Pulmonary Function Tests
By Ashok M. Karnik, MD; Faroque A. Khan, MB
From Resident & Staff Physician, April 1999

Interpretation of Pulmonary Function Tests:
A Step-by-Step Algorithmic Approach

The interpretation of the large number of available pulmonary function tests may appear daunting to the general internist. However, an understanding of basic pulmonary physiology relevant to these tests and a simplified approach help make the task manageable. This article presents an easy, step-by-step algorithmic approach to the interpretation of common pulmonary function tests.

A variety of pulmonary function tests can provide objective and quantifiable measures of lung function. These tests are commonly used to evaluate abnormal symptoms and signs in a patient not known to have respiratory disease and for detailed assessment and follow-up of patients with pulmonary problems. They are also used for monitoring certain groups of patients, for evaluation of disability and impairment, and for epidemiological surveys.

This article focuses on a simplified, step-by-step algorithmic approach to the interpretation of commonly performed pulmonary function tests. Relevant aspects of clinical physiology are discussed with each step, but no detailed description of basic physiology or technical aspects of the tests is given. The data obtained from spirometry, determination of lung volumes, diffusion capacity, and tests for muscle strength are used in the algorithms. The specialized tests (e.g., compliance, airways resistance, closing volume and other tests for small airways dysfunction, bronchial provocation tests, exercise testing, and preoperative assessment) are not discussed here. We would like to emphasize that the approach given below is a simplified one and is useful for most of the common problems seen by an internist. There are many exceptions and caveats, which are explained in Step 7.

Step 1: Technical Quality

The first step in interpreting a pulmonary function test is to assess the technical quality of the test (Figure 1). Spirometric tracings should be examined to make sure that they meet with the "acceptability" and "reproducibility" criteria as suggested by the American Thoracic Society. The individual spirograms are acceptable if they are free from artifacts, such as cough, early termination or cutoff, variable effort, leak, or obstructed mouthpiece, and if the patient has exhaled for at least six seconds or has reached a plateau in the flow-time curve. After three acceptable spirograms have been obtained, they are assessed for reproducibility. The two largest forced vital capacities should be within 0.2 L of each other and the two largest forced expiratory volumes in one second (FEV,) should be within 0.2 L of each other.

Figure 1

If the test does not meet with the criteria mentioned above, the results should be interpreted cautiously and the test may need to be repeated at a later date when the patient is less ill and able to cooperate better. If the technical quality of the test is satisfactory, go to the next step.

Step 2: Normal, Obstructive, or Restrictive Pattern?

The lung is physiologically divided into four volumes—tidal volume (TV), inspiratory reserve volume (IRV), expiratory reserve volume CF.RV) and residual volume (RV). Combination of two or more volumes gives capacities: TV + IRV = inspiratory capacity (IC); TV + ERV = functional residual capacity (FRC); TV + IRV + ERV = vital capacity (VC); the four volumes together = total lung capacity (TLC) (Figure 2).

Figure 2

Residual volume cannot be measured by simple spirometry but can be measured by helium dilution and other methods. The vital capacity can be measured as "slow" vital capacity (SVC) or "forced" vital capacity (FVC), a maneuver in which the patient breathes out forcefully and maximally after a maximal inspiration. By measuring the volume of air exhaled in one second, FEV, is obtained. A patient with obstructive airways impairment cannot empty his lungs as quickly as a healthy person, so the volume of air breathed out in the first second is decreased. FEV, is decreased, thereby decreasing the FEV/FVC ratio. Defining a fixed FEV/FVC ratio as a lower limit of normal is not recommended in adults by the American Thoracic Society because FEV/FVC is inversely related to age and height." However, for practical purposes, a ratio below 70% can be taken as suggesting airflow limitations.

The various lung volumes and capacities (pulmonary statics) can detect restrictive impairment, whereas dynamic flow rates (pulmonary dynamics) can detect obstructive lung diseased In restrictive defects, the lung volumes and capacities are decreased but the FEV/FVC ratio is normal, whereas in obstructive airways diseases, the flow is affected, thereby decreasing the FEV/FVC ratio, but the FVC is normal. In severe obstructive ventilatory impairment, however, the vital capacity may be decreased as the increased residual volume and functional residual capacity "encroach" on the vital capacity. Normally, the SVC and FVC are almost equal, but in obstructive ventilatory impairment, during the forced expiratory maneuver, the intrathoracic pressure increases, narrowing the compliant airways and thereby increasing the air-trapping; therefore, FVC is less than SVC.

