using pulmonary function testing in the diagnosis and treatment of asthma

in Using Pulmonary

the Diagnosis and Function Testing Treatment of Asthma

Allan D. SiefMn

Pulmonary Function Laboratories, University of California, Davis School of Medicine, Sacramento, CA 95817

~NTRODUCTION

The evaluation of lung function has a wide range of applicability in both pulmonary and nonpulmonary diseases. The clinician commonly employs pulmonary function tests (PFTs) to evaluate patients with complaints of dyspnea, wheezing, chronic cough, or with an abnormal chest radiograph. PFTs help differentiate organic from functional disease, aid in the differentiation of cardiac from pulmonary disease, and separate patterns of pulmonary dysfunction into obstructive airways diseases or restrictive lung or chest wall processes.

PFTs allow objective and quantitative assessment of the severity of a disease process. Disease activity can also be followed against time to predict prognosis and define the course of the illness~ Pulmonary function can also be followed in response to new or changing therapy. Prediction of surgical risk for both mortality and pulmonary morbid- ity can be satisfactorily estimated. The clinician has the benefit of an objective measure of pu!monary impairment to help with the often difficult decision regarding a patient's pulmonary disability.

Pulmonary function determination also has an important role in screening for unsuspected, early, or asymptomatic disease. This is especially valuable in the workplace, where exposures to inhalation hazards may result in clinicallyimportant lung disease. It is often important to establish baseline pulmonary function prior to initiation of

Cfinical Reviews in Allergy, vol. 8 Ed: M. Eric Gershwin �9 The Humana Press Inc.

179

180 Siefkin

therapy known to affect lung function, such as radiation, chemo- therapeutic antimetabolites, or lung surgery.

Nowhere in medicine is pulmonary function testing more valuable than in the diagnosis and management of asthma. PFTs help define the presence of bronchial hyperreactivity and measure the severity of the airway obstruction. PFTs are part icularly valuable in documenting the marked variabil i ty of the disease in response to multiple stimuli, treatment, and indeed to the time of day. Asthma can often be differentiated from other forms of lung disease. Every individual who cares for patients with as thma should unders tand how valuable PFTs are in providing objective and rapid information about the patient 's clinical state, and allowing direct comparison to the symptom and response to treatment.

ALTERED PULMONARY PHYSIOLOGY IN ASTHMA

Asthma is characterized by the widespread narrowing of the cross-sectional area of the conducting airway. This results in the dyspnea, chest tightness, cough, and wheeze seen in the mill ions of patients with this disease. The bronchial obstruction is par t ia l ly or totally reversible either spontaneously or after t rea tment with a bronchodilator medication. There is no single mechanism respon- sible for the narrowing. The luminal decrease in diameter is the result of

t. Bronchial smooth muscle hypertrophy and contraction; 2. Thickening of the airway wall because of chronic mucosal inflamma-

tion; and 3. A marked increase in airway mucous secretion resulting in the for-

mation of mucous and cellular plugs.

The reduced airway diameter results in impaired airway func- tiom Secondary abnormalit ies can then occur in ventilation, tung volumes, and gas exchange.

Airway hyperreactivity or bronchial hyperresponsiveness is a uniform feature seen in patients with asthma. This is an exaggerated narrowing of the airways compared to that in normal persons in response to a wide variety of stimuli. These may include inhaled drugs, chemicals, antigens, particulates, aerosols, or physical acts, such as exercise or hyperventilationo The mechanisms for this abnormal airway function are not totally known~

Pulmonary Function Testing 181

A wide variety of tests of airway hyperreactivity have been described (1-3). In practice, a reduction in baseline FEV 1 of greater than 20% is used to diagnose hyperreactivity. The determination of the presence and severity of airway hyperreactivity is particularly valuable in confirming suspected cases of asthma that do not show typical standard pulmonary function abnormality, tt is also a valuable test in some patients with episodic dyspnea or cough. The degree ofhyper- responsiveness can also change in response to therapy. This pheno- menon is comprehensively reviewed elsewhere in this chapter.

