Interpretation of Pulmonary Function Tests A Practical Guide, 3. ed

12. Patterns in Various Diseases

There are patterns of pulmonary function test abnormalities that are typical for most patients with a particular disease. Table 12-1 expands on Table 3-1, adding data on lung volumes, arterial blood gas values, diffusing capacity, lung compliance and resistance, the single-breath nitrogen test, and maximal respiratory pressures. It should be emphasized that a clinical diagnosis is not made from these test results alone. Rather they quantify the lung impairment and are to be interpreted in the context of the total clinical picture. For this discussion, obstructive disease is categorized into four conditions: emphysema, chronic bronchitis, chronic obstructive pulmonary disease, and asthma. Restrictive conditions are divided into those due to pulmonary parenchymal disease and extrapulmonary causes.


Pure emphysema (such as α1-antitrypsin deficiency) is associated with hyperinflation (increased total lung capacity [TLC]); a significant loss of lung elasticity (decreased recoil pressure at TLC and increased static compliance of the lung [PTLC and Cbstat]); and often a substantial decrease in the diffusing capacity of the lung (Dlco, reflecting destruction of alveoli). Resting arterial tension of oxygen (Pao2) and carbon dioxide (Paco2) are generally normal until the condition is far advanced. Bullae, predominantly in the lower lung fields, are typical in α1-antitrypsin deficiency.

*torr, equivalent to mm Hg.

A, often absent; N, normal; (N), occasionally normal; to; f, increased; f, decreased; Сьаупdynamic compliance of the lung; CLstat, static compliance of the lung; Dlco, diffusing capacity of carbon monoxide; Dl/Va, diffusing capacity of the lung/alveolar volume; FEF25-75, forced expiratory flow rate over the middle 50% of the FVC; FEF50, forced expiratory flow after 50% of the FVC has been exhaled; FEV1, forced expiratory volume in 1 second; FV, flow-volume; FVC, forced vital capacity; MVV, maximal voluntary ventilation; Расог, arterial carbon dioxide tension; Раог, arterial oxygen tension; PEF, peak expiratory flow; PEmax, maximal expiratory pressure; Pimax, maximal inspiratory pressure; PTLC, lung recoil pressure at TLC; Raw, airway resistance; RV, residual volume; Sa02, arterial oxygen saturation; TLC, total lung capacity.


Pure chronic bronchitis is typically found in heavy cigarette smokers with a chronic productive cough and frequent respiratory infections. In contrast to emphysema, lung recoil is often normal but the Pao2 may be low and associated with carbon dioxide retention (increased Paco2).


The lungs of most smokers in whom obstructive lung disease develops show a mixture of emphysema and chronic bronchitis. The tests reflect contributions of both disease processes. For example, hyperinflation tends to be greater than in pure chronic bronchitis, but carbon dioxide retention may not be present.


Because lung function may be normal between attacks, the data in Table 12-1 reflect those during a moderate attack in a nonsmoker. The changes are much like those in chronic obstructive pulmonary disease, except for the tendency toward hyperventilation and respiratory alkalosis (increased pH, decreased Paco2). Also, the response to bronchodilators (not shown in Table 12-1) is typically very striking and Dlco is often increased. In remission, all test results, with the occasional exception of the residual volume/total lung capacity ratio (RV/TLC), may return to normal; however, the methacholine challenge test is typically positive. The ratio of forced expiratory volume in 1 second to forced vital capacity (FEV1 /FVC) may be normal, especially in mild cases. The Dlco may be normal or increased. It is decreased only in very severe asthma.


Idiopathic pulmonary fibrosis is the classic example of an intrapulmonary restrictive process. Peak expiratory flows may be normal or low, the diffusion capacity decreased, PTLC generally increased, lung compliance decreased, and the slope of the expiratory flow-volume curve steep.

