Interpretation Of Pulmonary Function Tests.doc !!TOP!!
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Background: Appropriate interpretation of pulmonary function tests (PFTs) involves the classification of observed values as within/outside the normal range based on a reference population of healthy individuals, integrating knowledge of physiological determinants of test results into functional classifications and integrating patterns with other clinical data to estimate prognosis. In 2005, the American Thoracic Society (ATS) and European Respiratory Society (ERS) jointly adopted technical standards for the interpretation of PFTs. We aimed to update the 2005 recommendations and incorporate evidence from recent literature to establish new standards for PFT interpretation.
Conclusions: Interpretation of PFTs must be complemented with clinical expertise and consideration of the inherent biological variability of the test and the uncertainty of the test result to ensure appropriate interpretation of an individual's lung function measurements.
processing.... Drugs & Diseases > Clinical Procedures Pulmonary Function Testing Updated: May 14, 2020 Author: Kevin McCarthy, RPFT; Chief Editor: Nader Kamangar, MD, FACP, FCCP, FCCM more... Share Email Print Feedback Close Facebook Twitter LinkedIn WhatsApp webmd.ads2.defineAd({id: 'ads-pos-421-sfp',pos: 421}); Sections Pulmonary Function Testing Sections Pulmonary Function Testing Spirometry Lung Volume Determination Diffusing Capacity of Lung for Carbon Monoxide Assessment of Respiratory Muscle Strength Pulse Oximetry Methacholine Challenge Testing Six-Minute Walk Test Cardiopulmonary Stress Testing Arterial Blood Gases Exhaled Nitric Oxide Questions & Answers Show All Media Gallery Tables References Spirometry Description Spirometry assesses the integrated mechanical function of the lung, chest wall, respiratory muscles, and airways by measuring the total volume of air exhaled from a full lung (total lung capacity [TLC]) to maximal expiration (residual volume [RV]). This volume, the forced vital capacity (FVC) and the forced expiratory volume in the first second of the forceful exhalation (FEV1), should be repeatable to within 0.15 L upon repeat efforts in the same measurement unless the largest value for either parameter is less than 1 L. In this case, the expected repeatability is to within 0.1 L of the largest value. The patient is instructed to inhale as much as possible and then exhale rapidly and forcefully for as long as flow can be maintained. The patient should exhale until one of the criteria defining the end of a forced exhalation has been reached. At the end of the forced exhalation, the patient should again inhale fully as rapidly as possible. The FVC should then be compared with that inhaled volume to verify that the forced expiratory maneuver did start from full inflation.
Spirometry is used to establish baseline lung function, evaluate dyspnea, detect pulmonary disease, monitor effects of therapies used to treat respiratory disease, evaluate respiratory impairment or disability, evaluate operative risk, and perform surveillance for occupational-related lung disease. It may also be used in research and clinical trials and epidemiological surveys.
The 2017 ATS recommendations for a standardized pulmonary function report details recommendations for reporting of DLCO. [8] A major change is the recommendation to express the measured DLCO on a z-score scale, which expresses the result as the number of multiples of a standard deviation above or below a population mean.
CPX test is used for evaluation of dyspnea that is out of proportion to findings on static pulmonary function tests, preoperative evaluation of operative risk when lung function is compromised or removal of lung segments is contemplated, evaluation of disability, identification of exercise-induced asthma, and evaluation of therapy.
Cardiac limitation: This 48-year-old woman was referred for a cardiopulmonary exercise testing to evaluate her shortness of breath upon exertion over the last 6 months. Pulmonary function tests reveal a mild restrictive ventilatory defect with a normal DLCO, suggesting no active parenchymal disease.
The European Respiratory Society (ERS) and the American Thoracic Society (ATS) just published an updated technical standard on lung function interpretation. It's a critically important document written by a "Who's Who" in the lung function world. It's impossible to review in its entirety without more space, so I'll settle for covering what the authors say about bronchodilator testing. But before I do that, it's worth reviewing what we think we know about having a patient perform spirometry, inhale a bronchodilator, and then repeat it. This is colloquially referred to as pre- and post-bronchodilator testing.
Sarcoidosis is a granulomatous disease of unknown etiology that can affect any organ. Identification of sarcoidosis patients is key to improving their outcomes and reducing health care costs. Unfortunately, diagnosis can be complex and require significant testing. Pulmonary function testing (PFT), along with chest imaging, is often the initial testing obtained by the respiratory physician in evaluation of the patient with dyspnea and is often used to monitor response to therapy. PFTs are one of many potentially useful tools when following patients with pulmonary sarcoidosis. The goal of this review is to discuss the patterns and pitfalls of PFT interpretation in patients with sarcoidosis.
