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Pulmonary function testing in asthma

Pulmonary function testing in asthma
Author:
Charles G Irvin, PhD, FERS
Section Editor:
Peter J Barnes, DM, DSc, FRCP, FRS
Deputy Editor:
Helen Hollingsworth, MD
Literature review current through: Feb 2022. | This topic last updated: Nov 20, 2020.

INTRODUCTION — The "classic" signs and symptoms of asthma are intermittent dyspnea, cough, and wheezing. While typical of asthma, these symptoms are nonspecific, making it difficult to distinguish asthma from other respiratory diseases. The definitive diagnosis of asthma requires the history or presence of respiratory symptoms consistent with asthma, combined with the demonstration of variable expiratory airflow obstruction [1,2].

The use of pulmonary function testing in the diagnosis of asthma will be reviewed here. The diagnosis of asthma and the performance and interpretation of pulmonary function tests are discussed separately. (See "Asthma in adolescents and adults: Evaluation and diagnosis" and "Overview of pulmonary function testing in adults" and "Office spirometry".)

ADVICE RELATED TO THE COVID-19 PANDEMIC — Spirometry and other pulmonary function test (PFT) maneuvers can promote coughing and aerosol generation and could lead to spread of coronavirus disease 2019 (COVID-19; due to SARS-CoV-2) by infected patients. It is difficult to screen patients for active SARS-CoV-2 infection, particularly those with underlying respiratory symptoms, and infected but asymptomatic patients can shed the virus. Thus, we agree with expert recommendations that spirometry and other PFTs be limited to patients in whom results are essential to immediate management decisions [3]. Use of nebulizers to administer bronchodilators or methacholine for testing should be avoided. We also avoid other forms of bronchoprovocation testing due to the coughing induced by the testing and the need for multiple spirometric maneuvers.

Measures to prevent spread of COVID-19 should include hand hygiene and personal protective equipment (PPE; gloves, gown, face mask, and shield) for staff and anyone else in the testing space (eg, interpreters). N95 masks or powered air purifying respirators (PAPR) are preferred over surgical masks. Patients should be brought to a testing room using an approach that avoids queuing or grouping individuals in a waiting area. Enhanced cleaning of the testing area should be performed between patients.

TESTS FOR THE DIAGNOSIS OF ASTHMA — The diagnosis of asthma is based upon a compatible clinical history and characteristic findings from a series of pulmonary function tests (PFTs) [1,2,4,5]. An approach to the use of PFTs in the diagnosis of asthma is provided in the algorithm (algorithm 1). The clinical features and diagnosis of asthma are discussed separately. (See "Asthma in adolescents and adults: Evaluation and diagnosis", section on 'Clinical features'.)

The specific PFTs are selected to identify the characteristic features of asthma, which include [1,2]:

Variable airflow limitation, which can be either circadian or episodic in nature

Airflow limitation that reverses with bronchodilator administration

Airways hyperresponsiveness, which is an excessive decrease in airflow in response to specific stimuli or "triggers" (see "Risk factors for asthma")

The detection of airflow limitation in the patient with asthma can be accomplished with a variety of techniques. The most common are the measurement of spirometry pre and post bronchodilator, peak expiratory flow (PEF), and the flow-volume relationship [5-7]. It is important to realize that these techniques are not necessarily equivalent because of the complex physiology of the lung, the variable ability of patients to perform the tests, the accuracy of the tests themselves, and the underlying disease process.

Spirometry — National and international guidelines recommend the use of spirometry to diagnose and monitor asthma, as demonstration of reversible airflow limitation is a key component in the diagnosis of asthma [1,2,8]. (See "Asthma in adolescents and adults: Evaluation and diagnosis", section on 'Diagnosis'.)

Technique – Spirometry involves measurement of lung volumes during a forced expiratory maneuver (ie, a maximal inhalation to total lung capacity followed by a maximal exhalation) [7]. (See "Office spirometry".)

The three most important indices derived from spirometry are the forced vital capacity (FVC), which is the total volume of air exhaled, the forced expiratory volume in one second (FEV1), and the ratio of FEV1/FVC [6,7].