Pulmonary function is clearly affected by the autonomic neuro- nal control of the airway. Although there are many ~-adrenoceptors on the airway bronchial smooth muscle, the direct sympathetic inner- ration of the airways is very poorly developed. In contrast, there is a well-developed cholinergic nerve supply via the vagus nerve. The postganglionic fibers release the transmitter acetylcholine. Stimula- tion of the postganglionic receptors results in bronchoconstriction. This can be stimulated by inhalation of methacholine or another re- ceptor agonist, and blocked by inhaled atropine or another anticholin- ergic. Submucosal gland secretion is also modulated by cholinergic innervation. A third nonadrenergic, noncholinergic (NANC) autonomic nervous system~ sometimes called the "purinergic" or "pepti- dergic" system, is involved with both increasing smooth muscle tone and direct bronchodilation of the airway smooth muscle (4). This nonadrenergic inhibitory system may be an important component in maintaining airway patency balancing the primary bronchoconstriction of the parasympathetic innervation. The resting tone in the airway may be decreased by inhalation of ~-adrenoreceptor agonists or antichoiinergics in ashmatics and normals. However, ~-blockers, such as propranolol, cause bronchoconstriction in asthmatics, but usually not in normals. Asthmatics may be more dependent on circulating levels of epinephrine to maintain bronchoconstriction than normals.

There is a well-documented diurnal variation in resting airway tone in asthmatics. Airway tone is often highest in the early morning hours and may account for the increased incidence of nocturnal asthma attacks. The cause of this is unclear, but is probably related to circadian changes in circulating corticosteroids or epinephrine, cooling of the airway, mucociliary slowing, supine posture, or late- or delayed-phase allergic reaction (5). Although the mechanism for the nocturnal bronchoconstriction is unclear, the degree of abnormality appears to be related to the level of airway hyperreactivity.

182 Siefkin

During the acute as thma attack, there is a decrease in the cross- sectional area, often at multiple levels throughout the airway. This results in increased pressure gradient between the alveoli and mouth necessary to generate a given flow rate. This increase in airways resistance (Raw) is described by the equation:

Raw = Change in Pressure/Flow

Thus, for any given increase in airways resistance, there is a reduction in maximal flew rate with any given effort. Although airways resistance may be measured directly, it is technically difficult to assure reproducibly accurate values. In practice, this change in airflow resistance is usually evaluated by measurement of expiratory flow rates and evaluation & t h e forced expiratory maneuver. This is easily accomplished by the technique of spirometry (see below)~

It is also important to realize that flow rate depends on the lung volume at which the flow is measured. At high lung volumes, the airways are distended (larger cross-sectional area) result ing in higher flows. Conversely, at low lung volumes, flow rates are lower.

During forced expiration, an increase in intrathoracic pressure causes some dynamic narrowing of the airways. This is much more marked in processes like emphysema, where airway collapse can l imit expiratory flow in addition to the reduction in flow res.utting from loss of elastic recoil~ In normal individuals and in asthmatics, this dynamic compression of airways results in reaching a point at any given lung vol where additional increase in flow is not possible whatever the increase in effort. This is very helpful in the measurement of PFTs. If the patient makes a satisfactory effort, the measurement of the respiratory flow rate will be "effort independent" and, thus, very reproducible from measurement to measurement. This is not t rue at the beginning &the maneuver, where peak expiratory flows are effort dependent. At the very end of a forced expiratory maneuver, the subject may prematurely terminate the effort, which results in an underest imation of the forced vital capacity. During forced inspiration, however, inspiratory flows are not subject to these same factors, and the measured rates may vary considerably depending on effort and intrathoracic pressure generated. Inspiratory flow rates are much more affected by muscle weakness or submaximal effort.

The site of airway narrowing in as thma may vary from pat ient to patient. Some asthmatics never lose their "small airways obstruction," even during asymptomatic periods. This is presumably the re-


suit of the chronic inf lammation around these smaller airways. Other individuals have a significant component of episodic narrowing in the upper airways and even as high as the glottis (6). Most asthmatics have airway obstruction at multiple levels throughout the conducting airways.

