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hey^ '$iol American Thoracic Society S. Mecia. staglsudo 28:877< ! TheonjQ * laryvasea. , * 1984; MEDICAL SECTION OF THE AMERICAN LUNG ASSOCIATION ^ STANDARDS FOR THE DIAGNOSIS AND CARE OF PATIENTS l release of >e lungs. J 6. ; a$argj]c% 1: a release kbit lungs. WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) AND ASTHMA12 THIS Official Statement of the American Thoracic Society was adopted by the ATS Board of Directors, November 1986. D, e/o/.Al:nces PGI, helial cells, iger J, Jot* ndin D* in 1981; 240: i MA. Pm}. iary hyperdiatr 1982;' ''v / DC, He of PGDjOa' sin thece* 7-50. OL. cells .. .Titinol iy): # '.ffectsofu?1 >onsetova?: 1 1978; 234:. air. ana thront-: iary circuit ' rinatol 198ft. .ling pulm>: born infant;' ^ardiovasc*.' t.ColumbuiL; ;ymann MA1*; 1 ncrease pd-^,1 .m J Phys^f - r* I J, Heymanss .for the higfrlambs. P*sfe Contents Chapter 1............................ Chronic Obstructive Pulmonary Disease Chapter 2..................................................Asthma Chapter 3...................... Pharmacologic Therapy Chapter 4............................................02 Therapy Chapter 5..............Respiratory Care Modalities Chapter 6........................ Physical Rehabilitation and Home Care CHAPTER 1 Chronic Obstructive Pulmonary Disease I. Introduction Thirty years ago, British and North Ameri can terminology for the same major Jung con dition differed: The clinical term "emphy sema" in the United States was equivalent to "chronic bronchitis" in Great Britain. Gener ations of British physicians had recognized chronic bronchitis as a potentially disabling and even lethal affliction that was associated with cigarette smoking and dusty working en vironments (1). Attention in the United States somehow 1-ad been directed more to the pro found structural changes of emphysema that were first described by Laennec (2). The mor bidity and mortality due to these diseases in creased during the 20th century on both sides of the Atlantic. Improved physiological techniques were ap plied after World War II that rapidly advanced understanding of pulmonary pathophysiol ogy (3-6). The significance of reduced expi ratory airflow was widely appreciated. The first Aspen Conference in 1958 had interna tional representation, and appointed a com mittee on terminology, which agreed unani mously th :. emphysema must be defined mor phologically (7). British workers met in 1959 to discuss terminology, and published com prehensive suggestions (8) for an orderly tran sition to the newly recommended terminol ogy. The term "chronic non-specific lung dis use ' was devised, but proved too awkward (?). It also included a category of "obstruc ts lung disease" that could occur either with 0r without reversibility, and with or without Chronic Airways Obstruction Chronic obstructive pulmonary disease (COPD) and asthma are the major causes of pulmonary disability in the United States, with at least 10 million Americans suffering from COPD and up to 5% of the population afflicted with asthma. Over the past 20 years, major strides have been made in our understanding of the pathophysiology of these two disorders, although there are still large gaps In our knowledge. While a number of position papers and statements have been promulgated by the American Tho racic Society concerning various aspects of the diagnosis and treatment of COPD and asthma, it was felt that a review of the overall topic was timely. This statement represents the combined efforts of a Task Group appointed by the Scientific Assembly on Clinical Problems of the American Thoracic Society to accomplish this task. Clearly, we could not cover every aspect of this broad topic nor even provide a detailed review of those areas addressed. We elected instead to concentrate on clinically relevant topics and to provide sufficient data to be useful as a guide as well as to include selected, but in no way exhaus tive, references. The first two chapters define the entities and set forth recommendations for diag nosis, hospital admission, and discharge. The remaining four chapters critically review the various facets of therapy. We have noted controversial areas and those where conclusive experimental data are not yet available, in these situations, the committee often decided to take a position on one side or the other based upon the best available information. emphysema. The present recommendations continue along this line of reasoning. Chronic obstructive pulmonary disease (COPD) is defined as a disorder character ized by abnormal tests ofexpiratory flow that do not change markedly over periods of sev eral months observation. The qualification is intended to distinguish COPD from asthma. The airflow obstruction may be struc tural or functional. Specific causes of airflow obstruction such as localized disease of the upper airways, bronchiectasis, and cystic fibrosis are excluded. Bronchial hyperreac tivity may be present in patients with COPD as measured by an improvement in airflow following the inhalation of beta-adrenergic agents or worsening after inhalation of methacholine or histamine (10). Three disorders are incorporated in COPD: emphysema, peripheral airways disease, and chronic bronchitis. Of these, only emphysema is further classified. Any individual patient may have one or all of these conditions, but the dominant clinical feature in COPD is al ways impairment, or limitation of expiratory airflow. il. Definitions A. Emphysema The American Thoracic Society previously defined emphysema as an anatomic altera tion of the lung, characterized by an abnor mal enlargement of the airspaces distal to the terminal non-respiratory bronchiole, accom panied by destructive changes of the alveolar wails (11). This definition was reconsidered and modified by a recent workshop of the National Heart, Lung and Blood Institute. Our committee recommends adoption of the concepts and definitions published by that group in 1985 (12). Emphysema is defined as "a condition of the lung characterized by abnormal perma nent enlargement of the airspaces distal to the terminal bronchiole, accompanied by de struction of their walls, and without obvious fibrosis." Destruction in emphysema is de- 1 This project was supported by a grant from Boehringer Ingelheim Pharmaceuticals, Inc. 1 Reprints may be requested from your state or local lung associations. 225 226 fined as nonuniformity in the pattern of re spiratory airspace enlargement so that the or derly appearance of the acinus and its com ponents is disturbed and may be lost. It is recognized that emphysema, depend ing on its severity, may be diagnosed in a va riety of ways, including naked eye examina tion, by examination of an inflation-fixed lung slice using a dissecting microscope (sub-gross examination), or by light microscopic exami nation of thick (200 to 400 pm) or thin (4 to 6 pm) stained and mounted sections. Emphysema is recognized as a subcategory of respiratory airspace enlargement which in cludes: Respiratory Airspace Enlargement 1. Simple Airspace Enlargement a) congenital b) acquired 2. Airspace Enlargement with Fibrosis 3. Emphysema ' a) centriacinar b) panacinar c) distal acinar In simple airspace enlargement the pattern of the acinus is retained with no evidence of destruction. Congenital airspace enlargement occurs in Down's syndrome or congenital lo bar overinflation, whereas acquired forms of respiratory airspace enlargement include com pensatory overinflation and the uniform re spiratory airspace enlargement in the aging 'mg. It is still possible that the airspace en- rgement of age is not due to age alone, but due to the combination of age and environ mental conditions. However, the changes oc cur in nearly all subjects and it has been sug gested that these changes are therefore "nor mal." The term "aging lung" is preferable to the term "senile emphysema." A spectrum of airspace enlargement is usu ally associated with fibrosis of the lung. There is generally no difficulty recognizing honey combed interstitial pulmonary Fibrosis or air space enlargement associated with fibrosis in granulomatous lesions such as tuberculosis, sarcoidosis, or eosinophilic granuloma. Three subtypes of emphysema are recog nized: ' a) Centricinar emphysema. This is also re ferred to as proximal acinar emphysema be cause the proximal part of the acinus (respi ratory bronchiole) is dominantly involved. There are 2 subdivisions of this form of em physema. The first is classically associated with cigarette smoking and airflow obstruc tion, and is also referred to as centrilobular emphysema. Inhalation of coal dust and other mineral dust also results in dilatation of re spiratory bronchioles with accumulation of dust-laden macrophages in and around respi ratory bronchioles, and has been referred to focal emphysema. However, in those ex- ed to coal dust, the term coal pneumoconi osis is preferable. b) Panacinar emphysema. In this subtype, all components of the acinus tend to be in volved about equally. It is the form of em physema commonly associated with alpha- 1-antiprotease deficiency (13). It may also oc cur in the bases of the lung in patients with centrilobular emphysema, and as an inciden tal Finding in older subjects. c) Distal acinar emphysema. In this sub type the distal part of the acinus, alveolar ducts and sacs, are predominantly involved. Because of the association of this form with the secondary interlobular septa, it is also known as paraseptal emphysema; the distal acinus also abuts on pleuras, vessels, and air ways, and the emphysema may be worse in these regions. Additional types of emphysema have been suggested, but considerable overlap exists even with the types already described, and there seems to be little reason for further subdivi sions. When emphysema becomes severe, it is difficult to classify, and expert pathologists often disagree on the classification of such emphysematous lungs. Emphysema severity as assessed morpho logically is the single best correlate with an index ofairflow obstruction such as the forced expiratory volume in one second (FEV,) (14-16). Patients who have significant physi cal impairment due to COPD usually exhibit emphysema of at least moderate severity when examined postmortem. Occasionally, such pa tients have only minimal emphysema (17), and, rarely, it is absent (18). B. Peripheral Airways Disease A variety of morphologic abnormalities have been identified in the peripheral airways of patients with COPD. These include inflam mation of the terminal and respiratory bron chioles, fibrosis of airway walls with narrow ing, and goblet cell metaplasia of the bronchiolar epithelium (19). The distribution and severity of these changes varies considerably among individuals. Structure-function corre lations suggest that these lesions contribute to airflow obstruction in severe COPD, but that their importance is secondary to that of emphysema (14-16). In persons at risk for de veloping COPD (e.g., cigarette smokers), pathological changes in the peripheral airways appear to precede the development ofemphy sema (20). It has been suggested that inflam mation and other changes in the peripheral airways may be responsible for subtle abnor malities in pulmonary function tests that are not associated with physical impairment and that these physiological and pathological ab normalities may represent "early, or predinical" COPD (15,21). It is emphasized that these relationships remain unconfirmed by long term studies, and that their clinical relevance remains uncertain. C Chronic Bronchitis Chronic bronchitis, as previously defined, refers to "the condition of subjects with chronic or recurrent excess mucus secretion into the bronchial tree." Chronic was defined as "occurring on most days for at least three months of the year for at least two successive years" (8). The excess secretion should not be brought about by other diseases such as bronchiectasis or tuberculosis. Excess muli' secretion was empirically recognized production of any sputum, whether expect rated or swallowed, and in most instances^ turn production is accompanied by chrcmu z cough. Although not explicitly stated in | definition, it was generally held that ex& * mucus production is an important cause of airflow obstruction (19), and "chronic bron chitis has been commonly used to mean'e*. piratory airflow obstruction." . * Many patients with COPD have excess spu. turn production as well as hyperplasia of the mucus glands of the trachea and large bron chi. Both abnormalities have been linked etio. logically to cigarette smoking. However, avail, able evidence indicates that these effects of cigarette smoke are independent of those which cause airflow obstruction. Numerous structure-function correlative studies ha\t failed to identify a close relationship betweaj airflow obstruction and mucus gland hyperl plasia (6, 8, 22, 23). More importantly, lon gitudinal population studies have failed to identify an independent effect of cough and excess sputum production upon the develop ment of airflow obstruction (1, 24, 25). -v; HI. Diagnosis A. Clinical Assessment A complete history and physical examination should be performed during the initial assess-' ment of each patient suspected of haying COPD, and repeated on those occasions when the condition of the patient changes (e.g., hos-. pitalization). Limited histories and physical examinations should be performed at inter vals to evaluate the course of the disease and the response to therapy. . Characteristically, COPD affects middle- aged and older persons. The dyspnea due COPD cannot be reliably distinguished fro that due to other causes, and is frequently., associated with cough, wheezing, sputum production, and recurrent respiratory infefr tions. Occasionally, dyspnea is the only symp tom of COPD. In this situation it is insidious in onset and progressive in severity. Long-term^ cigarette use is the principal identified cause . of COPD, but these disorders do not occur exclusively in cigarette smokers and the" majority of smokers do not develop clinically;;' manifested lung disease (26). Inhaled toxins^ encountered in the workplace or in the envJ-| ronment pose additional risk factors for the;. _ development of COPD and a history ofsuch* j exposures should be sought. The inherited deficiency of plasma alpha-l-antiproteas* renders the patient more susceptible to tb . damaging effects of cigarette smoke and- predisposes to the early development COPD (13, 27, 28). Physical examination of patients COPD may reveal signs oflung overinflatioA;v. increased respiratory muscle effort, alteted,^ breathing patterns, and abnormal breathy sounds. Wheezes, especially on forced ratory and diminished breath sounds, may b> detected by auscultation. One or more ofthe *5 j 1` i. 1 r i: 2 e 1 v. d S a ii 0 tl Pg tl fe lt P O; ai di $r tr tii b\ nu ni Ci sh ex fo te: cli tin 30 thv sta in ma an- ( ere. urn ity I ;? micv' astht pccto- / sspu- S ironic m this excess use of bronan ex- ssspu- * of the ! bron:d etio availects of ' those nerous i s have etween , hyper- ly, Iondied to gh and eve) op25). \ .inati' 1 lasse. having ns when _> .g.,hos-': Physical 11 at interaseand middle- y1 a due to .. ed from . .quently ;, sputum j-ry infec-'l Iysymp- 5 nsidious jng-tenn . ed cause ot occur and the clinically v. :d toxins'; the envis for the j yof such ; * inherited t l iproteasejA le to the ;*! oke and ; 1 menr f { ;S Witu ' A fiation,!)