Typical results in asthma – During times when individuals with asthma are asymptomatic, spirometry is often normal. When asthma is symptomatic, airflow limitation is usually present on spirometry, as indicated by a FEV1 less than lower limits of normal (LLN; the fifth percentile of the confidence interval provided electronically by modern computerized spirometers) and a FEV1/FVC ratio below 0.7 or below the fifth percentile LLN. On the other hand, some patients with asthma have asymptomatic airflow limitation usually associated with long standing disease that has not been well controlled.

Similarly, FVC is normal or near normal, but can be decreased in the presence of air trapping or submaximal inhalation.

Accuracy – Measurements of FEV1, FVC, and FEV1/FVC ratio are reproducible, with coefficients of variation usually at 5 percent or less [6,7,9]. The FEV1/FVC ratio has also been shown in numerous studies to be sensitive to the presence of airflow limitation. FEV1 usually decreases more than the FVC if the airways narrow, whereas the decrease in FEV1 tracks the decrease in FVC if the airways close [10]. In patients with asthma, persistent reduction in FEV1 correlates with increased asthma symptoms and severity and is also predictive of poorer clinical outcomes [9,11].

The mean forced expiratory flow at 25 to 75 percent of forced vital capacity (FEF25-75), also known as the maximum mid-expiratory flow (MMEF), is highly dependent on the level of expiratory effort and the validity of the FVC maneuver. Thus, changes in the FEF25-75 observed over time or in response to bronchodilator are not used to diagnose asthma in adults.

Flow-volume relationships — The flow-volume relationship or loop is obtained by plotting flow against volume during the FVC (forced expiratory) maneuver. An inspiratory loop is obtained when a maximal inhalation to total lung capacity is performed after the FVC maneuver or from functional residual capacity. This measurement yields useful additional information beyond that obtained with measurement of FEV1 and FVC, specifically by providing rapidly recognizable patterns that permit the clinician to differentiate bronchial asthma from the airflow limitation due to other causes, such as paradoxical vocal fold motion or a fixed obstruction [12,13]. (See "Flow-volume loops" and "Inducible laryngeal obstruction (paradoxical vocal fold motion)".)

Lower airways – The flow-volume loops in the figure demonstrate some of the patterns that can be encountered (figure 1). The upper left panel shows intrathoracic airflow limitation, such as might be seen in asthma or COPD. The notable feature is the downward "scooping" of the expiratory curve. In milder airflow limitation or disease largely confined to the small airways, the "scooping" occurs at low lung volume, so the FEV1 may be normal, but the shape of the curve suggests airflow limitation.

Upper airways – When using the flow-volume loop to identify processes other than asthma that can cause similar symptoms, the reductions in maximal respiratory flow shown in the lower three panels often accompany clinical symptoms of dyspnea and wheeze. However, the cause of airflow limitation in these situations is central airway narrowing rather than asthma. Such patients will not respond to asthma therapy, since inflammation or bronchospasm are not the cause of the airflow limitation.

Once it has been determined that the patient has expiratory airflow limitation, the next step is to assess whether the airflow limitation is reversible.

Bronchodilator responses — Airflow limitation from asthma should usually demonstrate some degree of reversibility following acute treatment with a beta-agonist. The currently recommended criteria in adults for a significant response to a bronchodilator are that FEV1 and/or FVC should increase by 12 percent or more and by at least 200 mL, although there is not complete consensus on these criteria [6].

Withholding bronchodilators prior to testing – In preparation for assessing bronchodilator reversibility, ongoing bronchodilator medications should be withheld long enough for the bronchodilator effect to wear off, generally based on the duration of action (table 1). Short-acting inhaled bronchodilators (eg, albuterol, levalbuterol, ipratropium) should not be used for at least four hours prior to testing [7]. The long-acting beta-agonist bronchodilators (LABAs), salmeterol and formoterol, are omitted for 12 hours prior to testing, while vilanterol and indacaterol are omitted for 24 hours. The long-acting anticholinergic agents glycopyrrolate (glycopyrronium), tiotropium, and umeclidinium are omitted for 24 hours. Aclidinium would be omitted for 12 hours, based on twice daily dosing.

