Spirometry is Key in Asthma Management1

by: Thomas L. Petty, M.D.

Spirometry plays a vital role in assessing the severity of asthma by providing accurate measurements of air volume and airflow.

No one can manage asthma adequately without a spirometer. This fact is due to the nature of asthma: it is an acute, reversible, obstructive disease of the airways. It is caused by inflammatory processes that are triggered by environmental exposures (allergens, occupational hazzards, viral infections, or cold air); by exercise; or by release of inflammatory cytokines without an external provocation. In any case, inflammation drives bronchospasm; together, inflammatory swelling and muscular bronchospasm compromise airflow. Asthma may be acute and intermittent, chronic and persistent, or anything in between. In severity, asthma ranges from being a mild nuisance to being a life-threatening condition. Systematic use of spirometry is critical in assessing the severity of asthma, the patient=s responses to therapy, and the disorder=s course over a lifetime.

SPIROMETRY

Spirometry records airflow from fully inflated lungs. Expiratory airflow can be expressed as volume over time or as flow over volume, as seen in Figure 1. Only two measurements obtained through spirometry are of clinical value. These are the forced vital capacity (FVC), which is the volume of air that can be exhaled from fully inflated lungs, and the forced expiratory volume in one second (FEV1).

Although other measurements can be derived from the expiratory airflow curve, they do not have unique clinical value. Spirometers that employ a flow transducer can also measure inspiratory flow, which is valuable in assessing abnormalities of the upper airway that may mimic asthma. It must be emphasized that spirometric measurements are simple expressions of complex processes. Expiratory airflow is a function of elastic recoil, small-airway function, large-airway function, and the interrelationships among these factors.

Spirometry values are usually normal between asthma attacks, but may be dramatically abnormal during life-threatening attacks. Both major parameters (FEV1 and FVC) may be reduced in asthma because of obstruction to airflow, which can occur at any place along the tracheobronchial tree, or because of abnormalities in elastic recoil, which can come from inflammation of the alveolar attachments that surround and connect to small airways. Both FEV1 (airflow) and FVC (air volume) can be compromised due to airway narrowing, inflammatory and bronchospastic factors, and mucus plugging, which can shut off some of the small (or even large) airways.

Spirometry gives far more information than is available from simple peak-flow measurements because there is a record of the entire breath. Peak flow is only a snapshot of flow. It is possible for patients to give a falsely high peak-flow value by blasting air through pursed lips or a falsely low value by making only a poor effort.

TESTS FOR SMALL-AIRWAY FUNCTION

Historically, measurements of the midportion of the expiratory curve as forced expiratory flow, midexpiratory phase (FEF25-75%), has been believed to be a test of the function of the small airways, whereas FEV1 is a test for large-airway function. Studies of structure-function relationships in freshly excised human lungs, however, have shown that these conclusions are incorrect. After all, alveoli empty into small airways, and small airways, in turn, empty into large airways. All of the expiratory airflow finally reaches the spirometer for recording. These factors are all interrelated, so neither any single test (such as FEF25-75%) nor any one flow point on the expiratory flow curve can be taken as an index that distinguishes small-airway function from that of large airways.

It is a fact that isolated small-airway disease may be present, such as in bronchiolitis obliterans, but expiratory airflow is compromised in these situations, just as it is in asthma or chronic obstructive pulmonary disease (COPD). In fact, spirometry cannot be used to distinguish between asthma and COPD. Thus, most experts would prefer not to add confusion to the simple two-parameter measurement (FVC, FEV1, and the ratio between the two).

CLINICAL ASSESSMENT IN ASTHMA

Physical evaluation is not accurate in assessing the severity of airflow abnormalities in asthma. When the patient is in remission, normal air entry and exit can often be recognized by the experienced clinician. Likewise, there is no doubt about the severity of airflow obstruction in patients who are in status asthmaticus. In all states between those extremes, however, there is simply no way to judge the severity of asthma without spirometry. For example, blood gas levels are abnormal in asthma patients only during attacks. Similarly, a chest radiograph is not a pulmonary function test. In severe asthma, it may show severe hyperinflation, but it gives no information about the patient=s expiratory-airflow capability (see sidebar).

