Spirometry: Why, How, and When?

Office spirometry is essential, inexpensive, and profitable in the diagnosis and monitoring of chronic obstructive pulmonary disease (COPD). It is as essential to the outpatient clinic for assessing dyspnea as a sphygmomanometer is to assessing hypertension.

But why, how, and when?

Why Do Spirometry?

• To hunt for objective evidence of lung disease prompted by a chief concern of dyspnea and/or cough or exercise intolerance
• To confirm the presence of an obstructive or restrictive pattern to breathing
• To provide an index of lung disease severity and disease progression and prognosis over months and years
• To objectively assess the immediate response to and need for bronchodilator therapy
• To meet Centers for Medicare and Medicaid Services (CMS) and National Quality Forum (NQF) measures for quality performance (NQF measure 0091 for COPD and spirometry evaluation) and capture billing codes for reimbursement for procedures related to clinic care

Remember that spirometry cannot differentiate asthma from COPD. And COPD is not as irreversible as has been taught. A more relevant term is ROAD, or reversible obstructive airway diseases. ROAD could become a new taxonomic term for the syndromes of asthma, COPD, and asthma-COPD overlap syndrome (ACOS).¹

Up to 65.6% of COPD patients can experience a 15% or greater improvement in FEV₁ (forced expiratory volume in the first second of expiration) after bronchodilator challenge, meeting the reversibility criteria established by the American College of Chest Physicians,  and 54% of the same group of COPD patients can meet American Thoracic Society reversibility or responsiveness criteria (FEV₁ ≥ 12% and ≥ 200 mL) after bronchodilators.²

The key question to ask is: Does spirometry reveal a pattern of lung function that is normal, or does it reveal a pattern that is obstructive, restrictive, or both?

The finding of an obstructive pattern, or “chronic air constipation,” provides an opportunity for the patient and clinician to improve airflow obstruction and lung volumes with inhaled short- and long-acting bronchodilators and can lead to a diagnosis of asthma, COPD, or ACOS.

How Are Spirometry Tests Done? 

Two graphs or figures are created when a patient is asked to take a maximum breath (vital capacity) into the lungs and then to exhale completely as forcefully as possible. FEV₁, forced vital capacity (FVC, the lung volume representing the total amount of air a patient can forcibly exhale after maximum inhalation), and the FEV₁/FVC ratio pre- and post-bronchodilator are obtained from the spirogram, which records the volume exhaled from the lungs (L) against time (seconds, Figure 1). The patient should exhale for no more than 6 seconds. The patient does three FVC maneuvers, and the best or largest two FEV₁ and FVC efforts should be within 200 mL of each other.

Additional information can be collected by depicting the same breath into and out of the lungs as a flow-volume loop, which records and plots the flow of a breath (L/s) against the same forced vital capacity lung volume (L). Breath flowing into the lungs is negative flow, and out of the lungs is positive flow.

Spirometry interpretation is as follows:

In normal lung function, FEV₁ and FVC both are ≥ 80% predicted (range, 80% to 120% predicted), and FEV₁/FVC pre- and post-bronchodilator typically is from 0.70 to 0.80 but depends on age.³

FVC can be decreased to < 80% predicted in COPD, severe asthma, or ACOS because of static lung hyperinflation with lung air trapping. FVC also can be reduced in restrictive lung diseases, chest wall or pleural disease, obesity, or neuromuscular weakness. The patient’s history and physical examination findings will help differentiate the underlying lung disease or disorder.

In obstructive lung function, FEV₁ and FVC are ≤ 80% predicted, but FEV₁ is decreased relatively more than FVC, causing a FEV₁/FVC pre- and post-bronchodilator value of < 0.70, indicating airflow obstruction or limitation. Again, age can contribute to airflow limitation.