Dose of short-acting beta-agonist for testing – Most laboratories use two or four metered-dose inhaler inhalations of a short-acting beta-agonist, such as albuterol, via a valved holding chamber. For each puff of albuterol, patients are instructed to exhale slowly, then close their lips around the mouthpiece. One actuation of the inhaler is made into the chamber; the patient inhales fully to total lung capacity; the breath is held for 5 to 10 seconds before exhalation. The dose is repeated one to three times. The post-bronchodilator spirometry is performed after an appropriate delay for the bronchodilator used (10 to 20 minutes) to allow the beta-agonist to work.

Interpretation – For patients with baseline airflow limitation, an increase in FEV1 and/or FVC ≥12 percent over baseline and ≥200 mL is generally considered a positive response [6]. Lack of bronchodilator reversibility in patients with baseline airflow limitation may suggest airways inflammation that requires additional therapy (eg, glucocorticoids) or an alternate diagnosis (eg, COPD, bronchiolitis).

In patients with spirometry within normal limits at baseline, an increase in FEV1 of more than 8 percent following inhaled bronchodilator may suggest underlying airflow limitation, since the patient may have once had higher than predicted lung function [14,15].

Another response that can be observed after bronchodilator administration is a change in flow for a given volume, ie, an isovolume shift in the flow volume curve without a change in FEV1 [6]. This effect results from opening of lung units previously "trapped" at high lung volumes [10]. However, despite these units being open, their resistances remain high, and they do not contribute to the FEV1 except to the extent that FVC falls. The figure shows patterns of flow volume loop response following bronchodilator administration (figure 2). It is important to realize that not all of these responses result in changes in PEF, FVC, or even FEV1. In such cases, other measurements are needed, such as lung volumes. (See 'Lung volumes' below.)

Other measures of airflow limitation – It has been suggested that additional parameters of airflow obstruction be used to assess reversibility, such as specific airway conductance (SGaw) obtained with a plethysmograph. This approach increases the likelihood of observing airflow reversibility, although it is not universally accepted. As an example, one study of 100 patients with clinically suspected reversible airway obstruction reported that spirometry detected reversible obstruction in 82 [16]. Using body plethysmography revealed that 15 of the remaining 18 patients also responded to bronchodilators with either a change in SGaw or lung volumes. If a patient fails to show an improvement in FEV1 with albuterol treatment and a clinical response appears to occur, body plethysmography can be used to document this change.

Peak expiratory flow — Peak expiratory flow (PEF) is measured during a maximally forceful and rapid exhalation that immediately follows a maximal inhalation. An advantage is that small, portable devices can be used. PEF measurements are most often used to monitor patients with a known diagnosis of asthma or to assess the role of a particular occupational exposure or trigger, rather than as a tool for the primary diagnosis of asthma [1,2]. The technique of measuring PEF and the role of PEF monitoring in asthma management are discussed separately. (See "Peak expiratory flow monitoring in asthma".)

Measurement of PEF has several shortcomings for the diagnosis of asthma, the most serious of which is its significant dependence on effort [7,17]. In contrast to spirometry, it is difficult to apply quality control to PEF measurement, as PEF meters cannot be easily calibrated; and, the lack of graphic display makes it difficult to ensure optimal technique and maximal patient effort. Furthermore, the large variability of PEF between individuals (±30 percent) and for a given individual (±15 percent) makes PEF insensitive for detecting airflow limitation [6,7].

PEF is a useful method of monitoring changes or trends in the patient's lung function [1,2,7,8]. PEF results that vary little over time (less than 20 percent of the maximal value) argue against the diagnosis of asthma, while values that repeatedly fall by more than 20 percent when symptoms are present and return to baseline as symptoms resolve are consistent with asthma.

Bronchoprovocation challenge — A patient with mild or no airflow limitation may not show reversal after bronchodilator administration. In such cases, a bronchial challenge with inhaled methacholine or other modalities would be indicated to demonstrate reversible airflow obstruction. A discussion of methacholine inhalation challenge and other types of bronchoprovocation is provided separately. (See "Bronchoprovocation testing".)