Step 2 summarizes and uses these physiologic concepts (Figure 3). This step helps identify the major abnormal patterns, which can be further evaluated as described in the subsequent steps.

Figure 3

Step 3: Differential Diagnosis of Obstructive Airways Diseases

As mentioned above, a normal FVC but an FEV/FVC ratio below 70% suggests an obstructive pattern of impairment. Further differentiation between the various types of obstructive diseases depends on the clinical features, the response to inhaled bronchodilator, and the determination of lung volumes and diffusion capacity (Figure 4). According to the American Thoracic Society statement, chronic obstructive pulmonary disease is defined as "a disease state characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema; the obstruction is generally progressive, may be accompanied by airway hyperreactivity, and may be partially reversible." Chronic bronchitis is defined as "the presence of chron- ic productive cough for three months in each of two successive years in a patient in whom other causes of chronic cough have been excluded." Emphysema is defined as "an abnormal permanent enlargement of the air spaces distal to the terminal bionchioles, accompanied by destruction of their walls and without obvious fibrosis." Most asthmatic patients have reversible airways obstruction, but some patients with chronic asthma go on to develop irreversible airflow obstruction that is indistinguishable from chronic obstructive pulmonary disease. The pulmonary function tests mentioned in Step 3 help to identify typical cases of these disorders.

Figure 4

The airways obstruction in asthma is usually reversible with bronchodilators; a bronchodilator response is suggested by more than 12% increase in FEV1 The obstruction is "irreversible" or only partially reversible in chronic bronchitis and emphysema.

These two conditions can be differentiated by the determination of lung volumes and the diffusion capacity as measured by using carbon monoxide (DLCO). Because the diffusion capacity of carbon monoxide reflects uptake of carbon monoxide from alveolar gas, it needs to be corrected for alveolar volume (VA): DLCO/VA. The patients with simple chronic bronchitis do not usually have hyperinflation; therefore, their lung volumes are normal. Because their lung architecture is normal, the diffusion capacity is not affected. The diffusion capacity is decreased in patients with anemia, diminished pulmonary capillary bed, decreased pulmonary tissue resulting from resection, increased diffusion distance, or decrease in the alveolar surface area and capillary blood volume as happens in emphysema. In emphysema, where there is hyperinflation and destruction of the alveolar architecture, the lung volumes are increased and DL-CO/VA is decreased.

Step 4: Restrictive Defect: Intrapulmonary or Extrapulmonary?

Steps 4 and 5 outline the differential diagnosis of various types of restrictive defects. The physiologic mechanisms that can reduce lung volumes include:

  1. Space-occupying abnormalities within the chest—for example, pleural effusion, pneumonia, or tumor;
  2. Increased elastic recoil—for example, interstitial fibrosis;
  3. Weakness of the respiratory muscles—for example, diaphragmatic paralysis;
  4. Abnormalities of chest wall-for example, kyphoscoliosis, ankylosing spondylitis, or thoracoplasty;
  5. Elevation of diaphragm due to gross obesity, advanced pregnancy, or large ascites.

Although nonspecific, the pattern of alteration of various lung volumes may be useful in suggesting the type of restrictive process. All restrictive disorders, if sufficiently severe, cause reduction of both vital capacity and total lung capacity; most commonly, vital capacity falls below normal before the reduction in total lung capacity. However, it is recommended by the American Thoracic Society that the diagnosis of a restrictive abnormality should be based on reduced total lung capacity. A reduced vital capacity in the presence of a normal FEV,/VC may be used to suggest, but not diagnose, the presence of restriction.

Functional residual capacity would be:
  1. Reduced in diseases affecting the lung parenchyma (alveolar filling or alveolar process) or by thoracic cage processes (for example, kyphoscoliosis).
  2. Unaffected by neuromuscular disease, unless lung parenchyma is affected by atelectasis.
  3. Increased in other thoracic cage disorders (for example, ankylosing spondylitis).