In restrictive lung function, FVC is < 80% predicted, and FEV₁/FVC is > 0.85 without bronchodilator. This clinical profile should warrant further investigation in a pulmonary function testing (PFT) laboratory, including assessment of all lung volumes (slow vital capacity [SVC], total lung capacity [TLC], residual volume [RV], functional residual capacity [FRC]) and a carbon monoxide diffusing capacity (Dlco) test, to better define lung function abnormalities.

In mixed obstructive-restrictive lung function, FVC is < 80% predicted, and FEV₁/FVC is > 0.70 post-bronchodilator. Realize, however, that the reduction in FVC can be due to obstructive lung disease alone. This clinical profile definitely warrants further testing in a PFT laboratory, including all lung volumes and a Dlco test, to discern additional lung function abnormalities.

FEV₁ normally declines with aging by approximately 30 mL/y, but in susceptible smokers, the decline is greater (approximately 60 mL/y), resulting in the development of COPD.⁴ FEV₁ is a predictor of death from COPD, cardiovascular disease, cardiovascular accident, lung cancer, and all-cause mortality.⁵

The hallmark of COPD is a decrease in FEV₁ (< 80% predicted) with relative preservation of FVC, which brings the FEV₁/FVC to < 0.70. This is the “total cholesterol of COPD.” Severity of COPD and staging is based on the FEV₁ expressed as percent predicted. This is the “LDL of COPD” and can help determine COPD severity and selection of treatments.

FEV₁ is a good predictor of exercise tolerance and correlates with survival and quality of life. More rapid FEV₁ decline also is predictive of morbidity, mortality, and hospitalization rates regardless of whether the decline is associated with asthma, COPD, or ACOS. In addition to smoking, risk factors for accelerated decline in FEV₁ include frequent exacerbations, airway reactivity, and possibly chronic systemic inflammation.

Smoking cessation usually restores the normal or near-normal rate of FEV₁ decline, whereas intermittent quitting provides less benefit. Thus, smoking cessation is a critical component for the prevention of COPD progression. FEV₁ is central to the definition of COPD and classification of its severity. To date, only smoking cessation has been definitively shown to be effective in reducing the rate of FEV₁ decline, but other therapeutic strategies are under active research. Consequently, FEV₁ and its change over time are important outcomes in COPD and valuable measures for the assessment of disease progression.

When IS Spirometry Performed?

Tables 1 and 2 summarize the indications and contraindications, respectively, for spirometry. Spirometry should be performed whenever dyspnea, cough, or exercise intolerance is present. It should be performed as soon as possible, because CMS pay-for-performance incentives and NQF performance monitoring is ongoing, and compliance will be audited.

Spirometry is the best point-of-care tool to better define the type of dyspnea, shortness of breath (SOB), or chronic cough the patient is experiencing. Whether SOB is due to obstructive, restrictive, or mixed pathophysiology, the patient’s work of breathing is increased, resulting in the perception of dyspnea.

Spirometry is required to confirm the diagnosis of COPD. A post-bronchodilator FEV₁/FVC < 0.70 supports the diagnosis of COPD, but only if the clinical picture is compatible with COPD. For example, an 80-year-old man who is a retired schoolteacher and who never smoked, with an FEV₁/FVC of 0.69 without risk factors for asthma or COPD has no airway obstruction and has normal spirometry. On the other hand, a 50-year-old woman who smokes half a pack of cigarettes a day and works as a mortgage lender who has an FEV₁/FVC of 0.66 and symptoms of dyspnea or exercise intolerance and occasional cough probably has COPD in the absence of a history of asthma and/or atopy.

No reason exists for sending a patient to a PFT laboratory unless special testing is needed (eg, Dlco test, methacholine challenge test, lung volumes to discern whether lung volume restriction is due to parenchymal lung disease (all lung volumes reduced proportionally to the same degree), or neuromuscular/chest wall/pleural disease or obesity (SVC and TLC reduced but RV and FRC increased, often > 120% predicted).