During the asthma attack, in addition to reductions in flow rates, there is a reduction in the total air that can be expired, the forced vital capacity (FVC). In addition, the amount of air left in the lungs at end tidal breathing, the functional residual capacity (FRC), is increased. Figure I shows the divisions of the total lung capacity (TLC) in asthma, and contrasts those to normal and individuals with restrictive lung diseases, such as pulmonary fibrosis. Part of the increase in FRC may be because of the dynamic forces during expiration causing an increase in air trapping. However, part of the increase in FRC may be the result of persistent or increased activity in the inter- costals and diaphragm resulting in an enlarged chest cage at the end of expiration (7). This hyperinflation increases airway size and may increase expiratory flow rates. However, the increased resting length of the respiratory muscles probably increases the work of breathing. Some of the increase in FRC and perhaps much of the increase in TLC that has been reported in the past in asthma may be the result of arti- facts that occur during plethysmographic measurement of lung volumes (8). However, measurement of FRC by inert gas dilution, such as the helium dilution technique, also shows the increase in FRC during an asthma attack that is often almost totally reversible after airways function has normalized.

During the asthma attack, the narrowing of the airways is un- evenly distributed, leading to inequalities in ventilation in various parts of the lung. This results in a mismatch between the ventilation (V) and the perfusion (Q) going to those lung units. Diffusion usually remains normal. As a results of this V/Q mismatch, the gradient between the calculated partial pressure of oxygen in the normal alveolar units (PAO 2) and the partial pressure of oxygen in the arterial blood (PaO 2) widens. This gradient, the P(A-a)O2, becomes larger (usually >30 mm/Hg) as the mismatching is worsened by severely hy- poventilated lung units because of bronchospasm and mucous plug- ging. The PaO 2 may decrease, or it may remain in the normal range as the pat ient increases his or her min ventilation (pr imari ly by increasing rate and not tidal vol) and lowers his or her PaCO 2. Supple- mental oxygen usually increases the PaQ, and true right to left shunt is uncommon in asthma, even when gross atelectasis occurs.

184 Siefkin

IC

FRC

NORMAL

il _ TV

ERV

.o~. _ _ *,TLC

E~v !i FRC ~v

RV

IC =lnsplratory capacity ERV =explrutory reserve

volume RV =residual volume VC =vital capacity FRC =functional residual

capacity TLC =totsl lung capacity IRV Mnsplratory reserve

volume TV =tidal volume

OBSTRUCTIVE

l! ,B~ ii

TV ~!

_ ER'|.j 4Lc

RV

N o r L L o r N

H L o r N

H

H o r N N o r L

H o r L

N : normal, H = Increased, L = declreased

RESTRICTIVE

i I : TV I VCI

ER~

FRC ~- , :

RV LC

L L

L o r N L

L o r N

N o r L

Fig. 1, The total lung capacity is divided into four separate volumes. Sums of two or more volumes are called capacities, In asthma and other obstructive lung diseases, one may see increases in the residual volume and functional residual capacity. In restrictive lung diseases, all of the volumes are reduced.

USE OF PULMONARY FUNCTION TESTS IN ASTHMA

Normal Values

Before discussion of the specific tests used in diagnosing and treating the patient with asthma, it is important to realize what is "normal." Excellent discussions of the prediction of normal values are available (9). Obviously, the truest normal values for any patient are those obtained -when the patient is healthy and without lung disease. However, those measurements are often not available.

When PFTs are performed, the determination must be made if the values obtained represent abnormal function. Values are compared to those of a selected reference population. A regression equation is established for this population of presumably normal people for each type of PFT.


A n u m b e r of factors affect the predictions of normal . Some of these are included in the regression equations, and others are not. Height is an impor tan t variable, and since most s t andard tests predictions change d ramat ica l ly with each few inches in change height , th is var iable is included in most regression equations. An ind iv idua l 6 ft 4 in. in he ight has a FVC double that of an ind iv idua l who is 5 ft 2 in. Age is also a very impor tan t factor, since the FVC and the FEV 1 increase s teadi ly unt i l the late teens or early 20s, and then after a br ief decade of s tabi l i ty decrease steadily. The FEV~ or the FEF- 25-75% of a 20-yr-old m a y be twice tha t of the same ind iv idua l at age 80 (Fig. 2). Conversely, the res idual vol of the same 80-yr-old m a y b e a lmost twice as large as the 20-yr-old! Because of the growth dur ing childhood, he ight and not age is usua l ly used to es tab l i sh pedia t r ic predicted normals . Predicted values for chi ldren and aged individuals are more l ikely to be inaccurate than for the 20-60-yr-old groups.