TABLE 12-2. Causes of restrictive disease


Pulmonary fibrosis and interstitial pneumonitis


Neoplasms, including lymphangitic carcinoma



Bronchiolitis obliterans with organizing pneumonia (BOOP) or cryptogenic organizing pneumonia (COP)

Hypersensitivity pneumonitis

Alveolar proteinosis

Langerhans' cell histiocytosis (histiocytosis X or eosinophilic granuloma)

Lung resection Atelectasis


Pleural cavity Pleural effusion



Cardiac enlargement


Diaphragmatic paralysis

Neuromuscular diseases, including amyotrophic lateral sclerosis, myasthenia gravis, polymyositis

Chest wall


Ankylosing spondylitis

Chest trauma

Thoracic resection



Some other parenchymal conditions that cause restriction are listed in Table 12-2. However, not all of them always produce the classic picture described here. The slope of the flow-volume curve may not be increased and the lung recoil may not be altered, in part because restriction may be combined with obstruction. Examples are endobronchial involvement in sarcoidosis and tuberculosis. This mixed pattern is also frequent in heart failure, cystic fibrosis, and Langerhans' cell histiocytosis (eosinophilic granuloma or histiocytosis X) and is striking in lymphangioleiomyomatosis.


In the case of extrapulmonary restriction, the lung parenchyma is assumed to be normal. The most frequent causes of this type of restriction are listed in Table 12-2. The main abnormalities are the decreased lung volumes with generally normal gas exchange. Because the Dlco is somewhat volume-dependent, it may be reduced. Resection in an otherwise normal lung also fits this pattern.

Severe degrees of restriction, as in advanced kyphoscoliosis, can lead to respiratory insufficiency with abnormal gas exchange.


The hallmark of early neuromuscular disease is a decrease in respiratory muscle strength reflected in decreases in maximal expiratory and inspiratory pressures. At this stage, all other test results can be normal despite the patient complaining of exertional dyspnea. As the process progresses, the maximal voluntary ventilation is next to decrease, followed by decreases in the FVC and TLC with accompanying impairment of gas exchange. Ultimately, the picture fits that of a restrictive extrapulmonary disorder.

These patterns are most frequent in amyotrophic lateral sclerosis, myasthenia gravis, and polymyositis. They have also been noted in syringomyelia, muscular dystrophy, parkinsonism, various myopathies, and Guillain-Barre syndrome.


The effects of left-sided congestive heart failure with pulmonary congestion on the function of an otherwise normal lung are often not appreciated. In some cases, the predominant change is one of pure restriction with a normal FEV1/FVC ratio, flows decreased in proportion to the FVC, and a normal flow-volume curve slope. There is often associated cardiomegaly, which contributes to the restriction. The chest radiograph maybe interpreted as suggesting interstitial fibrosis, but the computed tomographic appearance is distinctly different.

In other cases, there may be a mixed restrictive-obstructive pattern with decreases in flow out of proportion to volume reduction. The FEV1/FVC ratio is reduced, as is the slope of the flow-volume curve. The obstructive component is in part due to peribronchial edema, which narrows the airways and produces ''cardiac asthma.'' Of interest, the result of the methacholine challenge test may be positive for reasons that are unclear.

In years past, the effectiveness of therapy for pulmonary congestion was sometimes monitored by measuring changes in the vital capacity. Congestive heart failure is highlighted here because it is often overlooked as a possible cause of a restrictive or obstructive pattern.


The changes in pulmonary function tests associated with obesity are indicated in Table 12-1. These changes do not seem to differ substantially between male and female patients. Some test results, such as the TLC, are abnormal only at very high body mass indexes. Others, such as decreases in functional residual capacity and expiratory reserve volume (not included in Table 12-1), occur with milder degrees of obesity. The results for RV and RV/TLC ratio may depend in part on whether the RV was calculated using the FVC or slow vital capacity (see section 3C, page 31). Even in the massively obese patient, the FEV1/FVC ratio can be normal. The adverse effects of obesity are greater in patients with a truncal fat distribution (''apple'' versus ''pear'') and may be greater in the elderly and in smokers, variables that are not always reported. In this respect, one study [1] found that male patients who had obstructive lung disease and gained weight after quitting smoking had a loss of 17.4 mL in FVC for every kilogram of weight gained. Their FEV1 also decreased by 11.1 mL per kilogram of weight gained. Similar but smaller changes of 10.6 mL FVC and 5.6 mL FEV1 were found in women.

A very interesting development has been the apparent association between obesity and asthma. Does obesity increase the risk of asthma? The final answer is not in. A recent rEV1ew [2] concluded that obesity has an important but modest impact on the incidence and prevalence of asthma.


1. Wise RA, Enright PL, Connett JE, et al. Effect of weight gain on pulmonary function after smoking cessation in the Lung Health Study. Am J Respir Crit Care Med 157:866-872,1998.

2. Beuther DA, Weiss ST, Sutherland ER. Obesity and asthma. Am J Respir Crit Care Med 174:112-119, 2006

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