Fraction of exhaled nitric oxide — Patients with airway inflammation due to asthma generally have high levels of nitric oxide in their exhaled breath, which is expressed as the fraction of exhaled nitric oxide (FENO); the FENO typically returns to normal after treatment with glucocorticoids. The measurement and interpretation of FENO are discussed separately. (See "Exhaled nitric oxide analysis and applications".)

MONITORING ASTHMA — Effective asthma management requires regular assessment of symptoms and pulmonary function, as suggested by national and international guidelines. (See "An overview of asthma management", section on 'Follow-up monitoring'.)

Peak expiratory flow (PEF) measurement can be a useful component of home self-assessment and can help the patient identify changes in lung function during exacerbations or trigger exposure. Ongoing twice daily PEF assessment is typically reserved for patients with severe asthma or those with impaired perception of airflow limitation [2]. (See "Peak expiratory flow monitoring in asthma".)

The optimal frequency of spirometry during follow-up office visits for asthma has not been determined. Guidelines suggest repeat spirometry three to six months after initiation of controller therapy and periodically thereafter [2]. We base the frequency of follow-up spirometry on the degree of asthma symptom control and the results of previous testing. If symptoms are well-controlled and prior spirometry was normal, follow-up spirometry can be obtained infrequently (eg, every one to three years). If the patient has persistent symptoms (eg, dyspnea, poor exercise tolerance, frequent short-acting beta-agonist use) or had baseline airflow limitation in the past, more frequent testing may be warranted (eg, at three to twelve month intervals). Test results can be used to determine whether symptoms reflect poor asthma control or an alternate process and whether therapy has improved lung function, or not. (See "An overview of asthma management", section on 'Pulmonary function'.)

Some experts obtain a PEF measurement at the time of initial spirometry to assess whether the percent predicted PEF correlates with the percent predicted forced expiratory volume in one second (FEV1). If so, PEF can be used at the time of follow-up office visits for objective monitoring of asthma control in the context of the comprehensive assessment of symptoms and risk of exacerbation. However, studies have not been done to validate this approach.

EFFECT OF ASTHMA ON OTHER PULMONARY FUNCTION TESTS — While the diagnosis of asthma is based on spirometric results, insights in to the pathophysiology of asthma can be gained from assessment of lung volumes and diffusing capacity for carbon monoxide (DLCO) [10,18,19].

Lung volumes — The main role for lung volume determination in patients with asthma is to exclude other causes of or contributors to dyspnea. Assessment of the severity of air trapping is of interest, but does not guide therapy. The measurement and interpretation of lung volumes is discussed separately. (See "Overview of pulmonary function testing in adults", section on 'Lung volumes' and "Overview of pulmonary function testing in children", section on 'Lung volume measurement'.)

Lung volumes provide indirect information about the elastic recoil of the chest wall and lung. At total lung capacity, the elastic recoil of the lungs is the key determinant of the driving pressure for expiratory airflow during passive exhalation. Hence, a decrease in TLC may indicate an increase in recoil whereas an increase in TLC may indicate a decrease in recoil.

Lung volume is an important determinant of airways caliber through the tethering effect of parenchymal attachments.

Measurement of lung volumes can be useful in the evaluation of other causes of dyspnea or periodic airflow limitation due to restrictive processes, which can masquerade clinically as asthma. As an example, in a patient who presents with episodic dyspnea after working in a barn or exposure to epoxy resin, a reduced forced expiratory volume in one second (FEV1) combined with a reduced total lung capacity (TLC) suggests a restrictive process, such as hypersensitivity pneumonitis, rather than asthma. This alternate diagnosis might be further evaluated with chest computed tomography, which would likely demonstrate centrilobular nodular opacities, consistent with hypersensitivity pneumonitis.

Overview — The relationships among lung capacities and volumes are demonstrated in the figure (figure 3). By convention, the term capacity is used for measurements that are composed of two or more volumes. Three of the lung volumes or capacities measured by plethysmography provide useful information about the pathophysiology of asthma and are described in the following sections:

TLC

Functional residual capacity (FRC)

Residual volume (RV)

In patients with asthma, determination of these lung capacities by plethysmography is preferable to dilution methods, because the presence of trapped gas can lead to falsely lowered values when measured by dilution and result in an erroneous conclusion that a mixed disease process is present [6].