Sex is also an independent var iable for predict ing normal values. Men have larger lung volumes than women of the same age and height. This may be the resul t of sex hormone effects on thoracic cage size and differences in muscle strength. Pu lmonary funct ion does vary with weight; being lower in both those underweight and in those who are obese. However, in most adul t studies, accurate regression equations for spirometic values can be predicted from age, height , and sex. Increase in weight is inversely related to expiratory reserve vol (ERV) and less so to FRC.

There clearly are racial differences in PFTs. Some of these differences are genetic, and some are nutr i t ional . Not all races have been adequate ly studied. In general , blacks and Asians have sma l l e r lungs t han whites by about 15% (10,11). Other variables , such as posture dur ing test ing, occupational exposures, smoking history, a l t i tude, and effects of muscle t r a in ing (athletes, musicians) , have all been considered possibly to have an effect on pu lmonary function, but are not usua l ly adjusted considerably (9).

Once the predicted value based on age, height, sex, and perhaps race is determined, how is i t best to compare the m e a s u r e d value? For m a n y years, _+20% of the value predicted from the ind iv idua l regression equat ion was considered an adequate measure of normal for values such as FEV 1 and FVC. This may lead to inaccuracies and is a gross oversimplif icat ion for every laboratory. The use of 95% confidence in terva ls may be somewhat better, but also does not consider the type of disease the specific laboratory is deal ing wi th or the pop- ulat ion studied. It is unreasonable to expect each laboratory to estab-

186 Siefkin

5

~" 4 UJ

==3 ..J O

2

MEN ~ FVC

FEV 1

00 10 2z0 --3~0 40 50 6~0 7~0 8~0 90 AGE (years)

Fig. 2. The FEV l and FVC change significantly with changes in age. The increase in lung volume up to approx age 20 is the result of growth of the chest cage and the lungitself. However, the reductions that occur with aging of the lung occur without changes in height~

fish its own regression equations. However, it is reasonable to have each laboratory, whether in the physician's office or in the hospital, test a group of normal individuals without lung disease and compare the results to those predicted from the regression equations that have been selected.

Spirometry: The Equipment and the Technique Determination of changes in pulmonary function is most easily

accomplished by measurements of change in exhaled or inhaled volumes as a function of time. This is called simple spirometry. A number of spirometers are available, including bellows type, water seal, or dry rolling seal. Flow rate or velocity can also be measured and compared directly to the vol at which the flow is measured. This is called the flow-volume curve. Flow is measured by pneumotachograph, mass flowmeter, or turbine flowmeters. Figures 3 and 4 show a direct comparison of these two techniques for a normal subject and a patient with asthma. Many types of modern office-based equipment will compute and display the information obtained from the FVC maneuver in both relationships, and often display "normal predicted curves" to allow direct visual comparison.

With the advent of microprocessors, many relatively inexpen- sive "office PFT systems" produce pages of figures and tables of numbers. As long as the interpreting physician understands the equipment and what is necessary to perform an accurate test, office


4 .,,J w 3

.=J 0 2 >

1

0 0

A. NORMAL

~ F F V C

I FEV1 ~ r - -

1 2 3 4

Bo ASTHMATIC

FEvl

0 g------ I~ ~ 1 ~ _____L.~ 0 1 2 3 4 5

TIME (sec)

Fig. 3. Lung mechanics are expressed by spirometry, where volume is expressed as a function of time. Examples of spirograms for a normal individual (A) and an asthmatic pat ient (B). Normal values for 50-yr-old, 5 ft 10 in, man are: FVC = 4.2L, FEV I = 3.3 L, FEVt/FVC% = 78%. The measured values for the same subject with moderate as thma show: FVC = 3.9 L, FEV I = 2.0 L, FEVJFVC% = 5t%.

t0 fA, N O R M A L

81 ~EF 25%

\

jO 2 5~176

0 LL - - . I I I " ~

0 1 2 3 4 5

10 B. ASTHMATIC

8~ FVC

61

0 1 2 3 4 5

VOLUME (liters)

Fig. 4. Expiratory flow-volume curves for the same subjects in Fig. 3. Note tha t in this figure flow is expressed as a function of volume. Forced expiratory flow at 50% of the FVC is called the FEF50%. There is no axis represent ing time, so the FEV I is shown by special time marks placed on the curve, usual ly at 0.5, 1, and 3s.