Residual volume may be:
  1. Reduced by space occupying processes or lung-resection;
  2. Less affected by the processes that predominantly decrease the compliance of the lung because lung recoil makes a minor contribution to residual volume;
  3. Increased by diseases with expiratory muscle weakness and some thoracic cage disorders, such as ankylosing spondylitis.

In Step 4, therefore, one looks at FVC, FEV/FVC, total lung capacity, expiratory reserve volume, inspiratory capacity, and DLCOAA (Figure 5). A decreased FVC with an FEV/FVC above 70% suggests a restrictive defect that may be extrapulmonary or intrapulmonary. Consideration of total lung capacity, expiratory reserve volume, inspiratory capacity, and DLCO/VA helps in differentiating these major types. The total lung capacity is reduced in both types, but may be normal in very early restrictive impairment or in pulmonary vascular disease. In these situations, the DLCO/VA may be abnormal. In extiapulmonary defects, such as obesity, the expiratory reserve volume is reduced out of proportion to inspiratory capacity, whereas in intrapulmonary restrictive impairments, both expiratory reserve volume and inspiratory capacity are affected equally. DLCO/VA is decreased in intrapulmonary problems, but would be expected to be normal in extrapulmonary defects like ankylosing spondylitis and obesity."

Figure 5

Step 5: Differential Diagnosis of Extrapulmonary Restrictive Defects

As mentioned above, normal or decreased total lung capacity, expiratory reserve volume that is decreased out of proportion to the decrease in inspiratory capacity, and normal DLCO/VA suggest extrapulmonary restriction that may be related to obesity, kyphoscoliosis, advanced pregnancy, massive ascites, and respiratory muscle weakness. Further analysis of these may be made by considering body-mass index, pressures generated against an occluded airway with maximal inspiratory effort while at residual volume (PImax) and with maximal expiratory effort while at total lung capacity (PEmax) (Figure 6).

Figure 6

In obesity, body-mass index is increased and expiratory reserve volume is decreased, but other pulmonary function parameters are normal. Functional residual capacity and residual volume are both increased in ankylosing spondylitis, whereas in kyphoscoliosis, functional residual capacity, and possibly residual volume are decreased. If the restriction is because of respiratory muscle weakness, differentiation between inspiratory- and expiratory muscle weakness may be made by consideration of PI vs. PE total lung capacity, and residual volume.

Step 6: What Does the Shape of the Flow-Volume Loop Reveal?

Look at the flow-volume loop in Figure 7. Does the shape support the assessment thus far? Is there a suggestion of upper airways obstructions?

Figure 7

The flow-volume loops are derived by plotting the airflow against the volume during a forced maneuver. The normal expiratory loop looks like a triangle sitting on the top of a semicircle of inspiratory loop (Figure 7A). In a patient with obstructive lung disease, the flow during the forced expiration is decreased, manifesting as a dip in the expiratory loop (Figure 7B). In a patient with severe obstruction, this pattern is more pronounced during a forced exhalation. The intrathoracic pressure increases, producing collapse of the bronchi, which may be exaggerated if the patient has emphysema (Figure 7C). A patient with restrictive lung disease tends to have low flows in absolute terms but normal or slightly high flows when compared at equivalent lung volumes. The flow-volume loop in restrictive defects, therefore, is small but of normal shape (Figure 7D). In a patient with upper airways obstruction, the shape of the flow-volume loop depends on whether the obstruction is fixed or variable and, if variable, whether it is extra- or intrathoracic. In fixed obstruction, the expiratory as well as inspiratory flows suddenly diminish at a particular volume, thereby truncating the peaks of both the loops and producing a box-like shape (Figure 7E). Due to negative pressure that is generated inside the airways during inspiration, the atmospheric pressure further increases the narrowing of the extrathoracic segment, thereby producing a flattening of the inspiratory loop in a patient with variable extrathoracic obstruction (Figure 7F). In the variable intrathoracic obstruction, on the other hand, because of the increase in the intrathoracic pressure during expiration, the worsening of narrowing occurs during exhalation, thereby flattening the expiratory loop (Figure 7G).

