Airway Function Tests

The most basic test of pulmonary function is the measurement of vital capacity (VC). This test simply measures the largest volume of air that can be moved into or out of the lungs. In the mid-1800s, a surgeon named Hutchinson developed a simple water-sealed spirometer that allowed measurement of what he named “vital capacity or vital breath” as he noted its relationship to survival. Hutchinson popularized the concept of using VC to assess lung function and named several other lung compartments that are still used today. He observed that VC was related to the standing height of the patient. He also developed tables to estimate the expected VC for a healthy patient. The VC was usually graphed on chart paper, which allowed subdivisions of the VC to be identified (see Chapter 2).

Forced vital capacity (FVC) is an enhancement of the simple VC test. During the 1930s, Barach observed that patients with asthma or emphysema exhaled more slowly than healthy patients. He noted that airflow out of the lungs was important in detecting obstruction of the airways. Barach used a rotating chart drum (kymograph) to display VC changes as a spirogram. He even evaluated the effects of bronchodilator medications, using the FVC traced as a spirogram.

In 1947, Tiffeneau described measuring the volume expired in the first second of a maximal exhalation in proportion to the maximal volume that could be inspired (FEV₁/IVC (inspiratory vital capacity)) as an index of airflow obstruction (i.e., the Tiffeneau index). Around 1950, Gaensler began using a microswitch in conjunction with a water-sealed spirometer to time FVC. He observed that healthy patients consistently exhaled approximately 80% of their FVC in 1 second, and almost all of the FVC in 3 seconds. He used the forced expired volume in the first second (FEV₁) to assess airway obstruction. In 1955, Leuallen and Fowler demonstrated a graphic method used to assess airflow. They measured airflow between the 25% and 75% points on a forced expiratory spirogram. This measure was described as the maximal midexpiratory flow rate (MMFR). This and similar measurements have been used to describe airflow from both healthy and airflow-obstructed patients. To standardize terminology, the MMFR is now referred to as the forced expiratory flow 25%-75% (FEF_25%-75%).

In addition to displaying FVC as a volume-time spirogram, it can also be represented by plotting airflow against volume. In the late 1950s, Hyatt and others began using the flow-volume display to assess airway function. The tracing was termed the maximal expiratory flow volume (MEFV) curve. By combining the forced expiration with an inspiratory maneuver, a closed loop can be displayed. This figure is called the flow-volume loop (see Chapter 2).

Peak expiratory flow (PEF) is measured using either a flow-sensing spirometer or a peak flow meter. In the 1960s, Wright and McKerrow popularized the use of peak flow to monitor asthmatic patients. Peak flow can be readily assessed from the flow-volume loop as well. Recently, portable peak flow meters that allow monitoring at home, as well as in the hospital or clinic, have been developed.

The FVC, FEV₁, and other flows, along with flow-volume loops, are all used to measure response to bronchodilator medications (see Chapter 2). Tests are performed before and after inhalation of a bronchodilator, and the percentage of change is calculated. The same tests may be used to assess airway response after a challenge to the airways. These tests are referred to as bronchial challenge or bronchial provocation tests. The challenge may be in the form of a nonspecific inhaled agent (e.g., methacholine) or a physical agent (e.g., exercise). In either case, airflow is assessed before and after the challenge. The percent change (normally a decrease) after the challenge is calculated (see Chapter 9).

Maximal voluntary ventilation (MVV) was described as early as 1941. Cournand and Richards originally called it the maximal breathing capacity (MBC). In the MVV test, the patient breathes rapidly and deeply for 12 to 15 seconds. The volume of air exchanged is expressed in liters per minute. The MVV gives an estimate of the peak ventilation available to meet physiologic demands.

Measurement of respiratory muscle strength is accomplished by assessing maximal inspiratory pressure (MIP) and maximal expiratory pressure (MEP). This is done using either a pressure transducer or a simple aneroid manometer. MIP and MEP are important adjuncts to spirometry for monitoring respiratory muscle function in a variety of pulmonary and nonpulmonary diseases. Black and Hyatt developed the first device to assess these parameters and termed the device a “bugle” because the expiratory maneuver was similar to blowing into a bugle.

Airway resistance (Raw) measurements date back to the development of the body plethysmograph in the early 1950s. Comroe, DuBois, and others perfected a technique that provided estimates of alveolar pressure. The patient sits in an airtight box called a plethysmograph (see Chapter 11). The plethysmographic method allows the calculation of the pressure drop across the airways related to flow at the mouth (see Chapter 4). This technique originally required complicated monitoring and recording devices. Microprocessors have simplified the measurement of the required signals so that plethysmography is now widely used. The same equipment can also be used to rapidly and accurately measure thoracic gas volume (V_TG).

Lung compliance is measured by passing a small balloon into the esophagus to measure pleural pressure. Intrapleural pressure can then be related to volume changes to estimate the distensibility of the lung (see Chapter 4). Other less invasive techniques are available but not widely used.

Lung Volume and Ventilation Tests

Measurement of lung volume dates back to the early 1800 s, well before Hutchinson’s development of spirometry. Various techniques have been used to estimate the volume of gas remaining in the lung after a complete exhalation. Davy used a hydrogen dilution technique to estimate residual air. This technique was later improved by Meneely and Kaltreider, using helium (He) instead of hydrogen. Around the same time, Darling, Cournand, and Richards began using oxygen breathing to wash nitrogen (N₂) out of the lungs. The collection and analysis of the volume of exhaled N₂ allowed the functional residual capacity (FRC) to be estimated. Using simple spirometry combined with FRC determinations allows total lung capacity (TLC) and residual volume (RV) to be calculated. The other commonly used method for measuring lung volumes uses the body plethysmograph to measure V_TG or FRC. Estimation of lung volumes from chest radiographs is possible but is not widely used. Lung volume can also be estimated from computerized tomography (CT) scans, but such measurements are seldom performed just for the purpose of measuring lung volume.

Closed-circuit (He dilution) and open-circuit (N₂ washout) techniques are both widely used to measure FRC. Besides determining lung volumes, each technique provides some limited information about the distribution of ventilation within the lungs. The pattern of N₂ washout can be displayed graphically. The time required for He to equilibrate during rebreathing provides a similar index of the evenness of ventilation. In the early 1950s and 1960s, Fowler developed a single-breath N₂-washout technique. This method plotted N₂ concentration in expired gas after a single breath of 100% oxygen. The single-breath N₂ washout also provides limited information about gas distribution in the lungs. It also allows estimates of the lung volume at which airway closure occurs when the patient exhales completely (see Chapter 4).

Measurement of resting ventilation requires only a simple gas-metering device and a means of collecting expired air. Portable computerized spirometers allow minute ventilation, tidal volume (V_T), and breathing rate to be readily measured in almost any setting. Determination of alveolar ventilation or dead space (wasted ventilation) requires measurement of arterial partial pressure of carbon dioxide (Paco₂) in addition to total ventilation. Alternately, the partial pressure of carbon dioxide (Pco₂) can be estimated from expired CO₂. The availability of blood gas analyzers and exhaled CO₂ analyzers makes these measurements routine.