188 Siefkin

PFTs can be extremely valuable in day-to-day patient management. Treating patients based solely on numbers generated from a "black box" without this simple knowledge can be quite dangerous and should be condemned. There is also considerable variability in the performance of various types of commercially available equipment (12).

The American Thoracic Society (ATS) has made recommenda- tions for the standardization of equipment to perform spirometry and the techniques to be used (13). The individual who performs or super- vises spirometry must review the ATS standards thoroughly. It is important that the technician, nurse, or physician who is directing the performance of the spirometry understand the equipment and the procedures. The subject should have the forced expiratory maneuver demonstrated, and a minimum of three FVC tests should be attempt- ed with significant verbal encouragement from the technician to elicit a maximum and complete effort. The technician needs to recognize when the test is unacceptable because of slow start, incomplete effort, premature cessation of expiration, excessive early coughing, or air leakage. The largest two FVC maneuvers and the largest two FEV~ volumes should not vary from each other by more than 5% or 100 mL, whichever is greatest.

Comparative tests should be performed at approx the same time of the day because of the variability in pulmonary function resulting from diurnal rhythms. All gas volumes must be corrected from room temperature and expressed as BTPS conditions. Without this correc- tion, volumes will artifactualty appear up to 10% lower. If patient cooperation is not optimal, it is important to note this.

Spirometry: The Forced Vital Capacity (FVC) Maneuver

The measurement of expiratory flow limitation in asthma can be accomplished by a number of techniques. The simplest and least specific is to watch the subject empty his or her lungs and record the expiratory time with a stop watch. The normal adult can almost reach residual vol in 3 s. Prolonged expirations beyond 5-6 s suggest obstructive airways disease; the longest forced expiratory times are seen in severe emphysema.

Peak flow meters are simple portable devices that can be used in the hospital ward, in the physician's office, and in the patient's home or work place. They are somewhat effort dependent. However, if the patient can be properly motivated and uses proper technique, the


results are quite reproducible. The peak expiratory flowrate (PEFR) will drop very significantly during asthma attacks and indeed may change as much as 50% because of diurnal variations alone in some patients. Serial PEFR measurements can help the patient and physician decide when medicines should be changed or added, or when the patient should seek medical consultation. Adequate patient moti- vation is required for successful home utilization. Such tests can be employed at the work place to document occupationally induced bronchospasm. Because the PEFR is reduced with poor effort, obstructive airways diseases, restrictive lung disease, and neuromuscular disease are nonspecific, but still can play an important role in the management of asthma.

The FVC is the maximal vol that can be expired after a maximally forceful inspiration (Fig. 3). The slow vital capacity or vital capacity (VC) is equal to the FVC in normal individuals; however, the FVC < VC when there is air trapping. This is seen primarily in emphysema, but may also be seen in asthma, especially during an acute attack. The FVC is reduced in both obstructive and restrictive lung disease. It is effort dependent in that it may be reduced with a poor effort, an inadequate effort, or if neuromuscular weakness is superimposed on asthma (as seen in respiratory muscle fatigue during a prolonged asthma attack).

The amount of the FVC that is expired in the first second is called the forced expiratory vol in one second (FEV~). This is a key vol in following the asthmatic patient. The FEV I is reduced in both obstructive diseases (asthma, emphysema, and chronic bronchitis) and in restrictive diseases (pulmonary fibrosis, kyphoscoliosis, muscular dys- trophy, and so forth). The key to differentiating these processes is the ratio of the FEV/FVC%o This value is reduced in asthma and the other obstructive diseases (<70-75%), but is normal or increased in the restrictive processes.