Spirometry measures several other volumes and capacities, but these volumes (inspiratory reserve volume, tidal volume, expiratory reserve volume) and capacities (inspiratory capacity) are not generally helpful in the clinical management of asthma [6].

Residual volume — An increased RV (≥120 percent predicted or greater than the upper 95th percentile) is the most consistently abnormal of all the lung volumes in asthmatic patients, and it is the last to return to normal following treatment (figure 4) [20]. However, measurement of RV is highly variable, and a value greater than approximately 150 percent of predicted is required before one interprets an abnormality [21]. If not due to poor expiratory effort, a high RV is interpreted as abnormal closure of airways, which can be confirmed by observing a fall in RV following bronchodilator therapy.

Functional residual capacity — A value for FRC greater than the upper 95th percentile (preferred) or ≥120 percent predicted suggests air trapping. Thus, the FRC may be elevated in asthma, especially during the acute phase of an asthmatic attack (figure 4) [20]. Several mechanisms are probably involved, but persistent or tonic activity of the inspiratory muscles is largely responsible for the rise in FRC [22]. The increase in FRC is important, because hyperinflation is thought to be responsible for sensations of chest tightness and dyspnea [23].

Total lung capacity — A value for TLC greater than the upper 95th percentile (preferred) or ≥120 percent predicted suggests hyperinflation. In asthma, the TLC can either be normal or elevated, although an elevated TLC is more commonly seen in chronic obstructive pulmonary disease (COPD) (figure 4). Elevation in the TLC is usually associated with more severe airflow limitation or asthma of longer duration. The likely physiological mechanisms for hyperinflation include a loss of lung elastic recoil, increased outward recoil of the chest wall, and increased inspiratory muscle strength [24].

Use of RV/TLC or FRC/TLC ratios can be quite helpful in patients for whom predicted values of the individual measurements are less reliable, eg, young children or patients with unusual ethnic origins. The RV/TLC is generally high, but must be greater than approximately 150 percent of predicted before it can be considered to be abnormal.

Patterns suggestive of restrictive (reduced TLC) or mixed processes should alert the clinician to consider other disease processes, such as chronic eosinophilic pneumonia, bronchiectasis, or concomitant pleural or neuromuscular disease and asthma.

Diffusing capacity — The DLCO (also called the transfer factor for carbon monoxide) measures the ability of the lungs to transfer gas from inhaled air to the red blood cells in pulmonary capillaries. The technique for measuring DLCO and its interpretation are described separately. (See "Diffusing capacity for carbon monoxide".)

In patients with asthma, the DLCO is usually either normal or high, and the degree of elevation is related to asthma severity. The mechanisms potentially explaining this elevation include the following [6,25,26]:

An increase in negative intrathoracic pressure during inspiration, which draws blood into the thorax.

Improved ventilation-perfusion matching due to increased perfusion of the apices.

Hemoglobin extravasation due to the inflammatory process, although evidence that this occurs in asthma is limited.

The main reasons to perform a DLCO measurement in an asthmatic patient are to distinguish between other causes of reversible airflow limitation and asthma (table 2) and to identify alternative diagnoses when dyspnea is not well explained by spirometric findings. As an example, patients who have COPD may present with a misdiagnosis of asthma; however, the DLCO should be decreased in emphysema, but not asthma.

ADDITIONAL TESTING IN PATIENTS WITH COMORBID DISEASE — Occasionally, patients have more than one process affecting respiratory function.

Asthma and COPD overlap – Approximately 15 to 20 percent of patients with asthma have concurrent chronic obstructive pulmonary disease (COPD), known as asthma-COPD overlap syndrome (ACOS) [27]. According to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) and Global Initiative for Asthma (GINA) consensus statement, ACOS "is characterized by persistent airflow limitation with several features usually associated with asthma and several features usually associated with COPD. ACOS is therefore identified in clinical practice by the features that it shares with both asthma and COPD" [27,28]. Measurement of lung volumes, variability in airflow limitation, and diffusing capacity for carbon monoxide (DLCO) may be useful in identifying features of concomitant asthma and COPD, such as hyperinflation, persistent but variable airflow limitation, or a reduced DLCO. (See "Chronic obstructive pulmonary disease: Definition, clinical manifestations, diagnosis, and staging", section on 'Asthma-COPD overlap'.)