Step 7: Do Not Forget the Limitations and Caveats

When interpreting pulmonary function tests, always correlate with the clinical picture and remember the limitations and caveats:

Early Stages. In the very early stages of the disease, results may be normal. In such a situation, patterns of changes may become apparent on serial measurements, and the patient's own baseline values provide the best reference values.

Obstructive Ventilatory Impairment. The following points should be remembered: (1) Vital capacity and particularly FVC may decrease in severe obstructive ventilatory impairment and not necessarily because of an additional restrictive defect; (2) After bronchodilator therapy, an apparent increase in FVC may be because of a better effort the second time rather than true bronchodilator effect; (3) If a patient makes a very poor effort, FEV/FVC ratio may be normal, thus "masking" a true obstructive ventilatory defect. Often, the use of SVC in the ratio will lead to a decrease in the FEV/SVC that is not observed in the FEV/FVC ratio; (4) A patient with asthma who has just received bronchodilator therapy may not show the expected 12% or greater increase in FEV and may thus be labeled "chronic obstructive pulmonary disease." Chronic asthmatics, on the other hand, eventually develop mucosal edema, muscular hypertrophy, and mucous plugging, and may not show the expected "reversibility"23; (5) Some patients with chronic bronchitis or "asth- matic bronchitis" may show reversibility; (6) The DLCO may not always differentiate between chronic bronchitis and emphysema. It may be normal in some patients with emphysema, whereas it may be decreased in patients with advanced chronic obstructive airways disease."

Restrictive Impairment. The following points should be remembered: (1) Low vital capacity may be due to a poor effort rather than a true restrictive defect; (2) The total lung capacity is decreased in restrictive impairment but does not always correlate with PImax (3) There is a considerable variation in the pattern of changes in lung volumes seen in restrictive defects. This may be due to intersubject variability in normal lung function or a combination of more than one mechanism, for example:

  1. An interstitial process, which in later stages may result in alveolar filling or airspace replacement;
  2. Compensatory processes - for example, hyperinflation in the remaining lung after resection;
  3. Secondary complications — for example, atelectasis or pneumonia associated with respiratory muscle weakness;
(4) In combined obstructive and restrictive defects, the lung volume measurements that are "within normal limits" may be inappropriately low for the obstructive defect but inappropriately high for restrictive defect. For example, a "normal" total lung capacity in the presence of other features of obstructive defect should suggest an associated restrictive defect. In combined defects, therefore, one needs to make the distinction between "normal" vs. "appropriate" values for the degree of obstructive or restrictive defect present.
Illustrative Cases

Each of the steps outlined above can be demonstrated by real-world examples.

Illustrations for Step 1.

• Case 1 — An 84-year-old woman is referred for pulmonary function testing. She complains of progressive exertional dyspnea. The test results are as follows: FVC, 0.82 L (44% of predicted); FEV, 0.81 L (58% of predicted); FEV/FVC, 98.9%; functional residual capacity, 2.15 L (110% of predicted); residual volume, 1.95 (130% of predicted); total lung capacity, 3.12 (95% of predicted); residual volume/total lung capacity, 62.39% (137% of predicted). The technician has commented, "Patient unable to properly perform pulmonary function tests. The DLCO deferred." The volume/time curve and flow-volume loop are shown in Figure 8.

Figure 8

As seen in Figure 8, the volume/time curve does not start at zero, and the exhalation has lasted for only about one second. The flow-volume curves show possible cough artifacts. Although the low FVC might suggest a restrictive pattern, by applying Step 1, it is seen that the patient has made a very poor effort and results of this study cannot be interpreted reliably.

• Case 2Figure 9 shows the flow-volume loop and volume/time curve obtained in a 51-year-old woman. The flow-volume loop shows variable effort and effects of coughing. The volume-time curves show efforts that are not reproducible. This is technically not a good test. The results cannot be interpreted reliably.

Figure 9

In Cases 3 through 5, the volume/time curve and flow-volume loop suggested a good patient effort and hence the test was acceptable.