Diffusing Capacity Tests

The basis for the modern single-breath diffusing capacity (Dlco) test was described by August and Marie Krogh in 1911. They showed that small but measurable differences existed between inspired and expired gas containing carbon monoxide (CO). This change could be related to the uptake of gas across the lung. Although they used the method to test a series of patients, they did not use the single-breath technique for clinical purposes. Around 1950, Forrester and others revisited the method. They developed it as a tool to measure the gas exchange capacity of the lung. About the same time, Filley and others were promoting other techniques, using CO to measure Dlco. Most of these techniques allowed patients to breathe normally, rather than hold their breath. These methods are called steady-state techniques. Each method has certain limitations. However, the single-breath technique is the most widely used and standardized in the United States and Europe (see Chapter 5).

Blood Gases and Gas Exchange Tests

Measurement of gases (O₂ and CO₂) in the blood began with volumetric methods used since the early 1900s. In 1957, Sanz introduced the glass electrode to measure pH of fluids potentiometrically. In 1958, Severinghaus added an outer jacket containing a bicarbonate buffer to the glass electrode. The electrode-buffer was separated from the blood being analyzed by a membrane that was permeable to CO₂. This allowed the pressure of CO₂ in the blood to be measured as a pH change in the electrode. In 1956, Leland Clark covered a platinum electrode with a polypropylene membrane. When a voltage was applied to the electrode, O₂ was reduced at the platinum cathode in proportion to its partial pressure. These three electrodes (pH, Pco₂, and partial pressure of oxygen [Po₂]) were the basic measurement device in blood gas analyzers for many years. Miniature electrodes gradually replaced the traditional electrodes. Today, blood gas analyzers use a variety of electrochemical techniques (see Blood Gas Analyzers, Chapter 11) to measure not only pH, Pco₂, and Po₂, but also the various fractions of Hb, such as O₂Hb and COHb. Similar methods to measure electrolytes (K⁺⁺, Na⁺⁺, Cl^–) are also included in many blood gas analyzer systems. Transcutaneous electrodes, using techniques similar to the classical blood gas electrodes, are available for the measurement of O₂ and CO₂ tensions (tcpO₂ and tcpCO₂).

Blood oximetry was developed during World War II to monitor the effects of exposure to high-altitude flight. During the 1960s, spectrophotometric analyzers that could measure the total hemoglobin (Hb), along with oxyhemoglobin (O₂Hb) and carboxyhemoglobin (COHb) levels, were perfected. Blood oximetry testing is commonly combined with blood gas analysis so that both can be accomplished with a single instrument. Pulse oximetry was developed in the 1970s as a result of efforts to monitor cardiac rate by using a light beam to sense pulsatile blood flow. It was quickly discovered that the pulse could be sensed, and changes in light absorption could also be used to estimate arterial oxygen saturation. Modern microprocessors have allowed pulse oximeters that are very small and portable, with some devices capable of measuring COHb in addition to O₂ saturation.

Capnography, or monitoring of exhaled carbon dioxide, was developed in conjunction with the infrared gas analyzer (see Chapter 11). This sensitive and rapidly responding analyzer allows exhaled CO₂ to be monitored continuously. Most critical care units, operating rooms, and emergency departments use some combination of blood gas analysis, pulse oximetry, and capnography for patient monitoring. Blood gas analysis is an integral part of routine pulmonary function testing because it is the definitive test of the basic functions of the lung.

Exhaled nitric oxide (eNO), although not a measure of blood gas or gas exchange, has emerged as an important parameter for assessing inflammatory changes in the lungs. Asthma, chronic obstructive pulmonary disease (COPD), and other pathologies characterized by inflammation of the airways or lung tissue, can be monitored by analyzing trace amounts of NO in exhaled gas.

Cardiopulmonary Exercise Tests

Exercise tests commonly use a treadmill or cycle ergometer to impose an external workload that stresses the cardiovascular and musculoskeletal systems. The simplest types of exercise tests are those in which the patient performs work and only noninvasive measurements are made. Such measurements include heart rate and rhythm monitoring using an electrocardiogram (ECG). Other simple, noninvasive measurements are blood pressure and respiratory rate monitoring. Analysis of exhaled gas is noninvasive, but the patient does have to breathe through a mouthpiece or mask. Ventilation and tidal volume (V_T) can be estimated by collecting the exhaled air. Analysis of expired gases permits oxygen consumption and CO₂ production to be measured. When invasive measures (blood gas analysis, arterial catheters, pulmonary artery catheters) are used, the entire range of physiologic variables that affect exercise can be monitored. Computerized exhaled gas analysis allows sophisticated measurements to be made rapidly while the patient continues to exercise (breath-by-breath gas analysis). Simple exercise tests, such as the 6-Minute Walk Test (6MWT), have become popular because the distance walked correlates well with more sophisticated exercise measurements and with clinical outcomes in a variety of diseases.

Metabolic Measurements

Measurement of energy expenditure and caloric requirements dates to the early 1900s. Basal metabolic rate (BMR) was measured by allowing subjects to rebreathe from a volume spirometer containing added oxygen. Plotting the rate at which oxygen was consumed derived an estimate of energy expenditure. Similar techniques are used today, except that oxygen consumption and carbon dioxide production are monitored using exhaled gas analysis. Resting energy expenditure (REE) has replaced BMR as the primary variable related to metabolic needs. Although BMR was used to detect disorders that affected metabolism, REE is used to manage critically ill patients whose caloric requirements may be difficult to estimate.

Spirometry

Spirometry is the pulmonary function test performed most often because it is indicated in many situations (see Box 1-2). Spirometry is often performed as a screening procedure. It may be the first test to indicate the presence of pulmonary disease. Spirometry is recommended as the “gold standard” for diagnosis of obstructive lung disease by the National Lung Health Education Program (NLHEP), the National Heart Lung and Blood Institute (NHLBI), the World Health Organization (WHO), and numerous other organizations concerned with the diagnosis of lung diseases. However, spirometry alone may not be sufficient to completely define the extent of disease, response to therapy, preoperative risk, or level of impairment. Spirometry must be performed correctly because of the serious impact its results can have on the patient’s life. It is one of the few tests that yields a false-positive response if performed poorly because low values are the result. These low results may lead to further testing, inappropriate diagnosis, treatment, and increased costs for the patient and the health care delivery system.

Lung Volumes

Lung volume determination usually includes the VC and its subdivisions, along with the FRC. From these two basic measurements, TLC and other lung volumes can be calculated (see Chapter 4). Lung volumes are almost always measured in conjunction with spirometry, although the indications for them are distinct (see Box 1-3). The most common reason for measuring lung volumes is to identify restrictive lung disease. A reduced VC (or FVC) measured with spirometry may suggest restriction, particularly if airflow is normal. Measurement of FRC and determination of TLC are necessary to confirm restriction because a low FVC can be caused by either restriction or obstruction. If TLC is reduced below the 5th percentile of the predicted value, restriction is present. The severity of the restrictive process is determined by the extent of reduction of the TLC. TLC and its components can be determined by several methods. For patients with obstructive lung diseases (COPD, asthma), lung volumes measured by body plethysmography may be indicated (see Chapter 4) because multiple-breath or single-breath dilution techniques may underestimate TLC. In obstructive lung disease, lung volumes are necessary to determine whether air trapping or hyperinflation is present. The degree of hyperinflation, measured by indices such as the IC/TLC ratio, correlates with increased mortality in patients who have COPD.