Sarcoidosis is a granulomatous inflammatory disease of unknown etiology that can affect any organ, but most commonly affects the lungs [1]. The diagnosis of pulmonary sarcoidosis can be difficult. Patients are often left undertreated or misdiagnosed due to the diverse presentation of sarcoidosis, which can be further confounded by the numerous possible findings noted on Pulmonary Function Testing. Unfortunately, pulmonary function tests (PFTs) are not a reliable means for detecting the presence of pulmonary sarcoidosis, nor do they provide an accurate estimate of the extent of parenchymal disease [2]. PFTs are only a piece of a puzzle when diagnosing pulmonary sarcoidosis (including a consistent clinical presentation, imaging, and biopsy). However, PFTs are often performed as part of the initial evaluation of a sarcoidosis patient and can be helpful in phenotyping pulmonary sarcoidosis as well as evaluating for alternative diagnoses.
Typical pulmonary symptoms include nonproductive cough and exertional dyspnea, and patients often report wheezing. Treatment of pulmonary sarcoidosis should be considered when patients have symptoms impairing quality of life or when the granulomatous inflammation causes progressive loss of pulmonary function, affects the heart, brain, kidneys, or causes hypercalcemia. PFTs can also provide evidence of worsening parenchymal disease in patients with symptoms that are unresponsive to treatment.
Pulmonary function testing is an essential tool for the pulmonologist. Insight into underlying pulmonary pathophysiology can be obtained from comparison to normal values (based on age, height, race and sex) and previous values from the same patient. The percentage of predicted normal is used to grade the severity of the abnormality.
PFTs provide objective assessment of lung function. This allows more accurate definition of respiratory mechanics, lung parenchymal function, gas exchange and cardiopulmonary interaction. These results are reproducible and quantitative, allowing monitoring over time. Respiratory symptoms alone tend to correlate poorly with disease severity and progression, so objective measurement is important [7]. PFTs are used to screen for the presence of obstructive and restrictive diseases, evaluate patients prior to surgery, document the progression of pulmonary disease, document the effectiveness of therapeutic intervention and monitor pulmonary drug toxicity [8]. Contraindications to PFTs include recent eye surgery, thoracic, abdominal and cerebral aneurysms, active hemoptysis, pneumothorax and unstable angina/MI within the past month [9].
However, pulmonary function testing may show normal results even when anatomic changes documented by imaging studies are severe [14]. In one study [13], only 14.6% of consecutive newly diagnosed sarcoid patients had restriction or mixed restriction and obstruction at presentation. Obstruction was noted in 9.7% of patients, with 47.9% having increased RV/TLC ratio consistent with air trapping and some element of obstruction. This mild obstruction was prevalent from early stages of the disease with the tendency to coexist with restriction as the disease advanced. The DLCO was reduced in 69.4% of patients, which tends to be a common finding in our practice as well.
Bronchial distortion caused by pulmonary parenchymal fibrosis results in lower expiratory flow rates. Interstitial disease can cause airway distortion caused by parenchymal changes or luminal stenosis, but sarcoidosis can also involve the large and small airways, causing obstructive airways disease. Sarcoidosis can affect the entire length of the respiratory tract, including the upper airway and the terminal bronchioles [16]. Mucosal erythema and edema and cobblestone mucosa (bunching of small yellow lesions, more common in lobar and segmental bronchi) can be seen. Bronchial stenosis can be seen in the lobar and segmental bronchi, but mucosal biopsy may or may not show granulomas [13,17]. Airway distortion leading to obstruction is more likely in advanced parenchymal disease. Airway hyperreactivity occurs in up to 20% of sarcoid patients [14]. Endobronchial involvement increases the risk of airflow limitation which can occur in up to 60% of sarcoid patients and can be seen in any stage [14]. Supraglottic structures can also be involved. Oral, nasal, and pharyngeal mucosal changes can lead to hoarseness, dysphagia, laryngeal paralysis, airway obstruction and obstructive sleep apnea. It has been reported that 2.3 to 6% of sarcoid patients exhibit involvement of the upper respiratory tract [18,19]. The trachea and main bronchi are less frequently affected than the lobar, segmental, subsegmental, and distal airways. Sarcoid granulomas of trachea, main carina, and major bronchi by themselves seldom produce significant obstructive symptoms or airway dysfunction, this is usually seen in involvement in the smaller airways [18]. Obstructive airway disease has been noted to be more common in African-American patients with sarcoidosis, compared with much lower rates in white European and American and in Japanese patients [20]. 2b1af7f3a8