The mean forced expiratory flow over the middle half of the FVC is the FEF25-75% (Fig. 5). This is a more sensitive measure of flow obstruction through smaller airways. It may be abnormal in early airways obstructive disease because of smoking. It may also be abnormal in the asthmatic patient who is asymptomatic or after treatment when the FEVI/FVC% has become normal. Although it is more sensitive, it is also more variable than the FEV~o The averaged flow over the middle half of the FVC may actually change before and after treatment in the asthmatic, so the values are not exactly comparable. This occurs because both the airway cross-sectional areas increase

190 Siefkin

5

FVC = 4.3L

"-'3

~ 2 / [ 2.21iterslO.8sec=2. 75LIseO

0 I , _ _ l 2 3 4 5

T I M E (seconds)

Fig. 5. Measurements of vent i la tory flow rates are made by m e a s u r e m e n t of slopes over various segments of the spirogram shown in Fig. 3. FEF200-1200 is a measurement of flow ra tes through larger airway; FEF25-75% is a measu remen t through smaller a irways; FEF75-85% is a measurement through even smaller airways.

and the FVC increases, potent ia l ly mak ing the m e a s u r e m e n t of FEF25-75% occur over different lung volumes.

The max ima l voluntary vent i la t ion (MVV) is the m e a s u r e m e n t of the total voi exhaled dur ing a series of rapid large expira tory efforts recorded over 10-15 s~ The MVV is expressed as total vent i la t ion that would occur had the maneuve r had been ma in t a ined at tha t level for I rain (L/rain). It is abnormal in m a n y forms of lung, neuromuscular , or chestwall disease. The MVV and FEV 1 are closely related in a i rway obstructive diseases, such as as thma, as they are in normals , pro- vided the subject makes a good effort, if the MVV is less than 40 x FEV I, the patient is either unable to cooperate with the test, or has neuromuscular weakness, easy fatigability, or a significant upper airway obstruction not obvious by FEVI.

Forced Expiratory Flow-Volume Curves or Expiratory-lnspirafory Flow-Volume Loops

A second technique for visual ly expressing lung mechanics is the f low-volume loop (Fig. 4). As described above, at each lung vol, there is a m a x i m u m achievable flow rate. Fu r the r expiratory effort will not increase flow, and thus, most of the middle 75% of the expira tory f low-volume curve is reproducible. F low-volume curves are plots of expiratory flow ra tes (usual ly measured with a pneumotachograph) , plotted against lung volumes. Flow rates are expressed in terms of

Pulmonary Function Testing I9I

the percentage of the FVC at which the flow is measured. Thus, the FEF50% is the maximal flow rate at the hmg vol point, which is 50% of the FVC. Any process that increases airway resistance, decreases elastic recoil of the lung, or abnormally compresses or obstructs the major airways will reduce the flow rate at a given lung vol. One major advantage of flow-volume loops is the visual pattern, which may itself be immediate ly diagnostic of the pat tern of abnormality, such as obstructive, restrictive, mixed obstructive-restrictive, or upper airway obstruction (Fig. 6).

Response to Bronchodilators Pulmonary function testing is usually performed before and after

bronchodilator administrat ion to establish if the obstruction is parti- ally or totally reversible. Although many subjects with chronic bronchitis show at least some improvement with bronchodilators, as thma by definition shows this improvement. The drug is usual ly delivered by giving two puffs from a metered dose inhaler (MDI), and after tak- ing a complete inhalation, the patient performs an FVC maneuver. Either simple spirometry or flow-volume loops can be obtained. Pre- and post-bronchodilator FEV~, FVC, FEF25-75%, PEFR, or FEF50% may be compared. Alternatively, Raw and FRC can be measured in the body plethysmograph. A maximal inspiratory maneuver may cause bronchoconstriction in the asthmatic, and use of part ial flow- volume curves can prevent this effect (14). Excellent reviews of the bronchodilator response and its evaluation are available (!5,16).