Diffusing Capacity

Diffusing capacity is measured by having the patient inhale a low concentration of CO and a tracer gas to determine gas exchange within the lungs (Dlco). Several methods of evaluating the uptake of CO from the lungs are available, but the single-breath technique (Dlcosb) is most commonly used. This method is also called the breath-hold technique because CO transfer is measured during 10 seconds of breath holding. Dlco is usually measured in conjunction with spirometry and lung volumes. Although many pulmonary and cardiovascular diseases reduce Dlco (see Box 1-4), it may be abnormally increased in some cases (see Chapter 5). Dlco testing is commonly used to monitor diseases caused by dust (pneumoconioses). These are conditions in which lung tissue is infiltrated by substances such as silica or asbestos that disrupt the normal structure of the gas exchange units. Dlco testing is also used to evaluate pulmonary involvement in systemic diseases such as rheumatoid arthritis. Dlco measurements are often included in the evaluation of patients with obstructive lung disease, particularly in emphysema. Dlco tests may be indicated to monitor changes in lung function (i.e., gas exchange) induced by drugs used to treat cardiac arrhythmias, as well as changes caused by chemotherapy and radiation therapy for lung cancer.

Blood Gases

Blood gas analysis is often done in conjunction with pulmonary function studies. Blood is drawn from a peripheral artery without being exposed to air (i.e., anaerobically). The radial artery is often used for a single arterial puncture or indwelling catheter. Blood gas analysis includes the measurement of pH, along with Pco₂ and Po₂. Other calculated parameters (HCO3−, base excess, etc.) are often included in the standard blood gas report. The same specimen may be used for blood oximetry to measure total Hb, oxyhemoglobin saturation (O₂Hb), carboxyhemoglobin (COHb), and methemoglobin (MetHb).

Blood gas analysis is the ideal measure of pulmonary function because it assesses the two primary functions of the lung (oxygenation and CO₂ removal). Evaluation of many pulmonary disorders may include blood gas analysis. Specific indications for blood gas analysis are listed in Box 1-5. Blood gas analysis is most commonly used to determine the need for supplemental oxygen and to manage patients who require ventilatory support. Some pulmonary function measurements require blood gas analysis as an integral part of the test (i.e., shunt or dead space studies). Blood gas analysis is invasive; noninvasive measurements of oxygenation or gas exchange are often preferred since they are safer or less costly. Many noninvasive techniques (e.g., pulse oximetry, transcutaneous monitoring, and capnography) rely on a blood gas analysis to verify their validity (see Chapter 6).

Exercise Tests

Physical exercise stresses the heart, lungs, and the pulmonary and peripheral circulatory systems. Exercise testing allows simultaneous evaluation of the cellular, cardiovascular, and ventilatory systems. Cardiopulmonary exercise tests can be used to determine the level of fitness or extent of dysfunction. Appropriately designed tests can determine the role of cardiac or pulmonary involvement. COPD, interstitial lung disease, pulmonary vascular disease, and exercise-induced bronchospasm are respiratory disorders that often require exercise evaluation. Understanding the physiologic basis for the patient’s inability to exercise is an important aspect in prescribing effective therapy (i.e., cardiac or pulmonary rehabilitation). Exercise testing may also be required for the determination of disability. Box 1-6 lists specific indications for exercise tests.

Equipment used to measure oxygen consumption and CO₂ production during exercise can also measure resting metabolic rates. This allows estimates of caloric needs in patients who are critically ill. Indications for performing studies of REE are detailed in Chapter 9.

Obstructive Airway Diseases

An obstructive airway disease is one in which airflow into or out of the lungs is reduced. This simple definition includes a variety of pathologic conditions. Some of these conditions are closely related regarding how they cause airway obstruction. For example, mucus hypersecretion is a component of chronic bronchitis, asthma, and cystic fibrosis (CF), although their causes are distinct.

Chronic Obstructive Pulmonary Disease

The term COPD is often used to describe long-standing airway obstruction caused by emphysema, chronic bronchitis, or asthma. These three conditions may be present alone or in combination (Figure 1-2). Bronchiectasis is sometimes considered a component of COPD. COPD is characterized by dyspnea at rest or with exertion, often accompanied by a productive cough. Delineation of the type of obstruction depends on the history, physical examination, and pulmonary function studies. Unfortunately, the term COPD is used to describe the clinical findings of dyspnea or cough without attention to the actual cause. This may lead to inappropriate therapy. Other similar terms include chronic obstructive lung disease (COLD) and chronic airway obstruction (CAO).

Emphysema

Emphysema means “air trapping” and is defined morphologically. The air spaces distal to the terminal bronchioles are abnormally increased in size. The walls of the alveoli undergo destructive changes. This destruction results in the overinflation of lung units. If the process mainly involves the respiratory bronchioles, the emphysema is termed centrilobular. If the alveoli are also involved, the term panlobular emphysema is used to describe the pattern. These distinctions require the examination of lung tissue either by biopsy or at postmortem. Because this is often impractical, emphysema is suspected when there is airway obstruction with air trapping. Physical assessment, chest x-ray or CT studies, and pulmonary function studies are the primary diagnostic tools. Spirometry (FVC, FEV₁, and FEV₁/FVC) is used to determine the presence and extent of obstruction. Lung volumes (TLC, RV, IC, and RV/TLC) define the pattern of air trapping or hyperinflation caused by emphysema. Dlco and blood gas analyses are useful in tracking the degree of gas exchange abnormality in emphysema. Exercise testing may be necessary if the emphysema patient is suspected of oxygen desaturation with exertion or to plan pulmonary rehabilitation.

Emphysema is caused primarily by cigarette smoking. Repeated inflammation of the respiratory bronchioles results in tissue destruction. As the disease advances, more and more alveolar walls are destroyed. Loss of elastic tissue results in airway collapse, air trapping, and hyperinflation. Some emphysema is caused by the absence of a protective enzyme, α₁-antitrypsin. The lack of this enzyme is caused by a genetic defect. The enzyme α₁-antitrypsin inhibits proteases in the blood from attacking healthy tissue. Deficiency of α₁-antitrypsin causes the gradual destruction of alveolar walls, resulting in panlobular emphysema. Chronic exposure to environmental pollutants can also contribute to the development of emphysema. The natural aging of the lung also causes some changes that resemble the disease entity. The natural decline of elastic recoil in the lung reduces maximal airflow and increases lung volume as people age. Surgical removal of lung tissue sometimes causes the remaining lung to overinflate.