Essential in Dyspnea Evaluation

Causes of inspiratory SOB and cough include diseases and disorders that affect the larynx (eg, vocal cord dysfunction [VCD], goiter, lymphoma, sarcoidosis, postnasal drip, gastroesophageal reflux disease). Pulmonary causes of inspiratory SOB include restrictive lung diseases and impeding respiratory failure from acute exacerbations of asthma or COPD. Causes of expiratory dyspnea include asthma, COPD, and ACOS.

Knowledge of whether the dyspnea, is inspiratory and/or expiratory will prepare the clinician to search for objective evidence in the shapes of flow-volume loops to confirm clinical suspicion.

FLOW-VOLUME LOOPS

Spirometry findings should be corroborated with flow-volume loops. Every clinician should be familiar with normal, obstructed, restricted, and VCD flow-volume loops, which technically represent a variable extrathoracic large-airway obstruction (Figure 2).

Inspiratory SOB will affect the shape of the inspiratory limb of the flow-volume loop below the x-axis (volume, L), whereas expiratory SOB will affect the expiratory limb. The site of inspiratory SOB or obstruction is laryngeal or throat; the site of expiratory SOB or obstruction is tracheal, bronchial, or both. The bottom of the inspiratory limb of the flow-volume loop should always be shaped like the bottom of a chicken egg.

The shape of the flow-volume loop should agree with your preliminary interpretation of the spirometry (Figure 3). A person can have significant upper airway obstruction and inspiratory airflow limitations and still have normal spirometry findings, since most spirometry tests document expiratory flow rates and expiratory volumes. A flow-volume loop may be the only clue to an extrathoracic problem causing inspiratory dyspnea.

Variable extrathoracic upper airway obstruction will truncate the inspiratory limb of the flow-volume loop to varying degrees. Fixed upper airway obstruction will flatten both the inspiratory and expiratory limbs (Figure 4).

PLENTIFUL PITFALLS

The pitfalls for clinicians (and the dangers to patients) are not employing or billing for spirometry in clinical situations that warrant spirometry, such as confirming the diagnosis of COPD, assessing asthma control, monitoring of inhaled insulin’s effects on patients with diabetes, and evaluating dyspnea or SOB in patients who misunderstand their symptoms of SOB and do not tell their physician or who relegate their symptoms to aging or a “safer” diagnosis of asthma.

If a patient presents with SOB, cough, wheezing or fatigue with physical exertion, sputum production, weight loss, chest tightness, frequent colds, barrel chest, and/or smoker’s cough, conduct a brief history and physical exam and order spirometry in the office. The ICD-10-CM diagnosis codes replace the ICD-9-CM codes for the signs and symptoms indicating consideration for spirometry.

For example, if the spirometry results of the 50-year-old mortgage lender described above are normal, bill for Current Procedural Terminology (CPT) code 94010 ($36). If spirometry findings show an obstructive pattern, have her inhale 4 puffs of albuterol and repeat spirometry in 15 minutes (the onset of albuterol’s bronchodilator effect usually is within 2 minutes), interpret the post-bronchodilator findings, and bill for CPT code 94060 ($61.50). A post-bronchodilator FEV₁/FVC < 0.70 confirms a COPD diagnosis in the correct clinical setting—that is, a current or former smoker with or without dyspnea (primarily exercise intolerance), cough, wheezing, and/or sputum production.

Excluding COPD as a diagnosis avoids unnecessary long-term treatment and promotes patient safety by avoiding potential adverse effects from a drug used as therapy for a disease that is not present. Nevertheless, the routine use of spirometry in the office and clinic remains poor despite strict CMS clinical process/effectiveness performance measures mandating that spirometry be used to confirm the COPD diagnosis (ie, NQF 0091).

For example, of the 12,491 patients with COPD as a primary or secondary diagnosis in the Lovelace Patient Database (which contains health data of 250,000 persons in New Mexico enrolled in the Lovelace Health Plan over more than 15 years), only 366 (2.9%) underwent spirometry to confirm a COPD diagnosis.⁶ Eight in 10 patients had COPD at a grade that warranted immediate maintenance treatment—50% had grade 2 (moderate) COPD, and 31% had grade 3 (severe) or 4 (very severe) disease—but the majority were not treated.⁶

Ironically, because of the use of inhaled insulin, diabetes mellitus, not COPD or asthma, will probably usher office spirometry into modern clinical practice.