| altered.^ breath a$ :d expi- y| maybe q of these AMERICAN THORACIC SOCIETY 227 physical signs are usually present in patients with advanced COPD, but the changes on physical examination may be sufficiently sub tle as to be overlooked even in the presence of moderate airflow limitation. The need for consv'mtive services may arise anytime the cond:::on of the patient deteriorates. B. Laboratory Tests ], Roentgenographic examination, A plain chest roentgenograph in posterior-anterior and lateral projections is necessary for the evaluation of patients with suspected COPD since the presence of regional hyperlucency and vascular attentuation confirm the existenceofemphysema. With severe emphysema, overinflation is present often, and bullous le sions are fairly common. It is pertinent, how ever. that roentgenographic studies have limit sensitivity for the detection ofemphy sema, and that the correlation of roentgeno graphic abnormalities with the severity of air flow obstruction or of anatomic emphysema is imperfect. Specialized studies such as com puted tomography are not usually necessary in patients with uncomplicated COPD. 2. Pulmonary function testing. Spirometric evaluation establishes the diagnosis ofCOPD. Testing should be performed by methods, and with instrumentation, that conform to stan dards established by the American Thoracic Society (29). The spirometric abnormalities asso ':^.ted with COPD consist ofa reduction in th. forced expiratory volume in one sec ond (FEV,) and in the ratio of the FEV, to the forced vita! capacity (FVC). Many other parameters may be calculated from the spiro gram (30, 31), but there is no evidence that they provide useful diagnostic information beyond that contained in the FEV, and FVC. It is desirable to perform spirometry in all patients who have unexplained dyspnea and/ or in whom COPD is suspected. It has been advocated that all individuals at risk for developing COPD (e.g., habitual cigarette smokers) be screened regularly by spirome try to detect mild abnormalities with the ra tionale that severe disease might be prevented by smoking cessation and early treatment measures. The efficacy of such programs has not been demonstrated. Repeat spirometric testing following medi cations (eg., bronchodiiators, corticosteroids) should be performed to determine to what extent the disease is reversible and to provide guidelines for rational therapy. The failureof forced expiratory flows to improve acutely af ter bronchodilator inhalation does not pre clude a long-term beneficial response to ei ther bronchodiiators or corticosteroids (10, 30, 32). The response of spirometric tests to the inhalation of bronchoconstrictor sub stances (e.g., methacholine) have been useful in asthma but their use in the diagnosis and management of COPD has not been defined, 2nd a role seems unlikely. COPD is frequently associated with an in crease in total lung capacity and residual vol ume, and a reduction in the diffusing capac ity for carbon monoxide (Dcco) (33). The measurement of lung volumes and of the Dlco may be helpful in the initial evaluation of patients suspected of having COPD. In sub sequent follow-ups, forced expiratory spirom etry alone usually suffices to demonstrate the response to therapy, or to explain symptom atic deterioration. COPD is also associated with abnormali ties in lung mechanics (e.g., compliance, air flow resistance), and abnormalities of vari ous tests of ventilation distribution (e.g., the single breath nitrogen washout test) have been described. The clinical relevance of these tests in the diagnosis and evaluation of COPD is unsettled, and their routine use is not recom mended. A reduction in exercise tolerance is com monly found in COPD, and routine evalua tion of exercise capacity is unnecessary. Such an evaluation may be indicated, however, when considering the need for supplemental oxygen therapy or when looking for additional causes of disability in patients whose exer cise tolerance seems out of proportion to the limitation of airflow. Any impairment in the efficiency of oxy gen uptake or carbon dioxide elimination by the lung can be detected by analysis of the arterial blood. COPD is characteristically as sociated with hypoxemia of varying severity and, in advanced stages, with hypercarbia. The efficacy of supplemental oxygen for pa tients with a defined degree of hypoxemia has been established. Arterial blood oxygenation should be assessed directly by measurement of Po* or indirectly by oximetry in ail patients with moderately severe airflow limitation (e.g., FEV, below 1.5 L) at the time of initial evalu ation, and subsequently, at appropriate in tervals. The adequacy of therapy in those pa tients receiving oxygen should be documented by repeated analyses. In patients hospitalized for respiratory insufficiency, frequent mea surements of arterial blood gases may be necessary to assess the adequacy of ventila tion and oxygenation, and to monitor acidbase balance. The methodology for measur ing arterial blood gases and for performing ear oximetry should conform to accepted lab oratory standards. 3. Additional laboratory tests. The need for other laboratory investigations in patients with COPD is defined largely by special cir cumstances and by complicating clinical con ditions. The detection ofsecondary erythrocytosis from periodic measurements of hemo globin or hematocrit levels suggests chronic hypoxemia and represents an indication to as sess the need for oxygen therapy. Addition al details about nocturnal hypoxemia are provided in the section on oxygen therapy. The presence or evolution of changes on the electrocardiogram consistent with right ven tricular enlargement suggests the need for ar terial blood gas analyses and supplemental oxygen. Many patients with severe COPD experi ence recurrent illnesses characterized by in creased cough and expectoration of purulent sputum. Although suspected of being infec tious in origin, the precise etiology of these episodes remains speculative. In the absence of clinical or radiographic signs of pneumo nia, bacterial or viral cultures of sputum usu ally provide little useful information. In a very small percentage of cases, COPD is associated with and is thought to result from a severe deficiency in the plasma level of alpha-l-antiprotease. Deficiencyof this inhib itor permits the early development of panacinar emphysema (13, 27, 28, 34). This genetic disorder should be suspected in patients who develop severe COPD at a relatively young age, especially if they have affected siblings or parents, and have smoked sparingly or not at all. The diagnosis can be made by mea surement of the serum alpha-I-antiprotease levels specifically, or by determining that the tiny sharp peak in the alpha 1-globulin re gion of the plasma electrophoretogram is ab sent. Quantitation of the alpha 1-globuiin fraction as usually reported from the auto mated densitometer readout of the serum pro tein electrophoretogram is worthless for di agnosing the deficiency since it is virtually always normal. Specific phenotype determi nations are desirable but not essential. At the present time, replacement therapy has not been completely assessed, and is not gener ally available. Thus, the practical implication of establishing this diagnosis, aside from admonishing against smoking, relates to its possible use in genetic counseling. Modestly reduced levels of alpha-l-antiprotease, asso ciated with the heterozygous deficient pheno type, do not pose a clear-cut risk of prema ture COPD (35). IV. Indications for Hospital Admission The principal indications for hospitalization of the patient with COPD include: (7) acute exacerbation of symptoms such as markedly increased dyspnea, cough, and sputum pro duction that have not responded to adjust ments in ambulatory care, (2) acute respiratory failure characterized by respiratory distress, hypercarbia, or worsening hypoxemia, (3) acute cor pulmonale with dependent edema, further impairment of exercise capacity, and hypoxemia, (4) complications of COPD such as acute bronchitis or pneumonia, (5) the per formance of invasive diagnostic procedures on the Jung such as bronchoscopy, transbronchial biopsy, or needle aspiration of nodules, (6) the need for surgery or other procedures that require significant amounts of analgesics, or anesthesia, and (7) diseases that might not require hospitalization by themselves, but that in the presence of severe COPD represent a significant risk to the patient. A continuing program of education is an important hospital function. Whenever pos sible the patient must know the schedule of each medication and understand its purpose. Guidelines for clinical response in the hospi tal include improvements in symptoms and signs, as well as in the results of spirometry and arterial blood gas analyses. Discharge Criteria Criteria for hospital discharge rest with im provement to the point that the patient is able to care for his personal needs and manage his medication, or that these requirements can be arranged for outside the hospital. References 1. Fletcher C, Peto R, Tinker C, Speizer FE. The natural history of chronic bronchitis and emphy sema. Oxford: Oxford University Press, 3976. 2. Laennec RTH. A treatise on diseases of the chest. Translated from the French by John Forbes. London: T. and C. Underwood, 1981. 3. Otis AB, Fenn WO, Rahn H. Mechanics of breathing in man. J Appl Physiol 1950; 2:592-607. 4. Harvey RM, Ferrer MI, Richards DW Jr, Cournand A. Influence of chronic pulmonary disease on the heart and circulation. Am J Med 1953; 10:719-38. 5. Fry DL, Ebert RV, Stead WW, Brown CC. The mechanics of pulmonary ventilation in normal sub jects and in patients with emphysema. Am J Med 1954; 16:80-97. 6. Bates DV. Chronic bronchitis and emphysema: the search for their natural history. In: Macklero PT, Permutt S, eds. The lung in transition between health and disease. New York: Marcel Dekker, 1979; 3-13. 7. Aspen Conference Report of committee on def inition of emphysema. Am Rev Respir Dis 1959; 79(Part II):114. 8. Ciba Guest Symposium Report. Terminology, definitions and classification of chronic pulmonary emphysema and related conditions. Thorax 1959; 14:286-99. 9. Fletcher CM, Pride NB. Definitions ofemphy sema, chronic bronchitis, asthma, and airflow ob struction: 25 years on from the Ciba Symposium. Thorax 1984; 39:81-5. 10. Ramsdell JW, Nachtwey FJ, Moser KM. Bron chial hyperreactivity in chronic obstructive bron chitis. Am Rev Respir Dis 1982; 126:829-32. 11. American Thoracic Society. Definitions and classification of chronic bronchitis, asthma, and pulmonary emphysema. Am Rev Respir Dis 1962; 85:762-8. 12. National Heart, Lung, and Blood Institute, Division of Lung Diseases Workshop Report. The definition of emphysema. Am Rev Respir Dis 1985; 132:182-5. 13. Carrell RW, Jeppsson JO, Laurel! CB, et al. Structure and variation of human alpha-1antitrypsin. Nature 1982; 298:329-34. 14. Mitchell RS, Stanford RE, Johnson JM, Sil vers GW, Dart D, George MS. The morphologic features of the bronchi, bronchioles, and alveoli in chronic airway obstruction: a clinicopathologic study. Am Rev Respir Dis 1976; 114:137-45. 15. Cosio M, Ghezzo H, Hogg HC, et at. The re lations between structural changes in small airways and pulmonary function tests. NEngi J Med 1977; 298:1277-81. 16. Nagai A, West WW, Thurlbeck WM. The Na tional Institutes of Health Intermittent positivepressure breathing trial: Pathologystudies II. Corre lation between morphologic findings, clinical find ings, and evidence of expiratory-airflow obstruc tion. Am Rev Respir Dis 1985; 132:946-53. 17. Hentel W, Longfield AN, Vincent T, Filley GF, Mitchell RS. Fatal chronic bronchitis. Am Rev Respir Dis 1963; 87:216-27. 18. Simpson T, Heard B, Laws JW. Severe irre versible airways obstruction without emphysema. Thorax 18:361-70. 19. Thurlbeck WM. Chronic airflow obstruction in lung disease. In: Major problems in pathology. Vol. V. Philadelphia: W. B. Saunders, 1978. 20. Niewoehner DE, Kleinerman J, Rice DB. Pathologic changes in the peripheral airways of young cigarette smokers. N Engl J Med 1974; 291:755-8. 21. Wright JL, Lawson LM, Pare PD Kennedy S, Wiggs B, Hogg JC. The detection of small air ways disease. Am Rev Respir Dis 1984; 129:989-94. 22. Thurlbeck WM. Aspects of chronic airflow obstruction. Chest 1977; 72:341-9. 23. Thurlbeck WM. Chronic airflow obstruction: correlation of structure and function. In: Petty T, ed. Chronic Obstructive Pulmonary Disease. 2nd ed. New York: Marcel Dekker, 1985; 129-203. 24. Bates DV. The fate of the chronic bronchitic: a report of the ten-year follow-up in the Canadian Department of Veterans Affairs coordinated study of chronic bronchitis. Am Rev Respir Dis 1973; 108:1043-65. 25. Sharp JT, Paul O, McKean H, Best WR. A longitudinal study of bronchitic symptoms and spirometry in a middle-aged, male, industrial popu lation. Am Rev Respir Dis 1973; 108:1066-77. 