The main symptom of emphysema is breathlessness, either at rest or with exertion. Hypoxemia may contribute to this dyspnea, particularly in advanced emphysema. However, the destruction of alveolar walls also causes loss of the capillary bed. Ventilation-perfusion matching may be relatively well preserved in patients with emphysema. As a result, oxygen levels may be only slightly decreased, particularly at rest. This type of patient is sometimes called the “pink puffer.” As the disease advances, the loss of alveolar surface causes a decreased ability to oxygenate mixed venous blood. Dlco is reduced. The patient becomes increasingly breathless, particularly with exertion. Muscle wasting seems to be common in emphysema, and patients are often below their ideal body weight. As noted, symptoms of chronic bronchitis and asthma may be present as well.

The chest x-ray film of a patient with emphysema shows flattened diaphragms and increased air spaces. The lung fields appear hyperlucent (dark) with little vascularity. The heart appears to be hanging from the great vessels (Figure 1-3). Computerized tomography (CT) scans, especially spiral CT scans, show a three-dimensional picture of enlarged air spaces and loss of supporting tissue. CT scans also delineate whether the emphysematous changes are localized or spread throughout the lungs.

The physical appearance of the chest confirms what is shown radiographically. The chest wall is immobile with the shoulders elevated. The diameter of the chest is increased in the anterior-posterior aspect (so-called barrel chest). There is little diaphragmatic excursion during inspiration. Intercostal retractions may be prominent. Accessory muscles (neck and shoulders) are used to lift the chest wall. Breath sounds are distant or absent. Patients may need to support the arms and shoulders to catch their breath. Breathing is often done through pursed lips in an attempt to alleviate the sensation of dyspnea (Figure 1-4).

Chronic Bronchitis

Chronic bronchitis is diagnosed by clinical findings. It is present when there is excessive mucus production, with a productive cough on most days, for at least 3 months for 2 years or more. The diagnosis is made by excluding other diseases that also result in excess mucus production. These include cystic fibrosis, tuberculosis, abscess, tumors, and bronchiectasis.

Chronic bronchitis, like emphysema, is caused primarily by cigarette smoking. It may also result from chronic exposure to environmental pollutants and second-hand smoke. Chronic bronchitis causes the mucous glands that line the airways to hypertrophy and increase in number. There is also chronic inflammation of the bronchial wall with infiltration of leukocytes and lymphocytes. The number of ciliated epithelial cells decreases. This causes impairment of mucus flow in the airways. Similar changes occur in respiratory bronchioles. Excessive mucus and poor clearance make the patient susceptible to repeated infections. Some patients who have chronic bronchitis caused by cigarette smoking experience a decrease in cough and mucus production after smoking cessation. Some airway changes, however, usually persist. Spirometry is useful in evaluating the extent of airway obstruction caused by bronchitic changes. Dlco may be helpful in distinguishing emphysema and chronic bronchitis; bronchitis patients may have preserved Dlco, whereas emphysema patients tend to have reduced Dlco. However, Dlco is usually not normal in chronic bronchitis because of the mismatching of ventilation and perfusion caused by bronchial obstruction.

Chronic cough is the defining symptom of chronic bronchitis. Some patients do not consider cough abnormal and refer to it as “smoker’s cough” or “morning cough.” In addition to cough, chronic bronchitis may produce dyspnea, particularly with exertion. Blood gas abnormalities usually accompany chronic bronchitis. Ventilation-perfusion mismatching causes hypoxemia. If hypoxemia is significant and persists, the patient may develop secondary polycythemia. Cyanosis may be present because of the combination of arterial desaturation and increased Hb levels. Chronic hypoxemia may also lead to right-sided heart failure (cor pulmonale) with peripheral edema, particularly in the feet and ankles. Advanced chronic bronchitis is also often accompanied by CO₂ retention (hypercapnia).

Unlike the emphysema patient, the patient with chronic bronchitis may show few clinical signs of underlying disease. Body weight may be normal or increased with minimal changes to the chest wall. Patients with bronchitis may appear normal except for cough and dyspnea. The chest x-ray film in chronic bronchitis differs markedly from that in emphysema. The congested airways are easily visible. The heart may appear enlarged with the pulmonary vessels prominent. The diaphragms may appear normal or flattened, depending on the degree of air trapping present. If there is right-sided heart failure, swelling (edema) of the lower extremities is often present.

Pulmonary infections can seriously aggravate chronic bronchitis, and patients who have chronic bronchitis tend to have an increased number of chest infections. The appearance of the sputum produced can help predict worsening function. If it is normally white, a change to discolored sputum indicates the beginning of an infection. This may be accompanied by worsened hypoxemia and shortness of breath. Early treatment can potentially reverse an otherwise serious complication. Failure to manage the chest infection can result in severe hypoxemia and hypercapnia, with exacerbation of right-sided heart failure. Acute respiratory failure superimposed on chronic failure is a common cause of death in patients with COPD.

Bronchiectasis

Bronchiectasis is pathologic dilatation of the bronchi. It usually results from the destruction of the bronchial walls by severe, repeated infections, but some individuals are born with it (congenital bronchiectasis). The terms saccular, cystic, and tubular are used to describe the appearance of the bronchi. Most bronchiectasis involves prolonged episodes of infection. Bronchiectasis is common in cystic fibrosis (CF), as well as following bronchial obstruction by a tumor or foreign body. When the entire bronchial tree is involved, it is assumed that the disease is inherited or caused by developmental abnormalities.

The main clinical feature of bronchiectasis is a very productive cough. The sputum is usually purulent and foul smelling. Hemoptysis is also common. Frequent bronchopulmonary infections lead to gas exchange abnormalities similar to those of chronic bronchitis. Right-sided heart failure follows advancement of the disease. Chest x-ray studies, bronchograms, and CT scans are used to identify the type and extent of the disease. As in chronic bronchitis, spirometry may be useful for assessing the degree of obstruction and response to therapy.

Treatment of bronchiectasis includes vigorous bronchial hygiene. Regular antibiotic therapy is used to manage the repeated infections. Bronchoscopy and surgical resection are sometimes required to manage localized areas of infection. Patients with recurrent hemoptysis may require a resection of the offending lobe.

Management of Chronic Obstructive Pulmonary Disease

The Global Initiative for Chronic Obstructive Lung Disease (GOLD), a World Health Organization(WHO) program, works with health care professionals to raise awareness and to improve the prevention and treatment of COPD. COPD is the third leading cause of morbidity and mortality throughout the world. COPD often includes components of emphysema and chronic bronchitis (see Figure 1-2). This association most likely is due to the common risk factor of cigarette smoking. Hyperreactive airways disease (asthma) may also be present. Reversibility of obstruction, however, is usually less than in uncomplicated asthma. Bronchiectasis and bronchiolitis are also commonly found in patients with COPD.

An essential ingredient in COPD management is early diagnosis. The NLHEP and the WHO both recommend spirometry as a primary tool in the early detection of chronic airflow limitation. Spirometry is recommended for all smokers over the age of 45 and for anyone with chronic cough, dyspnea on exertion, mucus hypersecretion, or wheezing.