Asthma and tracheal stenosis – A patient could have asthma and develop tracheal stenosis or vocal fold paralysis following endotracheal intubation. Dyspnea would likely be out of proportion to the expiratory flow limitation. Flow volume loops described above might help to identify fixed or variable upper airway flow limitation, although sometimes direct visualization is necessary. (See 'Flow-volume relationships' above and "Clinical presentation, diagnostic evaluation, and management of central airway obstruction in adults".).

Asthma and respiratory muscle weakness – A patient with asthma could develop diaphragmatic weakness or other respiratory muscle impairment as a comorbid disease or as a consequence of systemic glucocorticoid therapy. Respiratory muscle weakness is most often assessed by measurement of maximal inspiratory/expiratory mouth pressures, although other less well established measurements can also be performed. (See 'Research tools for assessment of airflow limitation' below and "Tests of respiratory muscle strength".)

In addition to maximal inspiratory/expiratory mouth pressures, examining lung volumes can help identify reduced muscular output (eg, due to respiratory muscle weakness), which is associated with the combination of high residual volume (RV) but low total lung capacity (TLC) without evidence of interstitial disease (figure 4).

RESEARCH TOOLS FOR ASSESSMENT OF AIRFLOW LIMITATION — Research tools are in development for the assessment of airflow limitation in patients with difficulty performing spirometry, identification of patients at increased risk of near-fatal or fatal asthma due to reduced hypoxic responsiveness, and evaluation of static recoil to better understand the overlap of asthma and COPD.

Tests not requiring patient effort – Assessment of lung functions such as forced expiratory volume in one second (FEV1) requires that the patient perform forced vital capacity (FVC) maneuvers reproducibly and with maximal effort (see 'Spirometry' above). However, a number of other techniques have been developed that yield similar information about airways function but do not require patient effort.

One such technique is the application of oscillatory pressure/flow to the lungs or the forced oscillation technique (FOT) or oscillometry where impulse oscillometry is one variant [29]. Pressure waves are applied at the mouth to measure resistance and reactance of the total respiratory system. A major advantage and attraction of FOT is that it does not require maximal efforts, but like specific airway conductance (SGaw) these endpoints are not always equivalent to the FEV1. (See "Asthma in children younger than 12 years: Initial evaluation and diagnosis", section on 'Children <5 years'.)

The forced oscillation technique is very useful in patients who cannot or will not perform the standard tests, such as the very young or old. These tests might also enable identification of obstructive airways disease in patients with respiratory muscle weakness. However, these measures have not been applied to large populations to generate predicted values and in some cases the endpoints show high variability. As a result, the response of these indices to bronchodilators or methacholine/exercise takes on more importance than does an isolated baseline result.

Control of breathing – Measurement of the ventilatory response to low oxygen (hypoxia) or high CO2 (hypercapnia) assesses the ability of the body to respond to respiratory stimuli. It has been shown that some patients with severe asthma have reduced hypoxic responsiveness in addition to a poor perception of dyspnea [30]. A potential application of this testing is to identify and characterize those patients at risk for near-fatal asthma exacerbations.

Lung static recoil – Lung static recoil refers to the elastic forces in the lung causing passive exhalation. As the lung expands during inhalation, the elastic recoil forces increase. At full inspiration after flow ceases, the lung static recoil is maximal. Elastic recoil is inversely proportional to compliance (volume/pressure), which is the slope of the pressure-volume curve. While it is generally believed that asthma causes a parallel upward shift of the pressure-volume (PV) curve of the lung [31], several studies have demonstrated a loss of elastic recoil, ie, decreased static recoil pressure at a given volume [32].  

Measurement of the static recoil of the lung is accomplished through determination of the PV relationship [33,34]. Static recoil is important because maximal expiratory flow, as measured with the FEV1 or flow-volume relationship, is determined both by airways caliber and the static recoil of the lung, which is the driving pressure for expiratory flow [18], whereas a static recoil is a measure of the elastic forces of the lung.