The degree to which the patient with as thma shows improvement after bronchodilators depends on many factors, including the seventy and the chronicity of the airways obstruction at the time of the test. The time of day of the test, the time of last bronchodilator use, the presence of recent lung infection, and the route and dose of bronchodilator drug may all have an effect. There is potential variabi l i ty in test results of 10-15% for FEV~ and FVC, and up to 25% for the FEF25-75% (17). For this reason, a 15-20% or greater increase in FEV 1 or a 25-30% or greater increase in FEF25-75% after bronchodilator adminis t ra t ion is considered necessary to define significant bronchodilator improvement. The marked exception to this occurs when the pat ient is suffering with a severe asthma att tack where little response may be seen. in COPD, the FEV t appears to be the most specific test, followed by the FVC, FEF25-75%, and the specific airways conductance (18). Some asthmatics show reduction in FRC

I92 Siefkin

Expiration A

JLC

t L

,~ NORNAL

Inspiration

Expiration +

C

(MtXED OBSTRUCTIVE/ RESTRICT VE)

T Inspiration

A B

EMPHYSEMA SCLERODERNA {SEVERE OBSTRUCTIVE) {RESTRICTIVE)

VOCAL CORD TUMOR (VARIABLE EXTRA- THORACIC UPPER

AIRWAY OBSTRUCTION)

TRACHEAL STENOSIS (FIXED UPPER AIR-

WAY OBSTRUCTION)

Fig. 6. Inspiratory and expiratory flow-volume curves show an example of severe obstructive lung disease (emphysema) (A), moderate restrictive lung disease (scteroderma) (B), mixed obstructive-restrictive disease (sarcoidosis) (C), variable extrathoracic upper airway obstruction (vocal cord tumor) (D), and fixed upper airway obstruction (tracheal stenosis) (E). Contrast these to Fig. 4.

after bronchodilator administration, implying a reduction in airtrap- ping, even when the FEV 1 or FEVJFVC% is not improved (19).

Although almost all laboratories use inhaled ~-agonists to assess bronchodilator response, there does not appear to be much difference in measurable response among the many agents available, with the possible exception of time of onset of action. Although most laboratories use two puffs of the drug given from an MDI, others emp]oy spacer devices to increase drug delivery. Isoproteronol, isoetharine, metaproteronol, and albuterol maybe delivered by mechanical nebu- lization, usuaity deIivering 10-20 times as much drug as the MDI. For smoking-related COPD, ipratropium is as effective as or more effective than the J3-adrenergic agonists as a bronchodilator, and thus may be used to assess bronchodilator response (20).


Lung Volume Measurement

As shown in Fig. 1, the TLC is subdivided into various volumes and capacities. At the end of quiet tidal expiration, the rot of air left in the chest at the point at which the recoil pressure of the chest watt outward to expand and the recoil of the lung inward to collapse are equal in the FRC. FRC and RV are often increased in obstructive airways diseases in proportion to the degree of airflow obstruction. Some individual patients may show significant degrees of this "hyper- expansion" during an asthma attack, although it is less commonly seen than in the patient with emphysema. Most laboratories utilize a gas dilution technique to measure the communicating gas vol in the chest. This technique may underestimate the FRC and TLC in individuals with a bullous disease, such as emphysema. Conversely, in some patients with severe obstructive disease, measurement of the compressible gas in the chest by the technique of body plethysmo- graphy may overestimate the TLC because of compression of com- pliant upper airways. In either event, for nonresearch purposes, the routine use of lung vol measurements in asthma is of limited clinical value, if other lung diseases are not suspected or coexistent.

Carbon Monoxide Diffusing Capacity (DLCO) The measurement of carbon monoxide uptake,, usually by single-

breath technique, allows an estimation of the available alveolar- capillary exchange surface. It is a valuable technique in the diagnosis and medical evaluation of treatment in patients with interstial lung diseases, collagen vascular diseases involving the lung, sarcoidosis, pulmonary vascular disease, and emphysema (21). The DLCO is usually normal in patients with asthma, but may be mildly increased or decreased, primarily because of changes in ventilation and perfusion matching. It is of primary value in the management of the patient with asthma in differentiating it from emphysema where a consistent reduction in DLCO is found.

~f~ONITORING THE PATIENT WITH ASTHMA AND GUiDELiNES FOR TREATMENT

The diagnosis of asthma is made by a combination of clinical symptoms and signs, by exclusion of other disease, by examination of the chest radiograph, and by the finding of obstructive airways

t94 Siefkin

disease that change rapidly over time and in response to therapy~ Table 1 shows the pulmonary pathophysiologic abnormali t ies seen in as thma in comparison to emphysema and restrictive diseases~ The spectrum of as thma is very wide, ranging from rare asymptomatic wheezing or coughing to such severe impairment that the pat ient is disab]ed and under continuous medical care. Chronic management of both the in termi t tent mild asthmatic and the severe as thmat ic requires objective measures with which to correlate signs and symptoms and to monitor results of therapy. The regular use of simple spirometry, flow-volume curves, or peak expiratory flow rates in managing the asthmatic has been likened to the use of the blood pressure cuff in following hypertension. Unfortunately, pat ient complaints of shortness of breath, dyspnea, and wheeze have only a fair correlation with the measured FVC, FEV1, or PEFR. Auscultation is also a relatively inexact method of assessing the degree of airflow obstruction.