Treatment of COPD begins with smoking cessation and avoiding irritants that inflame the airways. The rate of decline in lung function (FEV₁) in smokers is approximately twice that of nonsmokers. Smoking cessation decreases the accelerated decline in most, but not all, smokers. Other measures aimed at keeping the airways open are also important. Inhaled bronchodilators, especially β₂ agonist, are commonly used. Combinations of β₂ agonist and anticholinergic bronchodilators, together with inhaled corticosteroids (ICS), provide relief for many patients with COPD. This is often the case, even when there is little improvement in airflow assessed by spirometry. Some patients require oral steroids (e.g., prednisone) to manage chronic inflammation. Antibiotics are commonly used at the first sign of respiratory infections, and vaccination against viral and bacterial (pneumococcus) infection is recommended. Digitalis and diuretics are most often prescribed for the management of cor pulmonale.

Breathing retraining, bronchial hygiene measures, and physical reconditioning are important therapeutic modalities in addition to pharmacologic management. Breathing retraining is especially important for the patient with advanced COPD. Grossly altered pulmonary mechanics favor hyperinflation and the use of accessory muscles. Training in the use of the diaphragm for slow, relaxed breathing can significantly improve gas exchange. Pulmonary rehabilitation, particularly physical reconditioning, permits many patients with otherwise debilitating disease to maintain their quality of life (Figure 1-5).

Supplemental O₂ therapy is indicated in COPD when the patient’s oxygen tension at rest or during exercise is less than 55 mm Hg. Oxygen may also be prescribed when signs of cor pulmonale are present. Many patients desaturate with exertion only. Exercise testing is the only reliable method of detecting exertional desaturation. Low-flow O₂ therapy can be implemented by a number of methods, including portable systems. Chronic O₂ supplementation has been shown to improve survival in patients with COPD.

Single-lung transplantation has been used for patients with end-stage COPD who are younger than 60 years old. Although lung transplantation causes immediate improvement in pulmonary function, there are factors that need to be considered. The cost of hospitalization and follow-up care is extensive, and the lack of donor organs means that many patients with COPD die while awaiting transplantation. The prognosis for those receiving lung transplants is generally good. In some transplant recipients, a severe form of airway obstruction (bronchiolitis obliterans) has been found to occur in the transplanted lung. The reason for this obstructive process is unclear, but the progression is rapid. Spirometry is used to monitor transplant recipients to detect early changes associated with bronchiolitis obliterans. (See Figure 1-6).

Lung volume reduction surgery (LVRS) has also been used to treat end-stage COPD. In this procedure, lung tissue that is poorly perfused is surgically removed. This allows the remaining lung units to expand with improved ventilation-perfusion matching. This technique works particularly well when there are well-defined areas of trapped gas with little perfusion (bullae). The procedure can be performed by sternotomy or by using a flexible thoracoscope. With both methods, lung volumes (TLC and RV) are reduced and spirometry and gas exchange improve. Spirometry, lung volume measurement, and blood gas analysis are used to monitor changes in these patients. Lung volume reduction is expensive, carries significant risk, and does not appear to benefit all patients who have air trapping.

Restrictive Lung Disease

Restrictive lung disease is characterized by the reduction of lung volumes. The VC and TLC are both reduced below the lower limit of normal (LLN). Any process that interferes with the bellows action of the lungs or chest wall can cause restriction. Restriction is often associated with:

Diseases of the Chest Wall and Pleura

Several disorders involving the chest wall or pleura of the lungs result in restrictive patterns on pulmonary function studies. Conditions affecting the thorax include kyphoscoliosis and obesity. Pleural diseases include pleurisy, pleural effusions, and pneumothorax.

Kyphoscoliosis is a condition that involves abnormal curvature of the spine both anteriorly (kyphosis) and laterally (scoliosis). The degree of curvature is usually determined by x-rays, with curvature greater than 40 degrees requiring surgery. Patients who have kyphoscoliosis show rib cage distortion that can lead to recurrent infections as well as blood gas abnormalities. Depending upon the degree of spinal curvature, the patient may have normal lung function or restriction. Ventilation may be normal. Lung compression usually causes ventilation-perfusion mismatching and hypoxemia. In severe cases, there may be hypercapnia and respiratory acidosis. Treatment of the disorder involves prevention of infections and relief of hypoxemia, if present. Surgical correction is necessary, in many cases, and pulmonary function studies are used to evaluate patients both preoperatively and postoperatively.

Pectus excavatum (sunken chest) is a congenital abnormality affecting development of the sternum and ribs of the anterior chest. It is found more frequently in boys than in girls (approximately 3:1) and occurs in about 1 in 300-400 births, making it the most common congenital abnormality of the chest. The caved-in chest is usually obvious in infants but often does not cause significant limitations until adolescence. Pectus excavatum varies in severity but typically results in a restrictive pattern on pulmonary function tests. Exercise testing, or other tests of cardiac performance, may be indicated to assess functional limitations in severe cases. Pulmonary function and exercise tests may also be used to assess improvements following corrective surgery.

Obesity restricts ventilation, especially when the obesity is severe. Obesity is usually categorized using body mass index (BMI). BMI equals body weight in kilograms divided by height in meters squared (BMI = kg/m²). A BMI of 18.5–24.9 is normal; 25–29.9 is considered overweight, and 30 or greater is considered obese. A BMI of 40 or greater is sometimes referred to as morbid obesity. Increased mass of the thorax and abdomen interferes with the bellows action of the chest wall, as well as excursion of the diaphragm. TLC and VC are usually preserved in obese individuals, but FRC and expiratory reserve volume (ERV) are characteristically reduced. Obesity is also sometimes associated with asthma-like symptoms. It is not clear whether asthma is related to obesity, or if the restriction caused by obesity contributes to airflow limitation that mimics asthma. The airflow limitation occurs secondary to the subject breathing at or near RV.

Obesity may also be associated with a more general syndrome that consists of hypercapnia and hypoxemia, sleep apnea, and decreased respiratory drive. The combination of these findings is sometimes called the obesity-hypoventilation syndrome. Chronic hypoxemia in this syndrome results in polycythemia, pulmonary hypertension, and cor pulmonale. Not all patients who are obese show the signs of obesity-hypoventilation syndrome. However, pulmonary function studies often show restriction in proportion to the excess weight. Weight reduction relieves many of the associated symptoms. Respiratory stimulants, tracheostomy, and continuous positive airway pressure (CPAP) are used to manage the obstructive sleep apnea component.

Pleurisy and pleural effusions can each result in restrictive ventilatory patterns. Pleurisy is characterized by deposition of a fibrous exudate on the pleural surface. It is associated with other pulmonary diseases such as pneumonia or lung cancer. Pleurisy is often accompanied by chest discomfort or pain and may precede the development of pleural effusions. Pleural effusion is an abnormal accumulation of fluid in the pleural space. This fluid may be either a transudate or an exudate. Transudates occur when there is an imbalance in the hydrostatic or oncotic pressures, as occurs in CHF. Exudates are associated with infections or with inflammation as in lung carcinoma. Patients with pleural effusions usually have symptoms that relate to the extent of the effusion. Small effusions often go unnoticed. If the effusion is large, there may be atelectasis from compression of lung tissue and associated blood gas changes. Pulmonary function tests show restriction as a result of volume loss. In some cases, there is restriction caused by splinting as a result of pain. Treatment of pleurisy and pleural effusions is directed toward the underlying cause. Large or unresolved pleural effusions often require thoracentesis or chest tube drainage. Patients with painful pleural involvement may have difficulty performing spirometry or breath holding as required for Dlco.