A situation in which determination of the PV relationship might be helpful is in a patient with a low FEV1 of unclear etiology [33,34]. Theoretically, examination of pressure volume curves could help determine the cause by showing movement of the pressure-volume curve upwards and to the left in a patient with increased compliance and reduced elastic recoil due to emphysema. Conversely, movement downwards and to the right might indicate interstitial lung disease.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Pulmonary function testing".)

SUMMARY

An approach to the use of PFTs in the diagnosis of asthma is provided in the algorithm (algorithm 1). (See 'Tests for the diagnosis of asthma' above.)

Reversible airflow limitation is an essential component in the diagnosis of asthma. According to national and international guidelines, virtually all adolescents and adults being treated for asthma should have a baseline spirometry before and after inhaled bronchodilator. (See 'Spirometry' above.)

During times that individuals with asthma are asymptomatic, spirometry is often normal. When asthma is symptomatic, airflow limitation is usually present on spirometry, as indicated by a forced expiratory volume in one second (FEV1) <80 percent of predicted and a FEV1/forced vital capacity (FVC) ratio below 0.7 or below the fifth percentile lower limit of normal. (See 'Spirometry' above.)

While consensus is lacking on the exact criteria for reversibility following inhaled bronchodilator, a reasonable threshold is an increase in FEV1 ≥12 percent and ≥200 mL over baseline. Normal baseline airflow that increases by similar amounts is consistent with mild, reversible airflow limitation. (See 'Bronchodilator responses' above.)

For patients in whom the diagnosis of asthma is not clear after expiratory spirometry, we obtain flow-volume loops (inspiratory and expiratory) to exclude upper airway obstruction as a cause of the patient’s symptoms (figure 1). (See 'Tests for the diagnosis of asthma' above.)

For patients with suspected asthma, but normal airflow without a bronchodilator response, bronchoprovocation challenge testing may be useful to confirm (or exclude) the diagnosis of asthma. (See 'Bronchoprovocation challenge' above and "Bronchoprovocation testing".)

Lung volume measurements are indicated in the evaluation of asthma when the results from the above tests are suggestive of other processes (eg, a decrease in FVC) or the initial studies are equivocal. In asthma, the residual volume (RV) is the most consistently abnormal of all the lung volumes (figure 4). (See 'Lung volumes' above.)

The diffusing capacity for carbon monoxide (DLCO) has a limited role in asthma. However, it is useful in the evaluation of possible emphysema and in patients whose dyspnea is out of proportion to their airflow limitation. The diffusing capacity is usually normal or elevated in asthma and decreased in emphysema, interstitial lung disease, pulmonary embolism, and pulmonary hypertension. (See 'Diffusing capacity' above.)

Difficulty performing spirometry may indicate the need for either a neuromuscular evaluation or tests that do not require maximal patient effort, such as measurement of specific airway conductance (SGaw) by plethysmography or respiratory resistance with forced oscillations. (See 'Bronchodilator responses' above and 'Additional testing in patients with comorbid disease' above.)

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  26. Desjardin JA, Sutarik JM, Suh BY, Ballard RD. Influence of sleep on pulmonary capillary volume in normal and asthmatic subjects. Am J Respir Crit Care Med 1995; 152:193.
  27. Global Initiative for Chronic Obstructive Lung Disease. Asthma, COPD, and Asthma-COPD Overlap Syndrome. http://goldcopd.org/asthma-copd-asthma-copd-overlap-syndrome/ (Accessed on August 22, 2016).
  28. Irwin GC, Kaminsky DA. Physiology of asthma, COPD, and overlap. In: Asthma, COPD, and Overlap: A Case-Based Overview of Similarities and Differences, Bernstein JA, Boulet LP, Wechsler ME (Eds), CRC Press, 2018.
  29. King GG, Bates J, Berger KI, et al. Technical standards for respiratory oscillometry. Eur Respir J 2020; 55.
  30. Kikuchi Y, Okabe S, Tamura G, et al. Chemosensitivity and perception of dyspnea in patients with a history of near-fatal asthma. N Engl J Med 1994; 330:1329.
  31. Finucane KE, Colebatch HJ. Elastic behavior of the lung in patients with airway obstruction. J Appl Physiol 1969; 26:330.
  32. Gold WM, Kaufman HS, Nadel JA. Elastic recoil of the lungs in chronic asthmatic patients before and after therapy. J Appl Physiol 1967; 23:433.
  33. Irvin, CG, Cherniack, RM. Pathophysiology and physiologic assessment of the asthmatic patient. Semin Respir Med 1987; 8:201.
  34. Wagers, S, Jaffe, et al. Development, Structure, and Physiology in Normal and Asthmatic Lung. In: Middleton's allergy principles and practice, 6th Ed, Adkinson, NF Jr, Busse, WW, Yunginger, JW, et al (Eds), Elsevier, St Louis 2003.
Topic 569 Version 17.0