Illustration of Steps 2 and 3.
Case 3 Test Results
Prebronchodilator% PredictedPredicted
FVC (L)3.75884.28
FEV1 (L)2.05583.51
FEV1/FVC (%)54.506781.86
Functional Residual Capacity (L)4.491273.52
Residual Volume (L)2.781421.95
Total Lung Capacity (L)6.611066.23
Residual Volume / Total Lung Capacity (%)42.0413431.34
DLCO/VA (mL/min/mm Hg/L)1.77374.79
Postbronchodilator% Predicted% Change
FVC (L)3.8490+2
FEV1 (L)2.1361+4
FEV1/FVC (%)55.6368+2
Table 1

• Case 3 — The patient is a 46-year-old man. He is a chronic smoker with a history of progressive exertional dyspnea. His test results are presented in Table 1. The interpretation is as follows:

Step 1: Good test -> Step 2;
Step 2: FVC = normal; FEV/FVC <70%> limb b of Step 2 -> Step 3;
Step 3: Less than 12% improvement in FEV, after bronchodilator -> limb b of Step 3;
Limb b of Step 3: Lung volumes increased; DLCO/VA decreased -> limb d of Step 3.
Possible diagnosis: Emphysema.

Illustrations for Step 4.
Case 4 Test Results
Prebronchodilator% PredictedPredicted
FVC (L)3.22963.35
FEV1 (L)2.61932.81
FEV1/FVC (%)81.009763.72
Functional Residual Capacity (L)2.851022.81
Residual Volume (L)1.62961.69
Total Lung Capacity (L)4.76945.06
Residual Volume / Total Lung Capacity (%)34.0110233.31
DLCO/VA (mL/min/mm Hg/L)3.81715.33
Table 2

• Case 4 — The test results for this patient are presented in Table 2. The interpretation is as follows:

Step 1: Good test -> Step 2;
Step 2: FVC, FEV/FVC ratio normal -> limb a of Step 2;
Limb a of Step 2; DLCO/VA decreased -> Step 4;
Step 4: Total lung capacity and lung volumes normal; DLCO/VA decreased -> limb a of Step 4;
Possible diagnosis: Early restrictive impairment or pulmonary vascular disease.

Case 5 Test Results
Prebronchodilator% PredictedPredicted
FVC (L)2.13603.55
FEV1 (L)1.85642.91
FEV1/FVC (%)86.5910880.53
Functional Residual Capacity (L)1.79563.18
Residual Volume (L)1.09542.02
Total Lung Capacity (L)3.19575.62
Residual Volume / Total Lung Capacity (%)34.279535.99
DLCO/VA (mL/min/mm Hg/L)2.96585.14
Table 3

Case 5 — The patient is a 50-year-old woman with progressive exertional dyspnea for two years and clubbing. A chest radiograph reveals reticulonodular shadows at both bases. Her pulmonary function test results are presented in Table 3. The interpretation is as follows:

Step 1: Good test -> Step 2;
Step 2: FVC decreased, FEV/FVC > 70% -> Step 4;
Step 4: Total lung capacity, lung volumes, and DLCO/VA -> all decreased -> limb c of Step 4;
Possible diagnosis: Restrictive impairment, possibly secondary to interstitial lung disease.


It must be remembered that high-quality pulmonary function test results depend on accurately calibrated and well-maintained equipment, good test procedures and maximal effort by the patient, an ongoing program of quality control, and appropriate reference values.

The simplified interpretation method presented here obviously has its limitations and may not be accurate or applicable in all cases, but when used with an understanding of pulmonary physiology and correlation with the clinical picture, it would be useful in most common situations.

The Authors

Ashok M. Karnik, M.D.
Dr. Karnik is Attending Physician, Pulmonary Diseases, at Nassau County Medical Center, East Meadow, New York, and Associate Professor of Medicine at the State University of New Tork at Stony Brook, Stony Brook, NY. He received his medical degree from Lucknow University in India and completed a residency at Nassau County Medical Center.
Faroque A. Khan, M.B., M.A.C.P.
Dr. Khan is Chairman of the Department of MEdicine at Nassau County Medical Cetner, Easy Meadow, NY, and Professor of Medicine at the State University of New York at Stony Brook, Stony Brook, NY. He received his medical degreee from the University of Kashmir, India, and completed his training at Queens Hospital Center, Jamaica, NY, and Albert Einstein College of Medicine, Bronx, NY.