Pneumothorax is a condition in which air enters the pleural space. This air leak may be caused by a perforation of the lung itself or of the chest wall (e.g., chest trauma). A small pneumothorax may not cause any symptoms. A large pneumothorax can result in severe dyspnea and chest pain. Physical examination of the patient reveals decreased chest movement on the affected side. Breath sounds are usually absent. A chest x-ray study shows a shift of the mediastinum away from the pneumothorax. Small pneumothoraces usually resolve without treatment as gas is reabsorbed from the pleural space. Large air leaks usually require a chest tube with appropriate drainage to allow lung reexpansion.

Pulmonary function tests are usually contraindicated in the presence of pneumothorax. However, undiagnosed pneumothorax may present a risk if pulmonary function studies are performed. Maneuvers that generate high intrathoracic pressures (i.e., FVC, MVV, MIP/MEP) can aggravate an untreated pneumothorax. The potential for development of a tension pneumothorax exists when these maneuvers are performed. In a tension pneumothorax, air enters the pleural space but cannot escape. Increasing pressure compresses the opposite lung, as well as the heart and great vessels. Compression of the mediastinum interferes with venous return to the heart and can cause a rapid drop in blood pressure. A tension pneumothorax can be fatal if not treated immediately. Patients referred for pulmonary function studies that have a known or suspected pneumothorax should be tested very carefully, or not at all. In many instances, the information obtained may not justify the risk to the patient.

Neuromuscular Disorders

Diseases that affect the spinal cord, peripheral nerves, neuromuscular junctions, and the respiratory muscles can all cause a restrictive pattern of pulmonary function. Most of these disorders result in an inability to generate normal respiratory pressures. The VC and TLC are often reduced, while the residual volume (RV) may be preserved. Some chronic neuromuscular disorders are associated with decreased lung compliance. Blood gas abnormalities, particularly hypoxemia, may result if the degree of involvement is severe. Stiff lungs and rapid respiratory rates often result in respiratory alkalosis (hyperventilation). Progressive muscle weakness results in respiratory acidosis (hypoventilation) and respiratory failure.

Paralysis of the diaphragm may be bilateral or unilateral. Bilateral paralysis may be the end stage of various disorders. The most prominent finding is orthopnea, or shortness of breath in the supine position. In the upright position, the patient has a marked increase in VC and improvement in gas exchange. Simple spirometry in the supine and sitting positions can demonstrate the functional impairment. Unilateral paralysis often results from damage to one of the phrenic nerves (e.g., trauma, surgery, or tumor). As with bilateral paralysis, there is a marked change in VC from supine to sitting position. Diagnosis of which side is involved may require a chest x-ray or examination under fluoroscopy. Reduced inspiratory pressures may suggest diaphragmatic involvement.

Amyotrophic lateral sclerosis (ALS, or Lou Gehrig’s disease) affects the anterior horn cells of the spinal cord (motor neurons). Progressive muscle weakness results in a gradual decrease in VC and TLC, which is invariably fatal. Pulmonary function studies may be done serially to assess the progression of the disease.

Guillain-Barré syndrome is a progressive disease in which the body’s immune system attacks the peripheral nerves. Lower extremity weakness ascends to the upper extremities and face. There may be marked respiratory muscle weakness along with weakness of the pharyngeal and laryngeal muscles. Many patients eventually require mechanical support of ventilation. Serial measurements of the VC, MIP, and MEP are used to follow the disease progression.

Myasthenia gravis is a chronic autoimmune disease affecting neuromuscular transmission. In myasthenia gravis, antibodies produced by the body’s immune system block or destroy the receptors for acetylcholine at the neuromuscular junction which prevents the muscle contraction from occurring. It particularly affects muscles innervated by the bulbar nuclei (i.e., face, lips, throat, and neck). The patient with myasthenia gravis has pronounced fatigability of the muscles. Speech and swallowing difficulties can occur with prolonged exercise of the associated muscles. Administration of edrophonium chloride (Tensilon) is sometimes used to confirm the diagnosis of myasthenia gravis; the drug blocks acetylcholinesterase and temporarily increases muscle strength in patients who have myasthenia gravis. When the ventilatory muscles become involved, a myasthenic crisis occurs. Progression of a myasthenic crisis can be assessed using VC and respiratory pressures. Analysis of the flow-volume curve (see Chapter 2) may be helpful in detecting upper airway obstruction brought on by muscular weakness.

Congestive Heart Failure

Congestive heart failure is often used synonymously with left ventricular failure. Failure of the left ventricle may be caused by systemic hypertension, coronary artery disease, or aortic insufficiency. CHF may also be associated with cardiomyopathy, congenital heart defects, and left-to-right shunts. In each case, fluid backs up in the lungs. The pulmonary venous system becomes engorged. Fluid may spill into the alveolar spaces (pulmonary edema) or the pleural space (effusion).

The patient who has CHF usually has shortness of breath on exertion, cough, and fatigue. If coronary artery disease is the cause of CHF, there may be chest pain (angina) as well. Exertional dyspnea is related to pulmonary venous congestion. The fluid overload in the lungs reduces lung volume and makes the lungs stiff (decreased compliance). Dyspnea is usually worse when the patient is supine (i.e., orthopnea). This orthopnea results from increased pulmonary vascular congestion which happens when interstitial fluid becomes intravascular, causing increase in volume, causing vascular engorgement, promoting capillary leak. Dyspnea brought on by CHF may be difficult to distinguish from other causes (e.g., chronic pulmonary disease); therefore patients are often referred for pulmonary function studies. The chest x-ray film usually shows increased pulmonary congestion. The heart (left ventricle) may appear enlarged, particularly if systemic hypertension is the cause.

Treatment of CHF is directed at the underlying cause. Relief of systemic hypertension can reduce the myocardial workload. This is usually accomplished by vasodilator therapy. Reducing fluid retention is also important in managing CHF. Diuretics such as furosemide (Lasix) are commonly used to reduce the afterload on the ventricle. Oxygen therapy may also help reduce myocardial workload, especially if there is hypoxemia. If the cause of CHF is an arrhythmia, antiarrhythmic agents are typically used. Pulmonary function tests, particularly lung volumes and Dlco, may be used to monitor the effects of treatment.