SPIROMETRY AS A GUIDE TO THERAPY

The goal of asthma management is to achieve a symptom-free state with maximum improvement in both FEV1 and FVC. No one would treat hypertension without measurements of blood pressure, nor would anyone manage diabetes without blood-sugar measurements. It would be foolhardy to give anticoagulants without measurement of prothrombin time and international neutralization ratio. Few would give antiarrhythmics without electrocardiographic evidence of a cardiac-rhythm disturbance. Why, then, would anyone give powerful medications such as inhaled oral bronchodilators (or, particularly, corticosteroids, with their attendant adverse effects) without first measuring baseline lung function so that one can observe responses to therapy? How could anyone know when maximum therapeutic benefit had been achieved without airflow and air volume measurements? These questions demand the use of spirometry in all clinical situations.

Untreated or incompletely treated asthma may result in fixed changes to the airways and lead to irreversible airway obstruction, indistinguishable from other forms of COPD. Serial change in lung function, as shown by a decline in FEV1, is a powerful indicator of the course and prognosis of asthma, just as it is for COPD.

DISEASES THAT MIMIC ASTHMA

COPD, vocal-cord dysfunction, tracheal obstruction, and bronchopulmonary mycosis can appear to be asthma. COPD, of course, is a chronic progressive airflow disorder, but patients= responses to inhaled bronchodilators, particularly early in the course of disease, may equal the responses of patients with severe asthma.

Vocal-cord dysfunction most commonly affects young women who work in the health care field or who have a close family member or friend involved in some aspects of medicine. In many cases, it is considered a somatization disorder or a conversion reaction. Vocal-cord dysfunction is characterized by episodes of stridor, wheezing, and dyspnea. The sites of upper- airway obstruction can often be determined by auscultation over the trachea. An inspiratory crowing sound is characteristic. Flow-volume curves typically show normal expiratory airflow, but markedly flattened inspiratory flow (Figure 2), which is quite different from the pattern seen in asthma. If a vocal cord dysfunction is suspected, fiberoptic laryngoscopy or bronchoscopy can be confirmatory. This condition is not managed using asthma medications but, rather, through speech therapy, breathing training, and psychological counseling.

Tracheal obstruction is rare in adults. Children may have foreign bodies or upper-airway lesions, such as a tracheal web, following a prolong period of mechanical ventilation. A granulomatous reaction following use of an endotracheal tube for mechanical ventilation may cause obstruction. Rare tracheal tumors can also cause fixed upper-airway obstruction with a characteristic, fixed inspiratory and expiratory flow pattern (Figure 3).

Bronchopulmonary mycoses include aspergillosis and penicilliosis. A mycotic infection may complicate asthma and may result in airflow obstruction.

Spirometry is highly useful in assessing patients who have diseases that mimic asthma. The most commonly encountered is COPD, which is characterized by lack of reversibility and other tests of pulmonary function abnormalities, such as hyperinflation and reduced diffusion. Hyperinflation may, in fact, be present in asthma, but reduced diffusion is not found.

When spirometric measurements remain abnormal in spite of optimum therapy (including the use of anti-inflammatory agents and full doses of bronchodilators), the clinician should question the diagnosis of asthma (Table 1).

Use of spirometry, in concert with the answers to these questions, may allow clinicians to optimize therapy.

MEDICOLEGAL ISSUES

Over the past several years, I have been asked to give expert testimony in the defense of nearly a dozen physicians named in malpractice lawsuits. In these cases, steroid complications occurred (mostly in women) that were allegedly due to inappropriate use of corticosteroid drugs. Defense is difficult when systematic corticosteroids were prescribed, but there was no objective measurement of severe airflow obstruction and of response to therapy. In the rare case of aseptic necrosis of the femoral heads, which some believe may be a steroid-related event, it is difficult to argue that steroids were required for worsening disease, when, in fact, there were no spirometric measurements to establish this fact.