Inhaled Insulin

Rapid-acting inhaled human insulin is indicated to improve glycemic control in adult patients with diabetes mellitus.⁷ Among the important limitations of its use are that patients with type 1 diabetes must use it with a long-acting insulin, and that it is not recommended for use in patients with diabetes who smoke.

Inhaled insulin can cause acute symptoms of cough, wheezing, and SOB and is contraindicated by the FDA for patients with diabetes and asthma or COPD because of the risk of acute exacerbations brought on by the medication.

Human insulin inhalation powder can cause a decline in lung function over time as measured by FEV₁. In clinical trials lasting up to 2 years and excluding patients with chronic lung disease, inhaled insulin-treated patients experienced a 40-mL decline in FEV₁ that was greater than the decline in comparator-treated patients.⁷ The FEV₁ decline was noted within the first 3 months and persisted for the entire duration of therapy (up to 2 years of observation). An FEV₁ decline of ≥ 15% occurred in 6% of inhaled insulin-treated patients compared with 3% of comparator-treated patients.

Cough was reported in approximately 27% of patients with type 1 diabetes treated with inhaled insulin compared with 5.2% treated with placebo. In clinical trials, cough was the most common reason for discontinuing inhaled insulin (2.8% of treated patients).

The FDA requires all patients with diabetes who are prescribed inhaled insulin have documented spirometry testing prior to taking their first dose, then again after 6 months of treatment, and annually thereafter (even in the absence of symptoms) to detect evidence of FEV₁ decline indicative of a developing obstructive pattern to breathing.

In diabetics who have a decline of ≥ 20% in FEV₁ from baseline, consider discontinuing inhaled insulin. Consider more frequent monitoring of pulmonary function in patients with wheezing, bronchospasm, breathing difficulties, or persistent or intermittent cough.

The annual rate of FEV₁ decline did not appear to worsen with increased duration of use of inhaled insulin. The effects of inhaled insulin on pulmonary function for treatment duration longer than 2 years has not been established. There are insufficient data in long-term studies to draw conclusions regarding reversal of the effect on FEV₁ after discontinuation of inhaled insulin. The observed changes in FEV₁ were similar in patients with type 1 and type 2 diabetes. A fall in FEV₁ of 400 mL within 15 minutes has been observed in 29% of diabetic asthmatics in clinical trials, and a 200 mL fall in FEV₁ has been reported in COPD patients. Consequently, a dangerous pitfall is to prescribe inhaled insulin to a known asthmatic or COPD patient,.

CPT code 94010 should be used to report and bill CMS and third-party payers for initial and subsequent spirometry, whether for asthma control evaluation, COPD screening and severity staging, or inhaled human insulin therapy monitoring. The modifier code -32 should be appended to the 94010 code to indicate to third-party payers that the test is a mandated test in patients with diabetes.

The ICD-10-CM diagnostic code Z01.89 (encounter for other specified special examinations) should be used in conjunction with spirometry testing prior to initiation therapy, and Z51.81 (any therapeutic drug level monitoring) and Z79.4 (long term [current] use of insulin) should be submitted together for spirometry at 6 months and annually thereafter.

The American Thoracic Society and the European Respiratory Society have published detailed standards for quality control in pulmonary function testing and have adapted the standards to include the introduction of inhaled insulin.⁸ Contraindications are few but are important to ascertain before performing spirometry on a patient.