Lung Transplantation

Lung transplantation has evolved as an effective treatment for end-stage lung disease. Lung transplantation has been used for patients with CF, primary pulmonary hypertension, and COPD (Table 1-2). Double-lung transplants are usually performed in patients who have CF, generalized bronchiectasis, or in some types of COPD. Heart-lung transplants have been used for Eisenmenger’s syndrome, pulmonary hypertension with cor pulmonale, and end-stage lung disease coexisting with severe heart disease. Single-lung transplantation has been used effectively in patients with COPD who are younger than approximately 60 years old. Single-lung transplantation offers the benefit that two recipients can share a single donor’s organs. Survival rates for lung transplant recipients have steadily improved. Longer survival is mainly due to more potent anti-rejection drugs (e.g., cyclosporine) and better adjunctive therapy. Pulmonary function tests are used to both assess potential transplant candidates and follow them postoperatively.

Preoperative evaluation consists of documentation of the severity of the specific disease process. Spirometry, lung volumes, Dlco, and blood gas analysis are all used to rank the level of dysfunction. The same tests are also used to detect sudden worsening of lung function that might necessitate rapid intervention. Cardiopulmonary exercise testing may be indicated to determine the extent of the physiologic abnormality. For example, a patient with borderline pulmonary hypertension at rest may develop severe hypertension during even mild exertion.

Most transplantation programs list patients as prospective candidates when their pulmonary disease has advanced beyond predefined limits. An extended wait for lung transplantation is a direct result of the shortage of donor organs. Patients are often referred for transplant evaluation when a major decline in their condition is observed. The term transplant window has been used to describe the time period during which the patient is sick enough to require transplantation but healthy enough to have a reasonable chance of survival.

Posttransplant follow-up relies heavily on pulmonary function tests. Spirometry has been used extensively to monitor improvements resulting from transplantation. Recipients of double-lung transplants often show lung function values approaching those of normal patients within a few months. Blood gas changes usually occur immediately after surgery. Single-lung transplant (SLT) recipients show similar gains. However, because SLT patients retain a native lung, improvement in pulmonary function is usually less than when both lungs are replaced. Interpretation of spirometry, lung volumes, and blood gases in SLT patients is often complicated by the presence of the native lung along with the transplanted lung.

Besides monitoring improved lung function, pulmonary function tests are used to detect rejection and the development of bronchiolitis obliterans (BO). Rejection may be difficult to distinguish from other pulmonary complications (e.g., pneumonia) in patients who are immunosuppressed. There is some evidence that changes in spirometry (FVC, FEV₁, FEF_25%-75%) or distribution of gas (as measured by the single-breath technique) may signal episodes of acute rejection. Chronic rejection is thought to be associated with the development of BO. This pattern is characterized by the development of severe airflow limitation in the transplanted lung. Spirometry, particularly indices of small airway function such as FEF_25%-75%, may provide the earliest signs of BO.

Patient Preparation (Pre-Test Instructions)

Patient preparation for pulmonary function studies consists mainly of instructions given to the patient in advance of the actual test session. These instructions focus on taking or withholding specific medications, refraining from smoking, eating, and other guidelines related to specific tests (e.g., exercise tests, blood gases).

Withholding Medications

Patients referred for evaluation of airflow limitation are often already taking bronchodilators or related drugs. If response to bronchodilators is to be assessed, bronchodilators should be withheld before testing. The exact length of time to withhold a bronchodilator is dictated by the onset of action and how long it takes for the drug to be metabolized and/or excreted. Guidelines for withholding specific bronchodilators before simple spirometry are presented in detail in Chapter 2. Recommendations for withholding medications before a bronchial challenges test (methacholine, exercise, hyperventilation, etc.) are found in Chapter 9. Some patients may have difficulty withholding bronchodilators. In the case of simple spirometry, the test may be performed if necessary, with a technologist comment describing the use of bronchodilators before testing. The patient should be instructed to take the bronchodilator when breathing problems require it. Patients scheduled for a bronchial challenge who inadvertently take their bronchodilators may need to be rescheduled because bronchodilators can significantly alter airway response and lead to false-negative results.

Care should be taken when instructing outpatients about withholding medications. Some patients may be unable to correctly identify all of their medications. Therefore, it may be difficult for them to correctly withhold bronchodilators only. Some patients incorrectly withhold all medications. This may cause serious problems for patients who rely on insulin (diabetic patients), antiarrhythmics, or antihypertensives used for high blood pressure. If the patient is uncertain, it may be preferable to not withhold any medications.

Smoking Cessation

Patients referred for pulmonary function tests should be asked to refrain from smoking for 24 hours before the test. Smoking cessation is especially important if Dlco tests or arterial blood gas tests are ordered. Smoking has been shown to directly reduce Dlco. Smoking also raises the level of CO in the blood, which also interferes with the measurement of Dlco (CO back pressure in blood). Increased CO in the blood (COHb) also makes it difficult to interpret O₂ saturation measured by pulse oximetry (see Chapter 6). Smoking has been shown to reduce the levels of eNO, which may artifactually reduce the level of NO in patients who have airway inflammation.

Other Patient Preparation Issues

Patients referred for pulmonary function tests should refrain from eating a large meal immediately before their appointment. Two hours is usually sufficient to avoid vomiting or gastric distress during routine testing. The same is true if the patient will be exercising as part of the evaluation. Patients scheduled for a bronchial challenge test (see Chapter 9) should not drink beverages that contain caffeine or cola (theobromines) or eat chocolate. Outpatients scheduled for metabolic studies may need to fast for 8 hours before testing to assure a stable baseline. Patients should refrain from alcohol consumption for at least 4 hours before testing (see Box 1-8).

Patients should refrain from vigorous exercise immediately before testing and should be relaxed and comfortable during the test session. Exercise can result in circulating catecholamines, which affect airway tone. Depending on the time of exercise related to the testing time, exercise can also alter the subject’s cardiac output, resulting in a change to carbon monoxide uptake. Tight-fitting clothing (e.g., neckties) may need to be loosened during testing. Dentures should be left in place; many patients find it easier to hold the mouthpiece using their dentures. However, if the dentures are loose, they may obstruct the mouthpiece, particularly during forced expiratory maneuvers.

Some patients may require special accommodations for pulmonary function tests to be performed safely and accurately. Patients, or those referring patients, should understand the requirements of the tests requested. Patients who are unable to sit or stand may require additional time or equipment for testing to be completed. Patients who have a permanent tracheostomy may also require special devices to allow connection to standard pulmonary function circuits. Patients who do not speak the primary language used in the laboratory may require an interpreter to be present during testing. Asking appropriate questions before the patient’s appointment can identify each of these special needs.

Anthropometric Measurements

Various physical measurements are required for estimating each patient’s expected level of pulmonary function. Age, height, and weight are usually recorded in addition to the patient’s sex. Race or ethnic origin should also be recorded. Using the patient’s declared ethnic origin is preferred. Basic physical assessment of the patient’s respiratory status may be needed before and during testing.

The patient’s age should be recorded as of the last birthday. Some computerized pulmonary function systems store the patient’s birth date and calculate the age. This approach is helpful, especially when the patient returns periodically for serial testing. Care should be used when entering specially formatted data (such as dates) into a computerized system. Data entry errors can result in gross overestimation or underestimation of the patient’s expected values.

