPD in vivo and quantify its macroscopic pathology [1–3]. Emphysema and airway remodelling can be visually assessed and automatically quantified, and several studies have shown associations with morbidity and mortality [4–7]. In addition, CT can provide information on the spatial distribution of disease. In this issue of the European Respiratory Journal,KARIMI et al. [8] hypothesise that regional air trapping maybe a new imaging marker, in addition to emphysema, large-airway remodelling and diffuse air trapping. -
Learning Objectives
Restrictive Lung Diseases & Pulmonary Vascular Disease Pulmonary 2018 RESTRICTIVE LUNG DISEASES AND PULMONARY VASCULAR DISEASE Joel Thibodeaux, MD, Phone: 469-419-4535 Email: [email protected] INTRODUCTION This lecture will discuss basic concepts, etiologic factors, pathologic features, pathogenesis, and clinicopathologic findings in the different types of interstitial lung diseases. It also will touch briefly on pulmonary vascular diseases. LEARNING OBJECTIVES: • Acute respiratory distress syndrome (ARDS) (BP, pp. 460-461) o Define ARDS and list common causes o Illustrate the mechanism of lung injury in ARDS and the role of proinflammatory and anti-inflammatory mediators o Describe the morphologic features of ARDS. Understand how they evolve, and know what happens if the patient survives. • Diffuse interstitial lung disease (BP, pp. 472-474, 480-482) o List the major forms of diffuse interstitial lung diseases discussed o Be able to identify classic morphologic features of common interstitial lung diseases. o Recognize the major causes of pneumoconioses (BP, pp. 474-478) o Delineate the gross and microscopic features resulting from exposure to coal dust, silica, organic/animal dust, and asbestos. o Sarcoidosis (BP, pp. 478-480) . Define sarcoidosis . List the most common organs involved, and describe the characteristic histologic lesion . Describe the radiographic, gross, and histologic appearance of lesions in the hilar lymph nodes and lungs • Define primary pulmonary hypertension. Recognize the characteristic histologic -
Idiopathic Bronchiolocentric Interstitial Pneumonia Samuel A
Idiopathic Bronchiolocentric Interstitial Pneumonia Samuel A. Yousem, MD, Sanja Dacic, MD, PhD Department of Pathology, University of Pittsburgh Medical Center, Presbyterian University Hospital, Pittsburgh, Pennsylvania plugs of fibromyxoid connective tissue, and poorly The authors report 10 patients with a distinctive formed granulomas (1–3). This triad of morphologic idiopathic bronchiolocentric interstitial pneumonia changes allows the pathologist to direct the pulmo- having some histologic similarities to hypersensitiv- nologist to question the patient for specific inhala- ity pneumonitis. Bronchiolocentric interstitial tional exposures. We have accumulated 10 cases pneumonia has a marked predilection for women that have very similar morphologic findings to hy- (80%) and occurs in middle age (40–50 years). Chest persensitivity pneumonitis, with the exclusion of radiographs and pulmonary function tests show in- interstitial granulomas, in which extensive investi- terstitial and restrictive lung disease, while the his- gations failed to reveal a cause for the inflamma- tologic appearance is that of a centrilobular inflam- tion. The clinicopathologic features of this idio- matory process with small airway fibrosis and pathic bronchiolocentric interstitial pneumonia are inflammation that radiates into the interstitium of the basis of this report which suggests a more ag- the distal acinus in a patchy fashion. Granulomas gressive and life threatening biologic behavior for are not identified. At a mean followup of approxi- bronchiolocentric interstitial pneumonia than nor- mately 4 years in nine patients, 33% of patients mally associated with hypersensitivity pneumonitis were dead of disease and 56% had persistent or or some of the other conditions in the histologic progressive disease suggesting a more aggressive differential diagnosis. course than hypersensitivity pneumonitis and non- specific interstitial pneumonia, the two major dis- ease processes in the differential diagnosis. -
Imaging of Small Airways Disease
SYMPOSIA Imaging of Small Airways Disease Gerald F. Abbott, MD,* Melissa L. Rosado-de-Christenson, MD,w zy Santiago E. Rossi, MD,J and Saul Suster, MDz SECONDARY PULMONARY LOBULE Abstract: Small airways disease includes a spectrum of inflammatory The secondary pulmonary lobule (SPL) is a key and fibrotic pulmonary diseases centered on the small conducting structure in the lung anatomy and is distinguished as the airways. High-resolution computed tomography plays a key role in the detection and classification of small airways disease and, when smallest functioning subunit of lung that is bound by combined with relevant clinical and pathologic findings, leads to a connective tissue septa, supplied by a lobular bronchiole more accurate diagnosis. The imaging manifestations of small airways and arteriole, and drained by veins and lymphatics in the disease on high-resolution computed tomography may be direct or interlobular septa. Each SPL measures 1 to 2.5 cm and indirect signs of small airway involvement and include centrilobular contains 3 to 12 acini. The SPL are better formed and more nodules and branching nodular (tree-in-bud) opacities, or the easily recognized in the peripheral subpleural lung and demonstration of mosaic attenuation that is typically exaggerated on are smaller and less regular in the central lung. The SPL are expiratory computed tomography. This article reviews the normal not normally visible on radiography or computed tomo- anatomy and histology of bronchioles and the clinical, pathologic, and graphy (CT)/HRCT (Fig. 1). -
Restrictive Lung Disease
Downloaded from https://academic.oup.com/ptj/article/48/5/455/4638136 by guest on 29 September 2021 RESTRICTIVE LUNG DISEASE WARREN M. GOLD, M.D. RESTRICTIVE LUNG DISEASE is a These disorders can be divided into two pattern of abnormal lung function defined by groups: extrapulmonary and pulmonary. a decrease in lung volume (Fig. I).1,2 The In extrapulmonary restriction, an abnormal total lung capacity is decreased and, in severe increase in the stiffness of the chest wall (kypho restrictive defects, all of the subdivisions of the scoliosis) restricts the lung volumes, as does total lung capacity including vital capacity, respiratory muscle weakness (poliomyelitis or functional residual capacity, and residual vol muscular dystrophy). These extrapulmonary ume are decreased. In mild or moderately se causes of pulmonary restriction are treated vere restrictive defects, the residual volume may be normal or slightly increased. CLINICAL DISORDERS CAUSING TABLE 1 RESTRICTIVE LUNG DISEASE CAUSES OF RESTRICTIVE LUNG DISEASE Restrictive lung disease is not a specific clin I. Extrapulmonary restriction 3 ical entity, but only one of several patterns of A. Chest wall stiffness (kyphoscoliosis) B. Respiratory-muscle weakness (muscular dystrophy)4 abnormal lung function. It is produced by a C. Pleural disease (pneumothorax)5 number of clinical disorders (see Table 1). II. Pulmonary restriction A. Surgical resection (pneumonectomy)6.7 Dr. Gold: Director, Pulmonary Laboratory and Re B. Tumor (bronchogenic carcinoma or metastatic tumor)8 search Associate in Cardiology (Pulmonary Physiology), C. Heart disease (hypertensive, arteriosclerotic, rheu Children's Hospital Medical Center; Associate in Pedi matic, congenital)9 atrics and Tutor in Medical Science, Harvard Medical 10 11 School, Boston, Massachusetts.