PITFALLS TO AVOID IN SPIROMETRY 

• Forgetting to confirm the diagnosis of asthma anew in difficult-to-control cases.
• Not asking patients complaining of SOB whether dyspnea occurs while taking a breath into their lungs or out of their lungs.
• Omitting spirometry to confirm COPD with a post-bronchodilator FEV₁/FVC below 0.70 L.
• Omitting spirometry in favor of prescribing inhaled medications first for asthma, COPD, or ACOS.
• Prescribing inhaled human insulin without baseline spirometry and follow-up FEV₁ monitoring to detect decline in lung function, even in the absence of symptoms of cough, wheezing, and dyspnea.
• Forgetting that flow-volumes loops can detect large upper airway obstruction in addition to lower airways obstruction.
• Thinking that spirometry and bronchodilator reversibility can distinguish asthma from COPD.

GOLD Guidelines for COPD

The Global Initiative for Chronic Obstructive Lung Disease (GOLD) Guidelines (www.goldcopd.com), launched in 1997 in collaboration with the World Health Organization and the National Institutes of Health’s National Heart, Lung, and Blood Institute, provide a diagnostic screening tool for adult patients who may have COPD.

Grade I, mild COPD: FEV₁/FVC < 0.70 ± chronic symptoms. FEV₁ ≥ 80% predicted. Chronic cough and sputum production may be present.

Grade II, moderate COPD: FEV₁/FVC < 0.70 ± chronic symptoms. 50% ≤ FEV₁ < 80% predicted. Shortness of breath, typically developing on exertion. This typically is the stage at which patients seek medical attention.

Grade III, severe COPD: FEV₁/FVC < 0.70 ± chronic symptoms. 30% ≤ FEV₁ < 50% predicted. Greater shortness of breath, reduced exercise capacity, and repeated exacerbations that have an impact on patient’s quality of life.

Grade IV, very severe COPD: FEV₁/FVC < 0.70 ± chronic symptoms. FEV₁ < 30% predicted or < 50% predicted with chronic respiratory failure or cor pulmonale. Patients may have grade IV COPD even if the FEV₁ is > 30% whenever this complication is present.

The GOLD Guidelines do not adjust for age and may lead to the overdiagnosis of COPD in patients 70 years of age and older.

Spirometry measurements FEV₁ and FVC vary considerably in healthy people, which accounts for the wide range of normal predicted values. Predicted values for non-white populations are typically 10% to 15% lower than for the white population. Predicted values are calculated from spirometry reference equations derived from healthy persons of the same age, gender, height, and race. The predicted value actually is the average or mean value of a normal bell-shaped distribution or range of normal values for a given population tested.

Abnormalities detected by spirometry may show one of three patterns: obstruction, restriction, or mixed obstruction and restriction.

Patients with obstruction (eg, asthma, COPD) typically have an FEV₁/FVC and FEV₁ below the lower limit of normal (LLN), FEV₁ much more so than FVC. Patients with restriction have an abnormally low FVC, but FEV₁/FVC will be above the LLN. Mixed obstruction and restriction will cause a reduction in both FEV₁/FVC and FVC below the LLN.

Significant improvement in spirometry findings after bronchodilator challenge with 4 puffs of albuterol involves finding at least a 12% improvement or an increase by ≥ 200 mL in FEV₁ or FVC, or at least a 15% improvement in FEV₁ post-bronchodilators.

Other evidence of a positive bronchodilator response include a significant isovolume shift, which is defined as a decrease in total lung capacity or functional residual capacity (FRC) by plethysmography by ≥ 500 mL or ≥ 15%. FRC must be measured by body plethysmography or “body box” to accurately determine isovolume shift. This can be measured only in a pulmonary function laboratory.

Claudia M. Vukovich, RCP, RRT, AE-C, CCM, is coordinator of the Reversible Obstructive Airway Disease (ROAD) Center at UC Davis Medical Center (UCDMC) in Sacramento, CA.

Celeste Kivler, RCP, RRT, AE-C, CCRC, is coordinator of the UC Davis Asthma Network (UCAN) program at UCDMC in Sacramento, CA.

Samuel Louie, MD, is a professor of medicine in the department of internal medicine, division of pulmonary, critical care, and sleep medicine at UC Davis in Sacramento, CA.

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