Standing height, in either inches or centimeters (to the nearest ¼ inch or 0.5 cm), should be recorded with the patient barefoot or in stocking feet. A wall-mounted ruler (stadiometer) allows the patient to stand with the back against the wall and the head close to the ruler. If the patient is unable to stand upright, the arm-span method should be used. Patients who have a history of kyphosis, scoliosis, or related problems should also have the height estimated using their arm span. Arm span may be measured using a ruler placed on a wall or a tailor’s tape measure (Figures 1-8, A-C). The patient should extend the arms horizontally on both sides, and the distance between the tips of the middle fingers measured. Alternately, the distance from the tip of the middle finger to the center of the vertebrum at the level of the scapula is measured on each side and then summed. Height may then be estimated as arm span/1.06 or may be estimated using regression equations that account for race, sex, and age, in addition to arm span.

The patient’s weight in pounds or kilograms should be measured with an accurate scale. Although body weight is typically not used in the calculation of predicted lung volumes, subjects that are morbidly obese may demonstrate a restrictive pattern. Measurement of weight and calculation of BMI may be helpful for the interpretation of reduced lung volumes (e.g., FRC, ERV). Body weight is used to calculate other reference values (see Chapter 13). When weight is used to predict an expected value, the patient’s ideal body weight should be used, unless noted otherwise. Using actual weight in patients who are obese may overestimate expected values if the reference set is based on subjects with normal weights. Weight is also used to express oxygen consumption (i.e., milliliter/kilogram) for exercise and metabolic measurements. The patient’s weight may also be required when lung volumes are determined with the body plethysmograph. Weight is used to estimate body volume in the plethysmograph (see Chapter 4).

Physical Assessment

Physical assessment of patients referred for pulmonary function studies may be needed to determine whether the individual can perform the test. Documentation concerning physical assessment of the patient can also assist with interpretation of test results. Physical assessment should focus on breathing pattern, breath sounds (if necessary), and respiratory symptoms (Box 1-9). These can be observed simply and noted as necessary. Assessment of the patient’s oxygen status using pulse oximetry (Chapter 6) may be required, especially if the subject presents to the laboratory using oxygen therapy. Some test modalities require the patient to be off oxygen, and if the patient is intolerant, that portion of the test will not be performed. Documenting technologist/therapist comments regarding the patient’s signs, symptoms, and oxygenation status at the time of the test is a useful adjunct, especially if test performance is less than optimal.

Pulmonary History

Accurate interpretation of pulmonary function studies—from simple screening spirometry to complete cardiopulmonary evaluation—requires clinical information related to possible pulmonary disease. An ordered array of questions that can be easily answered by the patient provides the most useful history. The interpreter of pulmonary function studies may have little clinical information other than that obtained at the time of testing. A pulmonary history should be taken routinely before pulmonary function testing (Box 1-10).

Most of these questions can be answered by Yes or No, or by circling an appropriate response. Space should be provided so that the patient or history taker can enter comments. Computerized pulmonary function systems often allow history data to be stored in a database along with the patient’s test results. This is a useful feature but may limit the extent of the history that can be stored. In instances in which the physician performs the test, such history may be redundant if a medical history is available.

Interpretation of pulmonary function tests is best made if the clinical question asked of the test is considered. The clinician requesting the test should indicate the reason for the test. Examples of clinical questions asked of pulmonary function studies include, “Does the patient have airway obstruction?” or “Does the patient have hyperreactive airways?” The pulmonary history, including the reason for the test, should be used to decide what is normal or abnormal. Clinical information, as provided by the history, is especially important when the patient’s pulmonary function tests are near the lower or upper limits of normal. For example, an FEV₁ that is near the lower limit of normal (LLN) would be interpreted differently in a healthy patient tested as part of a routine physical than it would be in a smoker who complained of increasing dyspnea.

Technologist-Driven Protocols

As described previously, the basis for deciding which pulmonary function tests are needed is related to the clinical question being asked. The clinical question is often inappropriately stated as a diagnosis. In fact, many patients are referred for pulmonary function studies to establish a diagnosis. For example, a patient may be referred with a diagnosis listed as “asthma.” The clinical question is, “Does the patient have asthma?” Pulmonary function studies may be able to help answer this question, but the exact tests to be performed may not be defined. In this example, spirometry is indicated. Using an adaptive protocol, spirometry can be performed and, based on the results, appropriate additional tests selected (Figure 1-9). Bronchial challenge tests may be performed if spirometry results are normal. Alternatively, additional tests such as lung volumes or Dlco may be necessary.

The correct sequence (and timing) for performing tests is important. Many laboratories use a fixed order for component pulmonary function tests. This may include spirometry, followed by lung volumes and Dlco. In some instances, the order of tests may need to be altered. The methodology used for some tests has definite effects on the results of subsequent procedures. For example, the multiple-breath N₂ washout test to determine FRC has the patient inhale 100% O₂ for several minutes. If this test is performed immediately before a Dlco test, the elevated O₂ level in the lungs (as well as in the blood and tissues) may reduce the measured Dlco. Similarly, before repetition of the Dlco maneuver or FRC determination by gas dilution techniques, sufficient time must be allowed to wash out residual test gas.

Patient Instruction

Many pulmonary function tests are effort-dependent. To obtain valid data, patients must be instructed and coached for each maneuver. Instruction and coaching are particularly important for the FVC maneuver. Instruction should include a description of what the patient is expected to do, such as, “You will take a deep breath in, and then blow out as hard and as fast as possible.” In addition to a description of the test, the maneuver should be demonstrated. During the actual test, vocal encouragement should be given so that the patient knows what is expected and continues for an appropriate interval. Any problems that occur with the first few efforts should be explained before the patient attempts the test again. For example, “That was a very good effort, but you stopped before blowing out for six seconds. Let’s try that again, and keep blowing out until I signal you to relax.” This type of feedback is important because patients may be uncertain of what is required. Patients should be instructed that some maneuvers will be repeated so that their best effort can be obtained. They should be assured that repeating some tests is required and does not necessarily reflect a problem on their part.

Patients should also be carefully instructed for tests that require quiet breathing, such as lung volume determinations. Instructions about maintaining a good seal on the mouthpiece and continuing normal breathing can help reduce leaks or interrupted tests. Some maneuvers are very complicated and may be difficult to describe to the patient. The Dlco maneuver and panting in the body plethysmograph each consist of several steps. For these tests, a combination of demonstration and practice may be the most efficient means of instructing the patient.

Even after adequate instruction and demonstration, some patients may be unable to perform certain tests. This may be caused by lack of coordination related to illness, pain as a result of their condition, or inability to follow instructions. For example, a patient may experience uncontrollable coughing when asked to inspire deeply for an FVC maneuver. If the coughing prevents obtaining valid spirometry results, the fact should be noted in the technologist’s comments (see Chapter 12). Suboptimal effort by the patient can usually be detected as poorly repeatable results on effort-dependent tests (e.g., the FVC). Care should be taken that adequate instructions are given and a sufficient number of efforts recorded before deciding that the patient did not give a maximal effort. If the patient cannot continue or refuses to continue a test, the exact reason should be documented in the technologist’s comments.