26. Buist S, Ducic S. Smoking: evaluation of studies which have demonstrated pulmonary func tion changes. In: Macklem PT, Permutt S, eds. The lung in transition between health and disease. New York: Marcel Dekker, 1979; 271-86. 27. Tobin MJ, Cook PJ, Hutchinson DDS. Al pha 1-antitrypsin deficiency: the clinical and phys iological features of pulmonary emphysema in sub jects homozygous for Pi type Z: a survey by the British Thoracic Association. Br J Dis Chest 1983; 77:14-27. 28. Janus ED, Phillips NT, Carrell RW. Smok ing, lung function and alpha 1-antitrypsin defi ciency. Lancet 1985; 1:152-4. 29. American Thoracic Society. Snowbird work shop on standardization of spirometry. Am Rev Respir Dis 1979; 119:831-8. 30. Knudson RJ, Burrows B, Lebowitz MD. The maximal expiratory flow-volume curve: its use in the detection of ventilatory abnormalities in a popu lation study. Am Rev Respir Dis 1976; 114:871-9. 31. Knudson RJ, Lebowitz MD. Comparison of flow-volume and closing volume variables in a ran dom population. Am Rev Respir Dis 1979; 116: 1039-47. 32. Eaton ML, Green BA, Church MS, McGow an T, Niewoehner DE. Efficacy of theophylline in "irreversible" airflow obstruction. Ann Intern Med 1980; 92:758-61. 33. Bates DV, Macklem PT, Christie RV. Respira tory function in disease. 2nd ed. Philadelphia: W. B. Saunders, 1971. 34. LarssonC. Natural history and life expectancy in severe alpha 1-antitrypsin deficiency. Pi Z. Acta Med Scand 1978; 204:345-51. 35. Bruce RM, Cohen BH, Diamond EL, et al. Collaborative study to assess risk of lung disease in Pi M2 phenotype subjects. Am Rev Respir Dis 1984; 130:386-90. CHAPTER 2 Asthma I. Definition Asthma is a clinical syndrome characterized by increased responsiveness of the tracheo bronchial tree to a variety of stimuli. The ma jor symptoms of asthma are paroxysms of dyspnea, wheezing, and cough, which may vary from mild and almost undetectable to severe and unremitting (status asthmaticus) The primary physiological manifestation of this hyperresponsiveness is variable airways obstruction. This can take the form ofspon taneous fluctuations in the severity of obstruc tion, substantial improvements in the severity of obstruction following bronchodilators or corticosteroids, or increased obstruction caused by drugs or other stimuli. Histoiogically, patients with fatal asthma have evidence of mucosal edema of the bronchi; infiltra tion of the bronchial mucosa or submucosa with inflammatory cells, especially eosino phils; and shedding of epithelium and ob struction of peripheral airways with mucus. II. Diagnosis The diagnosis of asthma can occasionally be confusing because of its overlap with COPD. In addition, the diagnosis of asthma is occa sionally confused with other causes of air way obstruction such as tumors, foreign bod ies, laryngospasm, or even cardiogenic pul monary edema. Patients with COPD may have significant reversibility after treatment and patients with asthma may develop air flow obstruction with little to no reversibil ity. The separation of these overlap patients is often arbitrary and difficult, and from a ' clinical standpoint probably not important unless the diagnosis has therapeutic implica- '.. i tions, i.e., the bronchospasm results from a specific and avoidable etiologic agent. A. Clinical Assessment The symptoms of episodic cough, wheezing, . and dyspnea suggest a diagnosis of asthma. The history should explore these symptoms 1 in detail including: (J) family and personal history of allergic disease, (2) age at onset of ; symptoms, and frequency and severity of at tacks, (3) known provocative stimuli (table 1), and (4) prior pharmacologic and immunologictherapy, Initialsymptomsmaybeavague heavy feeling or tightness in the chest accora* ' panied in the allergic patient by rhinitis and ; conjunctivitis. The patient may complain of a nonproductive cough followed by wheezy ing and dyspnea. Although initially non*..>; productive; the cough frequently does become r productive of a viscous, mucoid sputum that. may contain casts of the distal airways or may ' appear purulent. A subset of patients with $ asthma are characterized by recurrent of chronic nonproductive cough without overt wheezing (1). .~y%% In the asymptomatic patient, the exanun*v -* tion of the chest may be normal, although. examination of the eyes, ears, nose, and may reveal concomitant serous otitis conjunctivitis, rhinitis, nasal polyps, PaI?j*~S nasal sinus tenderness, and signs ofposnas.4|j| drip, including pharyngeal mucosal lymph ,||| hyperplasia. In mild asthma, wheezing only be detected on forced expiration. . increasing degrees of severity, wheezing AMERICAN THORACIC SOCIETY 229 ezing, ; thma. . " ptoms ; rsonal.. lsetof of at- 'Su itable >; TABLE 1 STIMULATORS OF BRONCHOCONSTRICTION A. Nonspecific 1. Exercise 2. Cold air 3. Environmental pollutants and irritants 4 Pharmacologic agents, i.e., histamine, cholinergic agonists 5. Reflux esophagitis B. Specific 1. Aspirin and all nonsteroidal anti-inflammatory drugs (NSAID's) 2. Occupational antigens 4. Ingested antigens 5. Beta-adrenergic antagonists be heard on quiet expiration and on inspira tion. The findings of severe airways obstruc tion include restlessness, agitation, orthopnea, tachypnea, breathing through pursed lips with apr ' mged expiratory phase, using accessory musCies of respiration, diaphoresis, coughing, audible wheezing, and difficulty speaking. In the acutely ill asthmatic, the abatement of wheezing may occur with increasing severity of airways obstruction and must not be taken as a clinical sign of improvement. The evalua tion of the blood pressure may reveal that the patient has a widened pulse pressure, and a pulsus paradoxus (10 mm Hg or greater) may be present. The latter sign is a relatively reli able indicator of the severity of the asthma, the FEV, almost always being less than 40% predicted in this situation (2). The presence of fc - t is indicative of an infectious compli cation such as pulmonary infection. The tho rax is often hyperinflated. Patients with asthma and persistent sinusi tis and nasal polyposis with or without mid dle ear disease frequently benefit from an evaluation by an otorhinolaryngologist. Ag gressive management of sinusitis and correc tion of upper airway obstruction may improve the asthmatic condition. Patients with poorly controlled asthma requiring hospitalization should be evaluated by a specialist in pulmo nary disease or allergy. The accurate recogni tion of the importance of allergic disease in the asthmatic syndrome may require consul tation with a physician skilled in testing for allergic diseases. B. Laboratory Tests l. Pulmonary function tests. Spirometric studies of pulmonary function are valuable both in the diagnosis of asthma and in as sessing the severity of the disease and the re sponse of therapy (3). Spirometry and peak flow measurements are also useful on a regu lar basis during outpatient management. All measi able parameters of pulmonary function may be within normal limits when the patient with asthma is in remission. If the diagnosis Is suspected, bronchial provocation testing utilizing a cholinergic agonist, histamine, cold mr, or specific antigens or industrial agents may demonstrate significant airways obstruc tion with a quantifiable stimulus known to be tolerated by a normal individual (4). Induced airways obstruction may be severe and delayed for up to 24 h. Hospitalization may be war ranted when this approach is taken (see Indi cations for Hospital Admission). When preexisting airways obstruction is noted, bron chial provocation is contraindicated. The typical abnormalities noted with spi rometry in the asthmatic patient include a reduction in FEV,, peak expiratory flow rate, FEVj/FVC ratio, and an increase of 15% or greater in the FEV, in response to a bronchodilator. (Patients with asthma may not im prove their FEV, in response to bronchodilators during episodes of severe airways obstruc tion.) Abnormalities in lung volumes include a decreased vital capacity, an increase in func tional residual capacity, total lung capacity, and especially in the residual volume; how ever, it is not necessary to measure lung volumes in order to make the diagnosis of asthma. 2. Arterial blood gases. The measurement of arterial blood gases may be helpful in de termining the severity of disease in the hos pitalized patient. Hypercapnia and respira tory acidosis implies severe disease with FEV, ofless than 15% of predicted (5). Under these circumstances, frequent monitoring of arterial blood gases is essential in patient manage ment. Signs and symptoms of hypoxemia, such as cyanosis, are unreliable and should not be substituted for actual blood gas deter minations. With milder bronchospasm, the arterial blood gases usually reflect a respira tory alkalosis, with a near normal Po, and a widened alveolar-arterial oxygen gradient. In these milder cases the Po2 and Pco2 are relatively insensitive indicators ofairways ob struction (6). Normalization of the pH and Pcoj in the face of a falling Po2 usually indi cates worsening obstruction with an FEV, less than 25% of predicted. 3. Bloodleukocytes. Peripheral eosinophilia is common in both allergic and nonallergic forms of asthma; consequently, this parame ter cannot be used as a differentiating point between the two. Values of 5 to 15% of the total white blood cell count are common. To tal eosinophil counts provide a more accurate measure of peripheral eosinophilia. Although leukocytosis may suggest the presence of infection, leukocytosis with marked eosinophilia (greater than 3,000 per cubic mm) should raise the possibility of another diag nosis, such as Loffler's syndrome, the hypereosinophilic syndrome, allergic bronchopul monary aspergillosis, or Churg-Strauss aller gic granulomatous angiitis. 4. Sputum. Grossly purulent sputum may reflect eosinophilia rather than PMNs as sociated with infection. In this situation, mi croscopy may document eosinophilia, Curschmann's spirals, and Charcot-Leydon crys tals, all consistent with the diagnosis of asthma. 5. Electrocardiography. The electrocar diogram is of little value in the diagnosis or management of asthma. ECG changes are usually noted only in severe acute attacks of asthma, are nonspecific in nature, and include sinus tachycardia and rarely ventricular strain pattern and right axis deviation. 6. Radiology. The chest radiograph is not helpful for the diagnosis of asthma or for de termining the severity of the acute attack (7). It may be helpful in evaluating potential com plications of asthma, such as rib fractures, pneumothorax, pneumomediastinum, atelec tasis, and pneumonia. Paranasal sinus films may be of use in evaluation of the patient thought to have concomitant allergic rhinitis and sinusitis. 7. Measurement of serum IgE. A large proportion of the allergic asthmatic popula tion has normal IgE levels, and many condi tions other than asthma are associated with elevated IgE levels. Therefore, the usefulness of obtaining a serum IgE measurement in pulmonary conditions other than allergic bronchopulmonary aspergillosis has not been established. 8. Detection of IgE antibody. Tests to de tect antigen-specific IgE are indicated when the asthma is thought to be due to an iden tifiable and avoidable substance. Bronchial provocation testing with specific antigens (8) can also be used to demonstrate bronchial reactivity and is useful in the evalu ation of (I) the asthmatic patient with inter mittent episodes of asthma who presents for evaluation in the asymptomatic stage, and (2) a patient with suspected occupational asthma, since the use of skin testing in occupational asthma is complicated by a lack of specific antigens and the nonspecific irritating effect of the available antigens on the skin. Immediate-type hypersensitivity skin test ing remains the most important tool for the detection of IgE antibody and confirms the clinical suspicion of an allergic component to the patient's asthma as elicited by the his tory. Skin tests, which are done by prick, scratch, or intradermal methods, must be in terpreted in the light of a well-taken history, as false positive results may occur. A diagno sis of specific allergy should rarely be made in the absence of a correlating positive his tory. Skin testing is safe, sensitive, and use ful for the evaluation of allergy to inhalant aeroallergens that may be a trigger in airways obstruction. The RAST (Radioallergosorbent test) as say or ELISA (enzyme linked immunosorbent assay) permit the in vitro evaluation and semi quantitation of antigen-specific IgE antibod ies in serum (9). These tests correlate well with clinical provocation testing and are free of / 230 AMERICAN THORACIC society'' the risk of systemic reactions. They may be useful when the patient is currently receiving forms of symptomatic therapy that alter the interpretation of skin tests. Disadvantages in clude expense, a lag in the time from testing to the availability of results (at least 48 h), a lesser availability of potential antigens that may be utilized compared with skin testing, a decreased sensitivity, and the potential mis use of these assays by physicians not engaged in the evaluation of patients with allergic dis ease. III. Indications for Hospital Admission A. Diagnosis In general, the diagnosis of asthma or asth matic syndromes can be firmly established in outpatients. However, when inhalational challenge testing with environmental allergens or occupational substances are to be ad ministered and there is reason to believe a late response (one which occurs 4 h or later after inhalation) may occur, hospitalization may be required to firmly and safely establish a diagnosis (7, 10). The hospital facilities are used in this circumstance to confirm and quantitate obstructive airways dysfunction at a time of day that may preclude testing as an outpatient. Another indication for hospi talization is to establish a diagnosis of asthma when diagnostic challenge testing is planned in patients with possible or probable com plicating medical illnesses, such as cardiac dis ease, where close monitoring of cardiopul monary status is advisable. B. Treatment 1. Treatment oftheprimary disorder. Hospi talization for the treatment of asthma is in dicated for the acute onset of symptoms or physiological changes that are so severe as to preclude successful initial management as an outpatient or in an emergency room (1-5,7). This indication is more likely to occur in pa tients in whom the diagnosis of asthma had not been previously established, in patients who have not previously required treatment, or in patients whose treatment requirements have recently changed. Another indication is exacerbation of symptoms in individuals who are undergoing therapy as outpatients but in whom the control of symptoms or physio logical changes is such that outpatient man agement is no longer feasible. Rather than defining specific physiological or clinical cri teria for admission, the criteria should be the failure or probable failure ofoutpatient man agement as judged by the physician (11-16). Hospitalization is recommended for initi ation of therapy in asthmatic subjects with serious complicating medical conditions such as cardiac disease or pregnancy (17), depend ing on the severity of the asthmatic condi tion or the underlying medical complication. Hospitalization may be indicated for the purpose of removing the patient in exacerba tion from an unfavorable environment when there is substantial reason to believe that the environment is contributing to the patient's condition. 