CONCLUSION

Because of need for widespread use of spirometry in the assessment of asthma, COPD, and other chronic lung disease states, devices that are simple, handheld, accurate, and easy to use are now being produced. One such device is illustrated in Figure 4. Learning to use these simple spirometers is no more difficult than learning to measure blood pressure properly. These new devices will, one hopes, make spirometry as commonplace as blood pressure measurement in the future.

Spirometry measurements of airflow and air volume are extremely useful in the assessment of asthma and other respiratory disorders. In fact, spirometric abnormalities are predictive of deaths from many causes. Every practitioner should have a spirometer in his or her office. It is time for spirometers to join sphygmomanometers, clinical scales, and thermometers as critical instruments necessary for the management of asthma and many other common, chronic respiratory disorders such as COPD and interstitial inflammatory/fibrotic lung disease states.

FURTHER READING

Barnes PJ. A new approach to the treatment of asthma. N Engl J Med 1989;321:1,517-1,527.

Newman KB, Mason UG, Schmaling KB. Clinical features of vocal cord dysfunction. Am J Respir Crit Care Med 1995;152:1,382-1,386.

Petty TL. Difficult asthma: what next when therapy fails to control symptoms? Consultant 1998;38:1,011-1,028.

CASE STUDY

A 41-year-old man who was a successful lawyer and geologist had experienced cough and dyspnea for 4 years. He did not wheeze, but he did experience progressive exercise and work impairment. He had smoked for 20 years and had stopped only because of worsening symptoms of disabling cough and dyspnea.

On physical examination, the patient=s blood pressure was found to be 140 mm Hg/90 mm Hg. He was in respiratory distress, with a respiratory rate of 32 breaths per minute. Accessory muscles of respiration were in use. The patient had a hyperinflated chest, which was nearly silent; wheezes were not heard. The results of cardiac and extremity examinations were normal.

The patient=s posteroanterior and lateral chest radiographs showed only hyperinflation (Figure 5). His initial FVC was 1.45 L, and this increased to 1.88 L following inhalation of a bronchodilating aerosol. Predicted FVC was 4.87 L. The FEV1 was 0.57 L/s, increasing to 0.66 L/s after bronchodilator use. The predicted FEV1 was 3.52 L/s.

Because of the patient=s severe respiratory distress, he was admitted to the hospital and given inhaled B-agonists around the clock. There was some suspicion of asthma, since the patient=s brother had asthma, so corticosteroids were given. In 1 day, the patient=s FVC was elevated to 4.31 L; and FEV1, to 2.77 L/s. At this time, the patient=s single-breath diffusion test was normal at 29. The patient was immediately discharged from the hospital, but he continued to use tapering doses of corticosteroids. After 7 days, the patient=s FVC was 5.26 L and his FEV1 was 4.49 L/s (Table 1).

This is a classic example of hidden asthma. The clues, in this case, were the patient=s young age and his family history of bronchial asthma. At the author=s request, this patient returned for evaluation 11 years after diagnosis. He was following an all-inhaled medication program that included B-agonists, cromolyn sodium, and corticosteroids. The patient=s ventilatory function after 11 years of follow-up care is shown in Table 1. Unfortunately, this asymptomatic patient was using neither a peak-flow meter nor a spirometer to monitor his progress at home. One can hardly quarrel, however, with the success achieved in the management of this patient, whose asthma would otherwise have been life-threatening.



Table 1: Spirometric Documentation of a

Patient=s Response to Asthma Management

 
Measure-ment  

Predicted
 

Admission
Post-Broncho-dilator
1-day Cortico-steroids
7-day Cortico-steroids
11-year Follow-up (% predicted)
FVC (L)
4.87
1.45
1.88
4.31
5.26
3.81 (90%)
FEV1 (L/s)
3.52
0.57
0.66
2.77
4.49
2.45 (77%)
 Thomas L. Petty, M.D., is chairman of the National Lung Health Education Program and professor of medicine, University of Colorado Health Sciences Center, Denver. He is also on the Editorial Advisory Board at RT Magazine.
 

Published in: RT Magazine The Journal for Respiratory Care Practitioners 1999;12:57-61,75.