  1. American Thoracic Society: Standardization of spirometry: 1994 update. Am J Respir Crit Care Med 152:1107-1136,1995.
  2. Grippi MA, Metzger LF, et al: Pulmonary function testing. In: Pulmonary Diseases and Disorders, Fishman AP (Editor), 2nd Ed. pp 2469-2521. New York: McGraw-Hill, 1988.
  3. American Thoracic Society: Lung function testing: Selection of reference values and interpretative strategies. Am Rev Respir Dis 144:1202-1218,1991.
  4. Chemiack KM: Evaluation of respiratory function in health and disease. Dis Month 7:538,1992.
  5. Tisi GM: Clinical spilomelry. In: Pulmonary Physiology in Clinical Medicine. Tisi GM (Editor), 2nd Ed, pp 57-78. Baltimore: Williams & Wilkins, 1983.
  6. American Thoracic Society: Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 152:S77-S120,1995.
  7. Ries AL Measurement of lung volumes. Clin Chest Med 10:177-186, 1989.
  8. Bergofsky EH Respiratory failure in disorders of the thoraac cage. Am Rev Respir Dis 119:643-69,1979
  9. Haas A, Lowman EW, Beigpfsky EH: Impainnent of respiration after spinal cord injury. Arch Physical Med Rehab 45:339405. 1965.
  10. Inkley SR, Oldenbuig FC, Vignos PJ Jr: Pulmonary function in Duchenne muscular dystrophy related to stage of disease. Am J Med 56:297-306,1974.
  11. Kreitzer SM. Saunders NA, et al: Respiratory musde lunction in amyotrophic lateral sclerosis. Am Rev Respir Dis 117:437-447. 1978.
  12. Demedts M, Beckers J, et al: Pulmonary function in moderate neuromuscular disease without respiratory complaints. Eur J Respir Dis 63:62-67,1982.
  13. Braun NMT. Arora NS, Rochester DP: Respiratory musde and pulmonary function in polymyositis and other pioximal myopathies. Thorax 38:616-623.1963.
  14. Ray CS, Sue DY, et al: Effecis of obesity on respiratory function. Am Rev Respir Dis 128:501-506,1963.
  15. McCool FD. Rochester DF; The lungs and chest wall diseases In: Textbook of Respiratory Medicine. MunayJP, NadelJA (Editors), 2nd Ed, pp 2524-2543. Philadelphia: WB Saunders Company. 1994.
  16. Kelly BJ, Luce JM: The diagnosis and management of neuromuscular diseases causing respiratory failure. Chest 99:1485-1494, 1991.
  17. Aldrich TK, Rochester DF: The lungs and neuromuscular disease. In: Textbook of Respiratory Medicine. Murray JF, Nadel JA (Editors), 2nd Ed, pp 2492-2523. Philadelphia: WB Saunders Co, 1994.
  18. Miller RD, Hyatt RE: Evaluation of obstructing lesions of the trachea and larynx by flow volume loops. Am Rev Respir Dis 108:475-481,1973.
  19. Romian HH, Uss HP, WegJG; Diagnosis of upper airway obsttuction by pulmonary function testing. Chest 66:796-799,1975.
  20. Kryger M, Bode F. et al: Diagnosis of obstruction of the upper and central airways. Am J Med 61:85-93,1976.
  21. Crapo RO: Pulmonary function testing. N Engl J Med 331:25-30,1994.
  22. Girard WM, Light RW: Should the FVC be considered in evaluating response to bronchodilation? Chest 84:87-89.1983.
  23. Brown PJ, Greville HW, Finucane KE: Asthma and irreversible airflow obstniction. Thorax 39:131-136,1984.
  24. Morrison NJ, Abboud RT, et al: Comparison of single breath carbon monoxide diHusing capacity and pressure-volume curves in detecting emphysema. Am Rev Respir Dis 139:1179-1187.1989.
  25. Kinsella M, MuUer ML, et al: Quantitation of emphysema by computed tomography using a "density mask" program and correlation with pulmonary function tests. Chest 97:315-321 1990.


The authors wish to acknowledge Christina Esposito's help with the illustrations and Diane Canavan's secretarial work.

Resident & Staff Physician • Vol. 45, No. 4 - April, 1999. pp 45-63