2. Treatment of complications of the pri mary disorder. In addition to treatment of the asthmatic condition itself, a number of complications may arise that require hospi talization. These include serious infectious complications such as acute bronchitis, pneu monia, or sinusitis. Hospitalization is also in dicated for treatment of pneumothorax and pneumomediastinum. Hospitalization may be indicated for the treatment of iatrogenic com plications of the primary disorder, including medication overdose or severe adverse reac tion to medication, and complications of stan dard treatment, including severe side effects from steroid therapy, both acute, such as hyperglycemia or fluid retention, and chronic, including opportunistic infections, ocular, and skeletal complications. In the case of pa tients with status asthmaticus requiring treat ment with mechanical ventilation, there may be complications of the mechanical ventila tion, including disorders of the trachea or per sistent bronchopleural fistula, which may re quire prolonged hospitalization or readmis sion (18). 3. Treatment ofasthma in association with other disorders. Hospitalization may be in dicated prior to elective surgery or invasive diagnostic tests for the asthmatic subject who has required chronic treatment (19). The du ration of the in-hospital treatment would be proportional to the severity of the patient's disease and the likelihood of the surgery to result in respiratory insult, but usually would be 2 to 5 days. Asthma may be a factor that contributes to prolonged hospitalization in patients with non-pulmonary medical or sur gical disease. The combination of asthma with other forms of pulmonary disease may also extend the duration of required hospitaliza tion beyond that of the simple disorder; the duration of additional hospitalization will vary with the severity of the patient's asth matic condition. IV. Discharge Criteria In patients admitted to the hospital for the purpose of establishing a diagnosis of asthma, discharge is indicated when the diagnosis has been established, the diagnostic procedure has been completed, appropriate treatment be gun, and the patient's condition is stable. In those cases in which a diagnosis cannot be established but in which asthma has been reasonably excluded as a diagnostic possibil ity, discharge would be indicated depending upon the patient's overall condition. In patients admitted for the treatment of asthma as a primary diagnosis, discharge is indicated when a stable treatment regimen using oral or inhaled medications has been both established and demonstrated effective for 24 to 48 h after withdrawal of intravenous medications. Further, these patients should have documented clinical and physiological improvement (comparing the time of their ad mission to discharge) consistent with them pursuing activities of daily life. Subsequent monitoring of spirometry or peak flows af ter discharge is important in the patient's rou tine management. When complications ofth disease are the indication for admission, then appropriate diagnosis and treatment of these I complications should be instituted prior to fi discharge. This does not necessarily mean that t the treatment must be completed, but rather $ it must be demonstrated that an outpatient regimen is sufficient for the condition diag. nosed. In patients with pneumothorax and ; pneumomediastinum, the associated radio* - graphic changes must be demonstrated to have : improved or stabilized with implementation of a stable medical regimen. In circumstances in which complications arising from medica- tions were the indication for admission, these complications must be shown to be resolving or to have resolved prior to discharge. In dr- cumstances where the patient was admitted for other disorders but in which asthma oc- : curs in association with those disorders, the recovery from the primary disorder, or elec- tive surgery, must have progressed to the point where discharge is usually considered; at that - time the asthmatic symptoms must be under - control using oral or inhaled medications that ` can be administered by the patients or their families. In all hospitalized patients with asthma, definite plans for follow-up care are . an essential part of the management. ' References - 1. Corrao WM, Braman SS, Irwin RS. Chronic cough as the sole presenting manifestation ofbron- ` chial asthma. N Engl J Med 1979; 300:633-7. 2. Rebuck AS, Pengelly LD. Development of ; pulsus paradoxus in the presence of airways ob- - struction. N Engl J Med 1973; 288:66-9. 1 3. Gold WM. Clinical and physiologic evaluation of asthma. Chest 1985; 87(Suppl:30S-2S). : 4. Gershel JC, Goldman HS, Stein REK, Shelov SP, Ziprkowski M. The usefulness of chest radiographs in first asthma attacks. N Engl J Med 1983; 309:336-9. . ' 5. Tai E, Read J. Blood gas tensions in bronchial asthma. Lancet 1967; 1:644-6. 6. McFadden ER Jr, Lyons HA. Arterial-blood ' gas tension in asthma. N Engl J Med 1968; 278: . 1027-32. ; 7. Pepys J, Hutchcroft BJ. Bronchial provocation tests in etiologic diagnosis and analysis of asthma. ; Am Rev Respir Dis 1975; 112:829-59. - 8. Hargreave FE, Dolovich J, Boulet LP. Inhala- ; tion provocation tests. Semin Respir Med 1983; j 4:224-36. ' v. , 9. Wide L, Bennich H, Johansson SGO. Diagno- ' sis of allergy by an in vitro test for allergen anti- . bodies. Lancet 1962; 2:1105-7. . . ; 10. Pratter MR, Irwin PS. The clinical value of pharmacologic bronchoprovocation challengeChest 1984; 85:260-5. 11. McFadden ER Jr, Kiser R,deGrootWJ. Acute . 7 i bronchial asthma: relations between clinical and physiologic manifestations. N Engl J Med 1973; 288:221-5. .:7 7 12. Banner AS, Shah RS, Addington WW. Rapid . prediction of need for hospitalization in acute :. asthma. JAMA 1976; 235:1337-8. 7 13. KelsenSG.Kelsen DP, FleeglerBF, Jones RC. J Rodman T. Emergency room assessment and treat ment of patients with acute asthma: adequacy of the conventional approach. Am J Med 197?. _ ^eRlCAN THORACIC SOCIETY 231 It:r if l id o- ve )n es a- :$e. ng ired )c-he. ec-: l!int hat der hat ieir dth_ .. are . 7 ; ob-. b ition ielov adio1983; ichial '7 .. jlood. '7' ; 278: ,_v nation thma. "r4>i \*f vi ihala- ;* 1983; I . '-Ml iagno-1.;> r anti > ;* .lue of llenge. -gf' . Acute *^j :al and "& * 119: top** &->] i acute mI aes RC, 'J|| td treat-_a"' uacy of i 1978; ;622-$. 4 Fischl MA, Pitchenik A, Gardner LB. An in dex predicting relapse and need for hospitalization in patients with acute bronchial asthma. N Engl j Med 1981; 305:783-9. jj Arnold AG, Lane DJ, Zapata E. The speed of onset and severity of acute severe asthma. Bf j pis Chest 1982; 76:157-63. 16. Centor RM, Yarbrough B, Wood JP. Inabil ity to predict relapse in acute asthma. N Engl J Med 1984; 310:577-9. 17. Turner ES, Greenberger PA, Patterson R. Management of the pregnant asthmatic patient. Ann Intern Med 1980; 93:905-48. 18. Kingston HG, Hirshman CA. Perioperative management of the patient with asthma. Anesth Analog 1984; 63:844-55. 19. Westerman DE, Benetar SR, Potgreter PD, Fer guson AD. Identification of the high risk asthmatic patient. Experience with 39 patients undergoing ventilation for status asthmaticus. Am J Med 1979; 66:565-72. CHAPTER 3 Pharmacologic Therapy (. Introduction The use of pharmacologic agents is an im portant part of the management of patients with obstructive airways diseases, both dur ing exacerbations and during interim periods ofstability. This section will discuss the prin cipal pharmacologic agents and their use in the therapy of asthma and COPD. The infor mation in this chapter is based upon current medical knowledge, and, where controversy exists, upon accepted medical practice. The authors recognize that the following recom mendations may need to be revised as new information appears. II. Therapeutic Agents 1. Bela-adrenergic agonists. The sympathomi metic bronchodilators are the keystone of therapy in patients with obstructive airways disease. Because they can improve mucociliary clearance and serve prophylactically to pro tect against bronchospasm produced by vari ous stimuli, they may be of value even if they do not result in improvement of spirometric responses on pulmonary function testing. Aerosol formulations provide the optimal therapy for chronic outpatient use (1). In most patients, the metered-dose inhaler (MDI) is preferred, whereas for inpatient therapy pow ered nebulizers are often used (see Respi ratory Care Modalities, Chapter 5). Oral preparations are falling into disfavor, since they are no more effective than aerosols In most patients and they cause more side ef fects (2). Appropriate oral dosages are diffi cult to establish in Individual patients, since variables in bowel absorption and first-pass metabolism may markedly reduce the frac tion of the drug that enters the circulation Jn an active form. Aerosol dosages are easier to titrate, result in a more rapid onset of bronchodilation than oral preparations, and achieve a comparable peak response and per sistence of effect with a decreased incidence of tremor, nervousness, and palpitations. Fur thermore, aerosol bronchodilator delivery is more effective than oral dosing in the pro phylaxis of exercise-induced bronchospasm. Although many patients are unable to use the MDI optimally, repeated instruction results in a satisfactory outcome in the ma jority of cases (3). There is a small group of patients who fail to learn to use their MDI effectively, and for them the addition of a large volume reservoir or spacer can be ad vantageous (4). Optimal use of an MDI results in not more than 10% of the dose being deposited in the lung, while as much as 85% is deposited in the oropharynx. The use of a large volume reservoir may increase the amount deposited in the lungs to 15%, while reducing the oropharyngeal deposition to 5%. In contrast, a typical powered nebulizer unit will result in about 10% of the initial dose being depos ited in the lung, whereas only about 10% will be deposited in the mouth and pharynx; about 80% of the dose remains in the apparatus or is lost in the atmosphere (5). The actual amounts deposited will be determined by the apparatus used, the breathing technique, and the length of the treatment session, and there fore considerable variability in the effective dosage can result. The manufacturers' recommended dosages for use in powered nebulizers are compara ble to the oral dosages, and both are many times greater than the dosage delivered by the typical 2 or 3 actuations of an MDI (table 1). Since patients using powered nebulizers or oral tablets usually tolerate these much larger dosages, it is reasonable to evaluate the effect of increasing the number ofpuffs from an MDI beyond the customary 8 to 12 per day up to 16 to 24, and to add a large volume reservoir, before deciding to add an oral betaadrenergic drug to the regimen or to change to a powered nebulizer. The older sympathomimetic agents ephedrine, epinephrine, and isoproterenol have been generally replaced by the newer, longer act ing, more beta-2 specific bronchodilators (ta ble 1). Metaproterenol, albuterol, terbutaline, and bitolterol are mainly used as aerosols, but oral preparations of the first 3 are available and terbutaline can be given subcutaneously. In Europe, additional agents that are in use include fenoterol, pirbuterol, clenbuterol, reproterol, and rimiterol. Metaproterenol, al buterol, terbutaline, and bitoleroi, when given as aerosols, appear to be comparable enough in potency, length of action and side effects such that when used in recommended doses, they can be used serially or interchangeably. Individual patient preference and cost may be the best determinants for selecting one for chronic use. Intravenous sympathomimetic bronchodi lators have been recommended by physicians in Europe for treating severe bronchospasm, but experience in their use is limited. Only isoproterenol is available for intravenous use in the U.S. and it is not approved by the FDA for treatment of bronchospasm. 