References

1 : National Asthma Education and Prevention Program: Expert panel report III: Guidelines for the diagnosis and management of asthma. Bethesda, MD: National Heart, Lung, and Blood Institute, 2007. (NIH publication no. 08-4051) www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm (Accessed on August 31, 2021).

2 : Global Initiative for Asthma. Global strategy for asthma management and prevention (updated 2020). https://ginasthma.org/ (Accessed on September 26, 2020).

3 : American Thoracic Society. Pulmonary Function Laboratories: Advice Regarding COVID-19 https://www.thoracic.org/professionals/clinical-resources/disease-related-resources/pulmonary-function-laboratories.php (Accessed on October 19, 2020).

4 : Irvin, CG. Evaluation of Pulmonary Function. In: Physiologic Basis of Respiratory Disease, Hamid, Q, Martin, J, Shannon, J (Eds), Dekker, Ontario 2005.

5 : Pulmonary Function Testing: Principles and Practice, Kaminsky D, Irwin CG (Eds), Humana Press, 2018.

6 : Interpretative strategies for lung function tests.

7 : Standardization of Spirometry 2019 Update. An Official American Thoracic Society and European Respiratory Society Technical Statement.

8 : Standardization of Spirometry 2019 Update. An Official American Thoracic Society and European Respiratory Society Technical Statement.

9 : Asthma outcomes: pulmonary physiology.

10 : Older age and obesity are associated with increased airway closure in response to methacholine in patients with asthma.

11 : Performance Characteristics of Spirometry With Negative Bronchodilator Response and Methacholine Challenge Testing and Implications for Asthma Diagnosis.

12 : Detection of upper airway obstruction with spirometry results and the flow-volume loop: a comparison of quantitative and visual inspection criteria.

13 : Inspiratory flow-volume curve evaluation for detecting upper airway disease.

14 : Lung function testing: selection of reference values and interpretative strategies. American Thoracic Society.

15 : Evaluation of bronchodilator response in patients with airway obstruction.

16 : The utility of spirometry in the diagnosis of reversible airways obstruction.

17 : Physiologic measures: pulmonary function tests. Asthma outcome.

18 : Significance of the relationship between lung recoil and maximum expiratory flow.

19 : What long-term changes in lung function can tell us about asthma control.

20 : Acute bronchial asthma. Relations between clinical and physiologic manifestations.

21 : Pulmonary function testing. What is 'normal'?

22 : The role of respiratory muscles in the hyperinflation of bronchial asthma.

23 : Improvements in distal lung function correlate with asthma symptoms after treatment with oral montelukast.

24 : The mechanism of increase in total lung capacity during acute asthma.

25 : Single breath diffusing capacity for carbon monoxide in stable asthma.

26 : Influence of sleep on pulmonary capillary volume in normal and asthmatic subjects.

27 : Influence of sleep on pulmonary capillary volume in normal and asthmatic subjects.

28 : Influence of sleep on pulmonary capillary volume in normal and asthmatic subjects.

29 : Technical standards for respiratory oscillometry.

30 : Chemosensitivity and perception of dyspnea in patients with a history of near-fatal asthma.

31 : Elastic behavior of the lung in patients with airway obstruction.

32 : Elastic recoil of the lungs in chronic asthmatic patients before and after therapy.

33 : Pathophysiology and physiologic assessment of the asthmatic patient