At each office visit, measurement of simple spirometry with recording of the FVC, FEVt, and FEVI/FVC% allows the physician to assess the patient 's complaints objectively, to correlate what is heard with the stethoscope, and to assess the efficacy of the prescibed treatment plan. When the physician starts new therapy, serial PFTs will help decide i f it should be continued. Because of the multiple s t imuli that may cause changes in the FEV l or the PEFR, multiple measurements over weeks or months will help establish the patient 's baseline function. The goal of the physician should be to main ta in the highest possible FEV 1.

PEFR can be measured at home or at the work place. Pat ients who have considerable variabil i ty in their airways obstruction, and especially those who require continuous medication or frequent changes in their treatment, should consider self-monitoring with portable peak flow meters. Once the technique has been learned, the PEFR and the FEV 1 correlate reasonably well in the asthmatic patient. Patients can recognize deterioration at an earlier stage. Init ially, the patient should measure the PEFR four or more times a day, 10-20 rain after their inhaled bronchodilator and record the results in a diary. This allows the patient and the physician to gain confidence in the patient 's abili ty to reproducibly perform the test. It should be re- peated in the physician's office for corroboration. In addition, frequent PEFR measurements will allow the patient to determine his or her own "worst period of the day." This may be diurnal in pat tern or may help identify if an unsuspected environmental cause for the

Pulmonary Function Testing

Table 1 Typical Pulmonary Pathopsyiologic Abnormalities

Found in Various Lung Disorders

195

Lung Chest Wall

PFT Asthma Emphysema Fibrosis Restriction

FVC N or L L L L

FEV I L L L L

FEVI/FVC% L L N or H N

FEF25-75% L L L L

BD + +++ + or - - -

TLC N or H H L L

RV N or H H L N or L

DLCO N L L N or L

N = Normal, L = reduced, H = increased, + = positive

response, - = no change with bronchodilator.

hyperreactivity exists. It will also allow the patient to determine objectively when the standard drug regimen is no longer effective, which is a sign that more intensive intervention is needed. Once the pat ient and the physician are comfortable with the technique and that the pulmonary function is stable, less frequent determinat ion can be made, or the patient can only utilize home monitoring during periods of subjective problems or when therapy is being changed. PERF can be used to monitor bronchodilator or corticosterold therapy (22,23). Patients will learn to use their PEFR levels to help the physician adjust their management program.

In the case of the hospitalized patient, frequent determinations of PEFR and FEV 1 will help determine whether therapy should be altered. The arterial blood gas shoutd also be monitored. Normally, an increased P(A-a)O 2 is associated with hyperventilation and a low PaCO 2. As the airways obstruction becomes worse and the FEV1 and the FEVt\FVC% fall, the PaO 2 falls and the work of breathing increases. An increase in the PaCO 2 is an ominous sign that the patient is becoming exhausted, and that intubation and mechanical ventilation may be necessary. Intensive care of this patient includes intensive monitoring of the pulmonary function tests and arter ial blood gases.

SUMMARY

Asthmatics have remarkable changes in their pulmonary function in response to numerous external stimuli and internat controls.

196 Siefkin

Ser i a l p u l m o n a r y func t ion t e s t i n g in the office, hosp i ta l , a t home, or the work place a l lows the objective m e a s u r e m e n t t h a t is n e c e s s a r y to i n t e l l i g e n t l y d iagnose and t r e a t these pa t i en t s . Once t h e p a t i e n t a n d the p h y s i c i a n u n d e r s t a n d how to use the t echn iques for m o n i t o r i n g the degree of a i r w a y s obs t ruc t ion , t h e y become a k e y in med ica l m a n a g e m e n t decis ions.

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