2. Theophylline. Theophylline is usually given orally as sustained-release formulations for chronic maintenance therapy. Although the benefits of theophylline are difficult to prove in patients with COPD, its use is fa vored by most clinicians when appropriately used sympathomimetic agents fail to produce adequate bronchodilation. Twice-a-day ad ministration is generally adequate, although some patients are better controlled ifthe daily dose is given in 3 equal portions. Recently, some formulations have been demonstrated to provide effective airway dilation when given once a day to patients with less severe asthma. The reliability of longer-acting preparations can be ofconcern; established products should be favored, and their optimal bioavailability ensured by giving them before meals. Although some patients respond adequately when their theophylline serum levels are as low as 5 mcg/ml, most require 8 to 20 mcg/ml. A major problem with theophylline is that some patients experience toxic symptoms while blood levels are in the therapeutic range (6). The main side effects are nervous ness and tremor resulting from the endoge nous release of cathecholamines that theoph ylline causes, and gastrointestinal symptoms. When a patient begins to use theophylline, a relatively low dosage schedule should be selected; the theophylline serum level can be checked after a few days, and the dosage ad justed appropriately to maintain adequate bronchodilation without associated side ef fects. Therapeutic serum levels of theophyl line on stable doses of a sustained-release oral TABLE 1 SYMPATHOMIMETIC AGENTS Drug Recommended Dosage per Treatment Subcutaneous MDI Nebulizer* Oral (mi) (mg) (mg) (mg) Duration Of Action (A) Epinephrine (1MOOO solution) isoproterenol (soetharine Metaproterenol Albuterol Terbutaline Bitolterol 0.1-0.5 -- \\_ 0.25-0.5 - 0.32-0.9 0.16-0.39 0.68-1.02 1.3-1.95 0.18-0.27 0.4-0.6 0.37-1M 2.5-22 0.63-3.8 1.25-5 10-15 -- - - 5-20 1-4 1.25-5 - 1-2 1-2 2-3 3-4 4-6 4-6 4-6 ' Dosages vary widely. These are typical treatment doses, usually given at intervals of -6 h. | ( J .. : 1 ! ' , 232 AMERICAN THORACIC SQC^ theophylline preparation occur for about 8 to 12 h in most adults (7). The dosage of oral theophylline for the av erage nonsmoking, reasonably healthy adult is 10 to 12 mg/kg/day (e.g., 400 mg twice a day). Smokers may require up to 50% larger dosages, whereas hypoxemic patients or those with liver insufficiency may require a 25 to 50% reduction in dosage. If cimetidine therapy is given, the serum level of theophyl line may be rapidly increased by as much as 30 to 50%; the related agent ranitidine has little effect on serum theophylline levels (8). Many drugs (e.g., erythromycin) and other en vironmental conditions (e.g., diet, hydrocar bon exposure, illness) affect theophylline clearance, and a serum level determination is indicated when a serious environmental or health change alters the control of the bronchospasm. Aminophylline contains about 80% the ophylline solubilized by the addition ofethylenediamine. The latter can rarely cause hyper sensitivity reactions in susceptible patients. Aminophylline or theophylline can be given intravenously in critically ill patients, as is dis cussed later. 3. Anticholinergics. Atropine was used for many years for the management of asthma, but with the availability of potent beta-ad renergic agonists its use declined in the U.S. In recent years there has been an increased interest in inhaled atropine sulfate, especially for patients with chronic bronchitis associated with bronchospasm, although its use as a bronchodilator is not approved by the FDA (9). Atropine is usually given by powered nebulizer, often in combination with a betaadrenergic agent. Its side effects include tachy cardia, dryness of the oral mucosa, blurred vision, urinary obstruction, and constipation. Ipratropium bromide, a quaternary ammo nium derivative of atropine, is bronchoselective when delivered by inhalation (10). It is relatively free of systemic side effects because it is minimally absorbed into the systemic cir culation and does not cross the blood-brain barrier. It has been shown to be an effective bronchodilator in patients with COPD and in selected patients with asthma both alone and when used concomitantly with beta-2 agonists and theophylline (10). When ad ministered via MDI aerosol, the recommended dose is 2 puffs (40 meg) 4 times daily. 4. Cromolyn. Cromolyn is neither a bron chodilator nor an antagonist of anaphylactic mediators. However, it has been shown to in hibit histamine release from mast cells (11, 12). Cromolyn is poorly absorbed when given orally and must be given by inhalation, ei ther as a powder or as an aqueous solution available for nebulization and more recently as an MDI. Its advantages are its lack of tox icity and its effectiveness in preventing asthma when used properly, especially in younger pa tients. A trial period of 4 to 6 wk may be re quired to determine its usefulness. Cromo lyn has been found to be effective in prevent ing exercise-induced bronchospasm (EIB) and for this condition its preventive effects are im mediate (13). Because of its irritating effects on the airways, the powder form of cromo lyn should not be used in acute asthma attacks. 5. Corticosteroids. Corticosteroids are use ful in the management of acute exacerbations of most cases of asthma and for a minority of cases of chronic airways obstruction (14, 15). They may be given orally or intravenously during acute attacks along with bronchodi lator agents. Both oral and inhaled corti costeroids may prove beneficial in prevent ing acute asthma attacks, and oral therapy can help improve airflow in some patients with COPD. Response should be monitored with objective tests such as FEVi or peak flows, and therapy should be continued only if sig nificant improvement occurs (13). Oral cor ticosteroids are associated with significant toxicity when administered chronically, but alternate-day dosing (in which the entire twoday dose is given once in the morning on alter nate days) can be effective in asthma with fewer side effects (16). It is important to use bronchodilators concomitantly in an effort to re duce or discontinue steroid administration. 6. Mucolytics and expectorants. The most troublesome area in pulmonary pharmacol ogy is the treatment of abnormal mucus (17). Sympathomimetic bronchodilators and the ophylline offer the advantage of stimulating mucociliary clearance, and these drugs are in dicated for any obstructive disease syndrome that is accompanied by impaired mucokinesis. There is also evidence that corticosteroid therapy can improve mucokinesis in bronchitis and asthma. Inhaled atropine does not ad versely affect clearance, although systemic an ticholinergic and antihistamine therapy can impair mucociliary clearance. Oral expectorants are popularly used in over-the-counter preparations, e.g., guaifene sin, terpin hydrate, ammonium and other salts, iodide and ipecac. The only topical mucolytic available is n-acetylcysteine, which can be given by aerosol or instillation. The value of inhaled expectorants and mucolytic agents has not been demonstrated in objec tive studies (18). 7. Antibiotics. Although antibiotics have been used extensively for years to treat acute exacerbations of chronic bronchitis, as well as for prophylaxis in stable chronic bronchi tis, their value for either purpose has not yet been established (19-22). Bacterial infection or colonization of the trachea, bronchi, and small airways has been shown not to influence the natural history of COPD. It has been demonstrated repeatedly that the large air ways of most of these patients are colonized by the same aerobic bacteria that are found in the oropharynx (23, 24). TVvo organisms. Hemophilus influenzae and Streptococcus pneumoniae, have been cultured from spu tum and transtracheal aspirates more fre quently and in greater numbers from patients with acute exacerbations of chronic bronchi tis. The H. influenzae strains are almost al ways nonencapsulated and therefore ca^ be typed with specific antiserum, althc^t they can be studied biochemically and placM into "biotypes." Clinicians have prescribed short-term antimicrobial therapy directeda*, cifically against these 2 organisms. Thevalo. of such short-term treatment is difficult assess, although the few carefully control]^ and properly designed studies reported tho$ far have failed to show any clear-cut benefit. A few patients undoubtedly have repeatede* acerbations due to bacterial infection anddo benefit clearly from antimicrobial therapy; the clinician has little trouble identifying these : relatively uncommon individuals. Prophylac. tic therapy has not been shown to arrest de. terioration of pulmonary function over time or to decrease symptoms. If antimicrobial therapy is to be used in the patient with COPD, the microbial agents of most concern are H. influenzae and S. pneu moniae. The role of other bacteria that colo nize the bronchial tree is unknown, and in-' vestigators give them little or no place of im portance as this condition is understood at present. Since the value of antimicrobial ther apy for most patients is doubtful, any drag chosen for this purpose must be economical and nontoxic. The most suitable agents art ampicillin, amoxicillin, tetracycline, erythro mycin, and trimethoprim-sulfamethoxazole If antimicrobial therapy is to be given, an eo-, pirical choice is usually made without knowl edge of results from Gram stain of sputum, sputum culture, or studies for antimicrobial resistance. . 8. Vaccines. Influenza vaccine has been es tablished to be of great value in reduction of mortality and morbidity during epidemics of influenza. Most deaths from influenza result from bacterial pneumonia which leads to re spiratory failure, although influenza viral pneumonia is well documented. The adminis tration ofinfluenza vaccine is associated with a protection rate of 60 to 80%. Complications from the vaccine directed against Influenza A and B are relatively mi nor: 2% develop febrile reactions and mus cle aching that may last for a few hours, while hypersensitivity reactions can be seen in per sons allergic to egg protein. The severe reac tions observed following the mass vaccina tion for swine influenza in 1976 have not been noted with the vaccine containing types A and B. Since the mortality rate for pneumococcal pneumonia among persons over 60 yr of age has remained unchanged over the past 30 yr, attempts have been made to control this in fection with a vaccine containing purified cap sular polysaccharide from 23 pneumococcal serotypes. The vaccine is immunogenic in healthy, ambulatory, elderly persons, although its efficacy in preventing pneumococcal pneu monia in debilitated patients with COPD has not been established. The U.S. Public Health Service recommends use of the vaccine in all persons over 50 years of age and in patients with chronic disease including cardiopulmot 233 1 Placed ^ i scribed ' tedspe-/,. ie value i cult to'J strolled ed thus benefit.-'^ atedex.f;. iand do herapy*'" ng these'; 'phylacrest de-~; ver time id in the':* gents of ' S. pneuf> tat colo-^v and e of im--k >tood at ? rial ther-'S ny drug% nomical ents are erythro-^ oxazofe.|| t, an tknc sputum,^ itcrobial'.t: been esf iction of, emics of za result .ds to re* iza viral adminis* ited with directed jvively mi-**' nd mus--f is, while;?: n in per-^|' ere reac-S vaccina^ not been ^ types AaJ W iococcaljf^ yr of age ist30yr;;|-) 1 this in^f fiedcap-gf nococcalJs| igenic in alth' Jt DPD has.g| c Health ineinajl||| patientSM| opulmoi pary disorders. A single dose of the vaccine is judged to be sufficient, but experience is limited and the duration of protection after primary vaccination has not been determined. 9, Amantadine. Amantadine hydrochloride is a tricyclic amine that inhibits an early state ofreplication of the Influenza A virus. A num ber of controlled trials have demonstrated the prophylactic effectiveness of amantadine against the development of clinical illness in naturally-occurring and experimentally-in duced Influenza A infection. Estimates of ef ficacy range from 50 to 90%. Side effects in clude mental changes, ataxia, tremors, and convulsions, especially in the elderly. The recommended adult dose is 100 mg twice daily. Jn patients over age 65, renal excretion is de creased and daily dosage should be decreased to 100 mg after an initial loading dose of 200 mg. 10. Immunotherapy. Controversy persists concerning the use of immunotherapy in pa tients with allergic asthma and hay fever (25, 26). The repeated injection of extracts from substances that cause positive immediate skintest reactions results in the production of "blocking" antibodies, which may decrease the late, but not the early, IgE mediated al lergic response (27). Major problems with im munotherapy today include the lack of stan dardization of allergen extracts and dose, the lack of criteria for selection of those patients who might benefit, and the lack of objective studies to document its possible benefit in asthma (26). Pending the results of these in vestigations, it seems reasonable to employ immunotherapy for selected patients with epi sodic wheezing associated with rhinorrhea and conjunctivitis following exposure to known allergens (e.g., animal danders, rag weed pollen), provided contact with these al lergens is unavoidable. HI. Drug Therapy of Asthma i. Therapy ofthe acute attack. Management of the acute asthma attack is dependent upon the severity of the airway obstruction and the response to initial therapeutic maneuvers. Severity of the attack is determined by objec tive measurements, such as the FEV, or peak flow (28). The initial therapy of the acute at tack includes the administration of oxygen and bronchodilator agents (29). Beta-2 spe cific agents administered via a metered-dose inhaler or powered nebulizer are advised, par ticularly in older patients and those with car diovascular problems. Larger doses than those used in stable asthmatics may be required, to young, otherwise healthy asthmatics, sub cutaneous epinephrine or terbutaline give results that are comparable to inhaled betaudrenergic agents. in patients who have severe obstruction and have not responded to inhaled beta-adrenergic a8ents, theophylline should be added to the regimen. If intravenous aminophylline or theophylline is selected, an initial loading dose followed by a continuous drip is preferred TABLE 2 MAINTENANCE DOSAGES OF IV AMINOPHYLLINE AND THEOPHYLLINE* Aminophyline Theophylline Nonsmokers Smokers Cimetidine use Cor pulmonale Hepatic insufficiency Calculated (mg/kg/h) 0.5-0.7 0.9 0.3-0.4 0.2S-0.3 0.2-0.25 Typical Dose (mg/day) 900 1.300 600 500 . 450 Calculated (mgjkg/day) 0.4-0.6 0.75 0.25-0.3 0.2-0.25 0.18-0.2 Typical Dose {mg/day) 800 1,100 500 400 350 * Recommended loading doses of patients who have not been on maintenance oral therapy are: aminophytline. 5-7 mg/kg, or theophylline, 4-6 mg/kg. (table 2). If the patient has been on oral methybeanthines at home, a serum theophyl line level should be obtained and the initial loading dose decreased or eliminated. Serum levels should be maintained within the ther apeutic range of 8 to 20 mcg/ml and an im mediate reduction made if nausea, vomiting, severe nervousness, or cardiac arrhythmia de velop. Peak serum theophylline levels should be determined on 2 or 3 occasions when initiating therapy to obtain an estimate of daily requirements. Thereafter, they need not be repeated unless there is a change in the pa tient's status or new therapeutic agents are added. Severely ill patients may require fre quent determinations due to rapid changes in their clinical state. Corticosteroids should be administered promptly if the patient has had frequent re cent attacks, if steroids have been required in the recent past, or if the attack is severe and does not respond rapidly (within 30 to 60 min) to sympathomimetic and theophyl line therapy. In such cases, corticosteroids are given intravenously along with the bronchodilator agents; their onset of effect is not seen for 3 to 6 h, even with parenteral therapy (30). The dosage of corticosteroids for the acute asthma attack is still controversial; however, a loading dose of intravenous hydrocortisone of 4 mg/kg followed by 0.5 mg/kg/h or an equivalent dose of methylprednisolone (0.8 mg/kg initially followed by 0.1 mg/kg/h) is probably adequate for the initial therapy (30). As soon as flow rates improve, the patient may be switched to oral prednisone or methyl prednisolone. The initial maintenance doses should be about 40 mg ofprednisone per day or its equivalent; tapering should occur as rap idly as possible while the patient is monitored to avoid relapse. Weaning should be complete within about 2 wk and if this is not possible, a long-term maintenance regimen may be necessary. If attempts at weaning from cor ticosteroids fail, the lowest effective main tenance dose should be given, with repeated attempts at lowering the dose. Inhaled cor ticosteroids should be substituted if possible; if not, alternate-day therapy should be tried. Inhaled atropine, given by powered neb ulizer in doses of 0.025 to 0.035 mg/kg, may be given at intervals of 4 to 6 h if the acute attack does not respond to the above meas ures. The atropine may be combined with a beta-adrenergic agent. Inhaled corticoste roids, cromolyn, and n-acetylcysteine are in effective and may increase bronchospasm dur ing the acute asthmatic attack. Sedatives are also hazardous and should not be given dur ing an acute attack unless mechanical venti lation is required. 2. Preventive and long-term therapy. Ef fective management of patients with asthma is designed to prevent acute attacks. In the patient with mild, exercise-induced asthma, most agents have been shown to be effective, including the inhaled beta-adrenergic ago nists, oral sustained-release theophylline and cromolyn. The easiest and most convenient way ofpreventing exercise-induced asthma is by administration of a beta-2 adrenergic agonist from a metered-dose inhaler shortly before engaging in exercise. Inhaled cromo lyn is also effective in preventing exerciseinduced asthma (18). For more severe asthma (exercise-induced or otherwise troublesome), oral sustained-release theophylline twice daily may be combined with an inhaled betaadrenergic agent taken at regular intervals of 4 to 6 h. If long-term corticosteroid therapy is re quired, the dosage should be tapered to the lowest possible maintenance dose. At this time, patients should be tried on alternateday therapy, although this may be less effec tive. Inhaled corticosteroids (beciomethasone, triamcinolone, or flunisolide) may be ad ministered with the goal of eliminating oral steroids. The inhaled agents do not have sig nificant systemic effects, and their major side effects are sore throat and oral candidiasis. This is avoided by using an aerosol spacer and rinsing the mouth and throat with water af ter each inhalation. When switching from oral to inhaled corticosteroids, it is important to observe the patient for the development of adrenal insufficiency, especially during periods of stress; an overlap period is advised. Non-asthmatic symptoms such as rhinorrhea and arthralgias may appear if they were sup pressed by systemic steroid therapy. In patients with asthma inadequately con trolled by other therapy, a trial of inhaled cromolyn is indicated using either a spinhaler, MDI, or powered nebulizer. Cromolyn pow der by inhalation often causes bronchospasm and preceding the cromolyn with a betaadrenergic agent is generally advisable; when cromolyn is given by MDl, bronchospasm is uncommon, and this is the preferred method of administration. IV. Drug Therapy of Chronic Obstructive Pulmonary Disease (COPD) Many patients with COPD have a bronchospastic component, and these patients usu ally respond to appropriate bronchodilator therapy (14, 31, 32). While inhaled betaadrenergic agents are often effective, the ad dition of oral sustained-release theophyllines and/or an inhaled anticholinergic agent may be beneficial in some patients. For many years, corticosteroids were con sidered to be contraindicated for patients with COPD; however, investigators have recently shown that there is a subgroup of these pa tients who may benefit from oral corticoste roid therapy. These are usually patients who respond to inhaled beta-adrenergic agonists, but some patients with less reversible disease occasionally derive significant benefit from corticosteroid therapy (11). A therapeutic trial consists of determining baseline flow rates on optimum bronchodilator therapy, then ad ministering a dose of 32 mg of oral methylprednisolone or its equivalent once daily for 2 to 3 wk. Following this, flow rates are again determined and if no objective benefit is demonstrated by spirometry or peak flow, the corticosteroids should be discontinued. If there is significant improvement, the steroid dose is tapered as rapidly as possible until a maintenance dose is determined. At this time the patient may be changed to alternate-day therapy or an attempt may be made to sub stitute an inhaled corticosteroid; however, these methods of steroid administration are not effective in all patients with COPD who respond to oral steroids (33). In acute exacer bations of COPD, the addition of intravenous corticosteroids has been shown to be of ben efit (34). Benefits of long-term corticosteroids must be weighed against the multiple and var ied side effects of these agents. The prevention of acute attacks of bronchi tis includes influenza immunization in the fall of each year utilizing that antigenic combina tion recommended by the U.S. Public Health Service. This action will reduce death and morbidity from pneumonia and from influ enza-induced exacerbations of bronchitis. Amantadine is recommended for short term prophylaxis during presumed Influenza A outbreaks for high-risk patients who have not been immunized, and in situations where the vaccine may be ineffective, as in patients who may show a poor antibody response to vaccination. It should be given throughout the epidemic period for patients who cannot be immunized, but should not be a substitute for vaccination for most patients. In an out break, nonimmunized patients should be vac cinated and treated with amantadine for 2 wk. The usuai dose is 200 mg/day given in 2 di vided doses. For the patient who is hospitalized with an acute exacerbation of bronchitis, antimicro bial therapy is almost always given even though many of these episodes are induced by viral infection. When the patient is to re ceive intravenous drugs, ampiciJlin and/or amoxicillin are the drugs of choice. If allergy to penicillin is a concern, alternative agents include erythromycin, cephalosporin, tri methoprim-sulfamethoxazole, chloramphen icol, and tetracycline. The duration of treat ment must be individualized since these pa tients usually show a prolonged recovery period. For the patient with less severe dis ease who develops a sudden worsening of the bronchitis with increased cough and sputum production with or without fever, leukocyto sis, change in sputum volume and sputum purulence, symptomatic care, and rest are in dicated. Some physicians treat these patients with oral antibiotics for 1 to 2 wk, but there is little evidence to prove that this approach produces a more favorable outcome than symptomatic care and rest. References 1. Skidmore IF. Drugs acting on adrenoceptors. In: Buckle DR, Smith H, eds. Development of anti asthma drugs. London: Butterworths, 1984. 2. Popa VT. Clinical pharmacology of adrener gic drugs. J Asthma 1984; 21:183-207. 3. Shim C, Williams MH Jr. The adequacy of in halation of aerosol from canister nebulizer. Am J Med 1980; 69:891-4. 4. Sackner MA, Kim CS. Auxiliary MDI aerosol delivery systems. Chest 1985; 88(Suppl 2;161S--70S). 5. Newman SP. Aerosol deposition considerations in inhalation therapy. Chest 1985; 88(Supp] 2: 152S-60S). 6. Weinberger M, Hendeles L. Methylxanthines. In: Weiss EB, Segal MS, Stein M, eds. Bronchial asthma. Mechanisms and therapeutics. 2nd ed. Bos ton: Little, Brown and Company, 1985. 7. Goldstein RS, Allen LC, Thiessen JJ, Michalro K, Dayneka N, WoolfCR. Daily maintenancedose ofa long-acting theophylline from a single theophyl line serum level. Chest 1986; 89:103-8. 8. Brenn KJ, Bury R, Desmond PV. Effects of cimetidine and ranitidine on hepatic drug metabo lism. Clin Pharmacol Therap 1982; 31:297-300. 9. Gross NJ, Skorodin MS. Anticholinergic, antimuscarinic bronchodilators. Am Rev Respir Dis 1984; 129:856-70. 10. Pakes GE. Anticholinergic drugs. In: Buckle DR, Smith H, eds. Development of anti-asthma drugs. London; Butterworths, 1984. 11. George RB, Payne DK. Anticholinergics, cromolyn, and other occasionally useful drugs. Clin Chest Med 1984; 5:685-93. 12. Cox JSG. Disodium cromoglycate (FPL670). A specific inhibitor of reaginic antibody-antigen mechanism. Nature 1967; 216:1328-9. 13. Morton AR, Turner KJ, Fitch KD. Protection of exercise-induced asthma by pre-exercise cromo lyn sodium and its relationship to serum IgE lev els. Ann Allergy 1973; 31:265-71. 14. Mandella LA, ManfredaJ, Warren CPW, Anthonisen NR. Steroid response in stable chronic ob structive pulmonary disease. Ann Intern Med 1982; 96:17-21. 15. Sahn SA. Corticosteroid therapy in chronic obstructive pulmonary disease. Pract Cardiol 1995 11(No. 8):150-6. ' 16. Blair GP, Light RW. Treatment of chronic ob- structive pulmonary disease with corticosteroids. Chest 1984; 86:524-8. . 17. Zimentl.Hydration.humidiflcationandmu. cokinetic therapy. In: Weiss EB, Segal MS, Stein M, eds. Bronchial asthma. Mechanisms and ther apeutics. 2nd ed. Boston: Little, Brown and Com- pany, 1985. . 18. Brain J. Aerosol and humidity therapy. Am Rev Respir Dis 1980; 122(Supp!.i7-21). 19. Ziment I. Prophylactic and therapeutic management of chronic obstructive pulmonary disease In: Ziment I, ed. Practical pulmonary disease New York: John Wiley and Sons, 1983. 20. Leeder SR. Role of infection in the cause and course of chronic bronchitis. J Infect Dis 1975 131:731-42. ', 21. McHardy VU, Inglis JM, Calder MA, Crofton JW. A study of infective and other factors in ex acerbation of chronic bronchitis. Br J Dis Chest 1980; 74:228-38. . 22. Tager I, SpeizerFE. Role ofinfection inchronic bronchitis. N Engl J Med 1975; 292:563-71. * 23. Haas H, Morris JG, Samson S, Kilbourn JR, Kim PJ. Bacterial flora of the respiratory tract in chronic bronchitis. Comparison of transtracheal, fiberbronchoscopic and oropharyngeal sampling methods. Am Rev Respir Dis 1977; 116:41-7. * 24. Irwin RS, Erickson AD, Pratter MR, et el. Prediction of tracheobronchial colonization in cur rent cigarette smokers with chronic obstructive bronchitis. J Infect Dis 1982; 145:234-41. "-> 25. Lichtenstein LM. An evaluation of the role l of immunotherapy in asthma. Am Rev Respir Dis 1978: 117:191-7. ,-.i 26. Lichtenstein LM. A reevaluation of immuno therapy in asthma. Am Rev Respir Dis 1984; 129: 657-9. . . 27. Behrens BL, Marsh WR, Henson PM, Lar sen GL. Passive transfer of the late pulmonary re sponse in an animal model. Relationship of im munologic status to pulmonary physiologic changes (abstract). Am Rev Respir Dis 1983; 127 (Suppl:A65). 28. George RB. Some recent advances in the man agement of asthma. Arch Intern Med 1982; 142: 933-5. ' 29. Hopewell PC, Miller KT. Pathophysiology and management of severe asthma. Clin Chest Med 1984; 5:623-34. .< . 30. Collins JV, Clark TJH, Brown D, Townsend J. The use of corticosteroid in the treatment ofacute asthma. Quart J Med 1975; 174:259-73. , 31. Lertzman MM, CherniackRM. Rehabilitation of patients with chronic obstructive pulmonary dis* ease. Am Rev Respir Dis 1976; 114:1145-65. 32. Filuk RB, Easton PA, Anthonisen NR. sponses to large doses of salbutamol and theophy*" line in patients with chronic obstructive pulmonary -disease Am Rev Respir Dis 1985; 132:871-4. 33. Shim CS, Williams MH Jr. Aerosol be- clomethasone in patients with steroid-respona* chronic obstructive pulmonary disease. Am J Mr 1985; 78:655-8. .v'-' , 34. Albert RK, MartinTR, LewisSW. Control!*' clinical trial ofmethylprednisolonein patients - chronic bronchitis and acute respiratory >ns*}y: ciency. Ann Intern Med 1980; 92:753-8. , l < w 1 ( 1 1 ' ' . ' AMERICAN THORACIC SOCIETY 235 CHAPTER 4 02 Therapy j_ introduction Supplemental oxygen is one of the most com mon modalities used in treating patients with obstructive lung disease. The ultimate goal of such therapy is to prevent hypoxic tissue damage. In patients with obstructive lung dis ease, hypoxic tissue damage results primarily from arterial hypoxemia, which is efficiently treated with 02 therapy. When other diseases complicate obstructive lung disease, tissue hypoxia may result from other causes of in adequate 02 delivery to tissues, e.g., reduc tions in cardiac output or hematocrit. Inade quate 02 delivery in these situations obviously should be treated by maneuvers aimed at the basic abnormality and is not efficiently treated by 0: therapy, and will not be considered fur ther in this report. Arterial hypoxemia is one of the most ominous manifestations of ob structive lung disease and is at present the only acceptable indication for 02 therapy. The im mediate goal of 02 therapy, therefore, must be to increase arterial oxygenation to accept able levels. In general, 02 therapy in obstructive lung disease is used in 2 situations: in acutely ill hospitalized patients, and in chronically ill patients who are not in the hospital. II. O2 Therapy for Acutely 111 Patients A. General Guidelines As noted above, the indication for 02 ther apy is significant arterial hypoxemia. Arterial oxygenation is usually assessed by measur ing the partial pressure of 02 in arterial blood (Pao2), and when Pao2 < 60 Torr, hypoxemia sufficient to treat with oxygen is present. The goal of 02 therapy should be to increase Pao2 to at least 60 Torr, equivalent to an arterial 02 saturation of approximately 90%. On the other hand, increasing Pao2 beyond 65 Torr is associated with relatively minor further in creases in arterial 02 content (1,2), therefore, little purpose is usually served by increasing Paoi to values greater than 80 Torr, and 02 doses that do so should generally be avoided. The 02 dose that will increase Pao2 to 65 to 80 Torr in a given patient with obstructive lung disease can vary greatly, depending on the severity of the initial hypoxemia and the pre cise nature of the physiological disturbance. Attaining the correct dose is best done by trial and error, i.e., starting at a given dose (see below), measuring the Pao2 and adjusting the dose accordingly. It should be noted that in patients with severe COPD, it can take 20 to 30 min for a steady state to be achieved after a change in the inspired gas mixture, so that arterial blood should usually not be sampled at shorter intervals after changes in 02 dose. & 02 Therapy and C02 Retention In some patients with COPD, 02 therapy and the associated increase in Pao2 produce C02 retention, or an increase in arterial C02 ten sion (Pacoj) (3-5). This is a potentially seri ous problem in that C02 retention may pro duce coma. There is at present no good way to predict whether or not a given patient will develop a rising Paco2 with 02 therapy, though it generally occurs in very sick patients with Pao2 of < 40 Torr and with an elevated Paco2 while breathing room air, and very rarely oc curs in asthmatics (5-7). It follows that the only accurate way to assess the effect of 02 therapy on Paco2, as well as its effect on Pao2, is to measure Pao2 and Paco2 repetitively. In patients who demonstrate increases in Paco2 with b2 therapy, the latter should be used with caution. C02 produces central nervous sys tem disturbances by changing brain pH, so that the level of Paco2 that produces clini cally significant complications depends, in turn, on brain bicarbonate levels. C02 nar cosis, therefore, cannot be predicted on the basis of the Paco2, since no fixed level of Paco2 niay be defined as "too high," and C02 narcosis can only be diagnosed by careful serial clinical observations. In hypoxemic pa tients who develop C02 retention with 02 ther apy, the physician should attempt to increase the Pao2 without causing an increase of Paco2 sufficient to cause drowsiness or stupor. Of ten it is possible to produce clinically signifi cant increases in Pao2 that do not reach the ideal goal of 65 Torr, but are not associated with disturbances of consciousness. It must be recalled that severe hypoxemia causes death, whereas the disturbances associated with severe C02 retention are not usually le thal. In severe hypoxemia the first priority must be to increase Pao2- If excess 02 is given, and the patient develops signs and symptoms thought to represent C02 narcosis, the in spired 02 concentration should be reduced, but not to room air since abrupt cessation of all 02 therapy can produce fatal hypox emia. If adequate oxygenation cannot be achieved without progressive hypercapnia, mechanical ventiiation may be required (3, 5,6). C 02 Therapy in Emergency Situations The above discussion has assumed that the diagnosis of obstructive lung disease is clearly established and that measurements of Pao2 and Paco2 are readily available. These as sumptions do not always apply; patients are frequently encountered who are in respiratory distress for reasons that are not entirely clear, and, irrespective of diagnosis, 02 therapy is frequently undertaken without prior knowl edge of arterial blood gases. It is reasonable to treat all patients in respiratory distress with 02 before the results of blood gas analyses are known. If such patients clearly do not have COPD, short-term 02 therapy is essentially without risk, and any 02 dose--up to 100% -- may be safely employed. If, however, COPD is a diagnostic possibility, high-dose 02 ther apy carries the risk of C02 narcosis and should be avoided. The lower Che 02 dose, the lower the risk of COt retention. Inspired concen trations of less than 40% 02 are uncommonly associated with rapidly rising Paco2 and it is rare with inspired concentrations of less than 30%. Thus, when blood gas results are not available, patients suspected of having COPD should be treated with 02 concentra tions of 24 to 40%. In general, it is best to start at the lower end of the dose range, and to increase the dose only when there is clini cal or laboratory evidence that this should be done. These inspired oxygen concentrations are usually achieved by nasal flows on the or der of 1 to 5 L/min (see below). Oxygen therapy without arterial blood gas measurement is acceptable only under emer gency conditions. Ideally, arterial blood should be sampled in the emergency room as 02 therapy is started, and the procedure repeated some 20 to 30 min later. In acutely ill patients seen for the first time, prolonged (1 to 2 h) 02 therapy without measurements of Pao2 and Paco2`are acceptable only under exceptional circumstances. Though noninvasive measurements of Pao2 and Paco2 are available, they should not be relied upon in acute situations, or when rapid changes might be expected. D. Methods of 02 Administration In acute, inpatient situations, 02 sources are readily available, as are a variety of techniques of transferring 02 from the source to the pa tient (8). In general, there are 2 methods of delivering < 40% 02. Nasal "prongs" are popular because they do not interfere with eating and conversation. The 02 dose can be varied by varying 02 flow, but the precise in spired concentration achieved depends on the patient's ventilation and breathing pattern, and the dose delivered at a given 02 flow will show both interindividual and intraindividual variations. The inspired 02 concentration in % (Fio2) can theoretically be calculated as: Fio2 = 20 + 4 x 02 flow (L/min). This is, how ever, only an approximation. At flows of > 4 L/min, the 02 should be humidified, although at lower flow rates this is not necessary. Al ternative methods of administration of < 40% 02 are Venturi masks, which, though they in terfere with activities such as conversation and eating, supply fixed, known inspired 02 con centrations ranging from 24 to 50%. Oxygen at concentrations exceeding 40% can only be administered by mask. Masks vary in design, but those employing a high flow of 02 into a reservoir bag are most efficient in that they can deliver inspirates of up to 90% 02. As noted above, these systems are poten tially dangerous in patients with COPD. HI. 02 Therapy in Chronic Lung Disease A. 02 Therapy in Patients with Continuous Hypoxemia It has been conclusively shown that the sur vival of patients with hypoxemia COPD is improved by long-term 02 therapy, and that this benefit is greatest if the treatment is ap plied at least 18 h/day (9-13). Thus, chroni cally hypoxemia COPD patients should, in general, be treated in this way. There is no 236 AMERICAN THORACIC SOCIEf^ dence of benefit for long-term 02 therapy ,,,>ed less than 12 to 15 h/day. Benefits from home 02 therapy have been demonstrated in stable patients with Pao2 < 55 Torr (arterial 02 saturation, < 90%), and in patients with Pao2 55 to 59 Torr with evi dence of polycythemia or right heart failure when stable; it is, therefore, to this group that the treatment should be applied. Stability is best defined in terms of arterial blood gas measurements. Patients are defined as chron ically hypoxemic if, when clinically stable, they meet the above criteria during an observation period of 2 wk. Patients with Pao2 of 45 to 60 Torr can usually undergo the observation period as outpatients, but sicker patients may have to be stabilized in the hospital. Patients who qualify as outlined above should receive continuous 02 therapy, i.e., as close to 24 h/day as possible, and the dose should be sufficient to raise resting Pao2 to 65 to 80 Torr (saturation, 91 to 95%). The dose should be increased by I L/min while the patient is sleeping or exercising to elimi nate hypoxemic episodes during these activi ties. With such a regimen, specific studies of oxygenation during sleep and exercise are sel dom necessary. The appropriateness of the daytime resting 02 dose should be assessed periodically. 8. Patients with Intermittent Hypoxemia Some patients with COPD --not asthma-- who have Pao2 of at least 60 Torr while awake and at rest develop more severe hypoxemia while sleeping or exercising (14). At present there are few data to indicate whether, in such patients, 02 therapy during sleep or exercise are of benefit, so any standards suggested must be regarded as provisional. C Nocturnal Hypoxemia There appears to be little question that some COPD patients who do not qualify for con tinuous home 02 therapy have episodes ofse vere hypoxemia (arterial saturation, < 85%) while sleeping. Though it is not established that such episodes are harmful, it is probably unwise to assume that they are harmless, and we believe nocturnal 02 therapy can be justi fied in such patients. Detection of nocturnal hypoxemic episodes in patients who are not hypoxemic during wakefulness requires study during sleep; the criteria for patient selection for study has not yet been determined (9). COPD patients with Pao2 > 60 Torr who are obese, or who have C02 retention, polycythe mia, or evidence of right heart failure, prob ably merit sleep studies. The 02 dose required to eliminate severe nocturnal hypoxemia in these patients can also only be determined with accuracy by sleep study. A minimum noc turnal oxygen saturation of approximately 90% is a reasonable therapeutic goal. It should be noted that 02 therapy may not be appropriate for obstructive sleep apnea, which may coexist with COPD. In patients with nocturnal hypoxemia due to obstructive sleep apnea, therapy should be aimed at reliev ing nocturnal upper airway obstruction. D. Exercise Hypoxemia Some COPD patients--usually those with very severe airway obstruction--develop hy poxemia during exercise while maintaining Pao2 ^ 60 Torr at rest. Home oxygen has been prescribed for use during exercise in such pa tients, though there is no solid evidence for long-term benefit. Since most ofthese patients spend relatively little time exercising, it is dif ficult to believe that the hypoxemia of exer cise affects survival or function at rest. Thus, the best rationale for supplemental 02 dur ing exercise is that it will increase exercise toler ance and useful daily activity. However, it is not clear that arterial hypoxemia limits exer cise tolerance in all of these patients. Sup plemental 02 during exercise should probably be prescribed only when it has been shown by appropriate testing to increase exercise tolerance significantly. The simplest way to measure the benefits of 02 during exercise is to conduct exercise tests with the patients breathing both room air and supplemental 02. These tests are best conducted in such a way that the patient is not aware of whether 02 or room air is being supplied (15). E. Methods of 02 Delivery The only practical way of delivering home 02 to patients is via nasal prongs (8). Recently, prongs that supply 02 only during inspira tion have been developed in an attempt to conserve gas; oxygen has also been delivered directly to the sublaryngeal trachea via a chronic transtracheal cannula. These systems have not yet been fully evaluated, and can not be recommended at present. Sources of 02 suitable for use in the home vary, and each has advantages and disadvan tages. Liquid 02 systems were used early in home 02 therapy, and are the most versatile because of their easy portability: patients can easily carry an 02 supply for shopping excur sions, etc. Liquid systems are also more ex pensive than any other, and can only be used in urban areas near a source of liquid 02. Steel cylinders containing compressed gas can be used as sources for home 02. These are available in towns large enough to have welding suppliers. They are nearly as expen sive as liquid systems, and afford much less portability. Small steel 02 cylinders are too heavy to carry and must be moved in wheeled carts, which is frequently difficult for sick pa tients. Recently, aluminum compressed gas cylinders have become available. These are light enough to carry while containing sev eral hours of 02 supply and are, in theory, an improvement over steel cylinders. How ever, the most efficient use of aluminum cylinders involves filling them from large steel cylinders in the home, which is regarded as dangerous by many municipal safety authori ties. The cheapest source of home 02 is the socalled concentrator, which separates atmos pheric 02 from N2 and supplies the former. Though there is a substantial initial cost for these machines, they require little subsequent service and maintainance. They operate usia*'' electrical power and can be used in any hom* with electricity. Their major drawback is that they are non-portable; If the patient leaves the home, it is either without 02 or with an.' other portable system. Most programs sup. ply a large steel cylinder of compressed o along with the oxygenator, to provide against electrical failure. * I References 1. Campbell EJM. Oxygen therapy in disease of the chest. Br J Chest Dis 1964; 58:149-57. 2. Campbell EJM. Management of respiratory failure. Br Med J 1964; 2:1328. 3. Seiker HO, Hickham JB. Carbon dioxide in toxication. The clinical syndrome, its etiology and management with particular reference to the use of mechanical respirators. Medicine 1956; 35 389-423. ' 4. Lopez-Majano V, Dutton RE. Regulation of respiration during oxygen breathing in chronic ob structive lung disease. Am Rev Respir Dis 1973 108:232-40. 5. Bone RC, Pierce AK, Johnson RL Jr. Coo- trolled oxygen administration in acute respiratory failure in chronic obstructive pulmonary disease Am J Med 1978; 65:896-902. ' 6. Aubier M, Murciano D, Miltc-Emili J, et a!. Effects of the administration of 02 on ventilation and blood gases in patients with chronic obstruc- ' live pulmonary disease during acute respiratory fail ure. Am Rev Respir Dis 1980; 122:747-54. v 7. Anthonisen NR. Hypoxemia and O, therapy. Am Rev Respir Dis 1982; 126:729-33. \ 8. Fulmer JD, Snider GL. ACCP-NHLBI national conference on oxygen therapy. Chest 1982; 86: 234-47. ./, 9. Anthonisen NR. Long-term oxygen therapy. Ann Intern Med 1983; 99:519-27. >- 10. Levine BE, Bigelow DB, Hamstra RD. The role of long-term continuous oxygen administration in patients with chronic airway obstruction and hy poxemia. Ann Intern Med 1967; 66:639-50. 11. Abraham AS, Cole RB, Bishop JM. Reversal of pulmonary hypertension by prolonged oxygen administration in patients with chronic bronchi tis. Circ Res 1968; 23:147-57. 12. Nocturnal Oxygen TherapyTrial Group. Con tinuous or nocturnal oxygen therapy in hypoxemia chronic obstructive lung disease: a clinical trial. Ann Intern Med 1980; 91:391-8. -- 13. Medical Research Council Working PartyLong-term domiciliary oxygen therapy in chrome hypoxic cor pulmonale complicating chronic bron chitis and emphysema. Lancet 1981; 1:681-6. / 14. Block AJ. Dangerous sleep: oxygen therapy for nocturnal hypoxemia. N Engl J Med 1982; 306:166-7. - 15. Longo AM, Moser KM, Luchsinger PC. The role of oxygen therapy in rehabilitation of patients with chronic obstructive pulmonary disease. Affl Rev Respir Dis 1971; 103:690-7. J. CHAPTER 5 Respiratory Care Modalities : 1. Introduction Respiratory care modalities are valuable ^ adjunctive therapy in the care of patients with, obstructive airways diseases. Patients, fa*/. ^XERICAM THORACIC society 237 M ; that ;j 1 aij. ' ir sup. , \ d0j { ainst j 'i e of j atory | ie inyand e u* ; 35: on of j I j } ! icob- } 1973; [ Conatory tease. i | j et at. - | ation * ;truc* i i ny fail- , * :rapy. lional * 86: '' j J:rapy. . .erok I ion in . V .d by* J /ersal | <ygen nchi- / Con<emia .Ann | 'arty. ,t l ronic f bron- , i 6. .-I erapy. } 1982; I .The. dents ,, Am ! le as "r , with ; 1 fam- | .. members or other caregivers should be lrained in the use of these modalities by quali fied practitioners, usually respiratory ther ms and respiratory therapy technicians un- jgr the aegis of a medical director who has been trained in the care of acute and chronic pulmonary diseases (1, 2). This section will cover the indications and guidelines for the use of incentive spirometry, intermittent posi tive pressure breathing (IPPB), intermittent continuous positive airway pressure (CPAP), bland aerosol and humidity therapy, medi cated aerosol therapy, chest physiotherapy (in cluding postural drainage), chest percussion and vibration, and breathing exercises. Oxy gen therapy is discussed in Chapter 4. These modalities may be administered separately or concomitantly. f(. Measures for Lung Expansion Incentive spirometry is a technique to en courage a patient to take a sustained, deep breath, utilizing a measuring device for di rect visual feedback. It is indicated as an aid to facilitate lung expansion in hospitalized pa tients both to prevent and to treat pulmonary atelectasis. It may be particularly useful be fore and after major surgical procedures as part of a regimen to help prevent postopera tive atelectasis and other respiratory compli cations (3,4). The deep breathing maneuvers may also stimulate patients to cough and thereby aid in the removal of abnormal bron chial secretions. The frequency of use usually depends upon the clinical condition of the patient. In the initial treatment of pulmonary atelectasis, in centive spirometry may be used hourly, at least during the waking hours. With improvement of atelectasis or with prophylactic use of in centive spirometry, the frequency of therapy may be less. It is critical that patients receive instruction in the proper use of incentive spirometry from individuals trained in respi ratory care, with the emphasis on sustained maximum inhalation for 5 to 6 s, and 5 to 10 sequential deep breaths (6). Subsequent use of the incentive spirometer may be super vised by nursing personnel, but it is reason able to provide periodic follow-up assessment by respiratory care personnel to assure that incentive spirometry is being properly ad ministered and utilized. Although chronic use of lung expansion maneuvers in the home or at other commu nity living sites may be indicated in persons with severe restrictive pulmonary dysfunction, there is no evidence that this form of therapy is useful in patients with obstructive airways diseases. Breathing exercises with a simple in spiratory resistance device or with an incen tive spirometer may be of value as a means to increase inspiratory muscle strength and endurance (6), but studies of long-term ben efit are still lacking. The use of the IPPB in patients with COPD |s controversial. There is no evidence that it >s helpful or desirable for home use (7). Pos sible selected indications for IPPB in the hos pital may include the following (8); (!) The management of atelectasis that has not improved with voluntary deep breathing or incentive spirometry, when it can be doc umented that the inspiratory capacity is in creased by at least 25% using IPPB (9). In these patients, IPPB should be administered by a volume-oriented technique. IPPB can not be recommended as a routine prophylac tic technique to prevent atelectasis. (2) As a measure to provide frequent peri odic deep breathing for a patient with acute ventilatory failure in an attempt to avoid in tubation or reintubation. In such circum stances, IPPB is a temporizing procedure and not meant to normalize arterial blood gases, allowing the patient time to improve by vir tue of correction of reversible factors that have precipitated the acute ventilatory failure. (3) For the delivery of aerosol medications, primarily bronchodilators, in pateints who are unable to breathe slowly and deeply because of acute respiratory distress. It is doubtful, however, that IPPB is more effective in the delivery of nebulized bronchodilators or in causing bronchodilatation than is a nebulizer operated by a constant pressure compressed gas source. Continuous positive airway pressure (CPAP) by mask has been used in the past for treatment of pulmonary edema. Recently, the use of intermittent CPAP by mask has been investigated in the management of pul monary atelectasis (10,11). This modality re quires further study in patients with COPD before specific recommendations for its use can be made. In particular, the possible det rimental effects of further hyperinflation on cardiac function and respiratory muscle efficiency must be evaluated. The use of in termittent mask CPAP would appear to have no place in the management of respiratory failure associated with obstructive airways diseases. III. Bland Aerosols and Humidity Therapy The use of bland aerosols and humidity ther apy in patients with obstructive airways dis ease centers primarily on humidification of the inspired gas being delivered through an artificial airway (endotracheal tube or tra cheostomy). Any patient with obstructive air ways diseases and respiratory failure who requires hospitalization and who has an ar tificial airway, either with or without mechan ical ventilation, should be provided with a heated and humidified gas source during the period of tracheal intubation. In patients with chronic obstructive airways diseases who have permanent tracheostomies, the need and method for continued humidification of the inspired gas after discharge must be individ ually assessed. Further studies are needed to determine if adequate long-term humidifica tion using a moisture-exchange device ("ar tificial nose") connected directly to the air way opening can be efficacious. Bland aerosols, utilizing either water or sa line, have not been shown to aid in the clear ance of abnormal secretions. They neither thin secretions nor enhance bronchial clearing and may precipitate bronchospasm (12,13). Room humidifiers should be discouraged because of their ineffectiveness in providing increased hu midity for the patient and because of their high rate of bacterial and fungal contamina tion. Hypertonic saline delivered by ultrasonic nebulization may be used for short periods of time to induce sputum for diagnostic studies, although there is no evidence it is su perior to coached coughing. IV. Medicated Aerosol Therapy It is well established and generally agreed that bronchodilator drugs, administered to pa tients who demonstrate symptomatic or ob jectively measured improvement, are useful both in the hospital and in the home. Advan tages of aerosol versus oral bronchodilator delivery include: more rapid, predictable on set of therapeutic effect, smaller quantity of active agent required for given degree of ob jective response, generally greater attainable response at tolerated doses, and fewer systemic side effects. Bronchodilators may be given as aerosols via a metered-dose inhaler (MDI), with or without a variety of spacer devices (tube, col lapsible bag, cone or pear-shaped) introduced to improve the efficiency of delivery of the bronchodilator agents (14,15) in patients who are unable to use a MDI properly (16, 17). Alternatively, they may be administered with a nebulizer powered by compressed gas or by a small electrical air compressor. Patient in struction in the proper technique of using a nebulizer or an MDI with or without a spacer is essential. This may be done by respiratory care personnel, a specially trained nurse, or by a knowledgeable physician. In the hospital, aerosolized bronchodila tors are usually delivered by nebulizers, al though recent studies have demonstrated that, in patients not severely ill, the effects of metaproterenol administered by MDI plus spacer were the same as metaproterenol ad ministered by a nebulizer (18, 19). Adminis tration of the aerosol bronchodilators by either MDI or nebulizer should be performed by respiratory care personnel or other trained hospital personnel for patients who are acutely ill, confused, or feeble. In the stable patient who has demonstrated proficiency in using an MDI, with or without a spacer, little su pervision may be required. The frequency of administration of aero solized bronchodilators will depend upon the severity of the illness but may be required as often as every hour in those patients with acute severe asthma (20). As the patient improves, the frequency of administration should be dictated by the duration of action of the drug administered (see Pharmacologic Therapy, Chapter 3). In the patient with ob structive airways disease who requires surgery, particularly of the thorax or upper abdomen, aerosolized bronchodilator agents should be started preoperatively and continued in the postoperative period, in order to reduce post operative pulmonary complications (21,22). Outside the hospital, aerosolized bron- -hodilators are usually delivered with a nered-dose inhaler with or without a spacer. When inhaled corticosteroids are required, the use of spacer devices with a MDI results in a substantially lower incidence of thrush, and fewer problems with dysphonia, than when the MDI alone is used (14). Some outpatients, particularly those who are unable to use an MDI, derive benefit from aerosolized bronchodilator agents delivered by a nebulizer. If the nebulizer is used on a daily basis, it may need to be powered by an air compressor since hand-bulb nebulizers may be difficult to coordinate with inhala tion. These devices are portable. Patients using a nebulizer in the home should be instructed by trained personnel in the proper use and cleaning of the equipment. Periodic servic ing and inspection of home nebulizer equip ment may be necessary for some patients. V. Chest Physical Therapy Chest physical therapy (or chest physiother apy) encompasses the use of postural drain age, chest percussion and vibration admin istered by hand or by mechanical percussion, as well as cough and deep breathing. The ra tionale for this therapy in the treatment of patients with obstructive airways diseases is the belief that gravity and applied external force to the chest wall will facilitate mobili zation and clearance of secretions from the .irways, leading to an improvement in pul monary function. In order for chest phys iotherapy to be effective in the home or hos pital, the patients must have excessive secre tions (30 cc/day or greater) that are difficult to expectorate (23-27). In the hospital setting, chest physiother apy is indicated in chose patients who have great difficulty raising secretions and in those patients who develop atelectasis either postoperativeiy (28) or under other circumstances (29, 30). Fiberoptic bronchoscopy can be ef fective in acute lobar atelectasis, but is no more effective than vigorous chest physiotherapy given by experienced personnel (27). Chest physiotherapy may be effective in acutely ill patients with obstructive lung diseases who expectorate large sputum volumes (30, 31) even if they require mechanical ventilation (30, 32). Use of chest physiotherapy has not been shown to be effective in acute exacerbations of chronic bronchitis (33-35), in patients with scant secretions receiving mechanical venti lation (31), in patients with status asthmaticus (26), or in patients who have pneumonia (36). Chest physiotherapy is indicated either in the hospital or at home in stable patients with bronchiectasis, cystic fibrosis, and chronic bronchitis who chronically produce large spu tum volumes (37-41). It is not effective in pa tients with COPD who produce less than 30 cc/day (42). To facilitate bronchodilation and mucociliary clearance, chest physiotherapy should be delivered after the administration of an aerosolized bronchodilator (35). The frequency of administration of chest physiotherapy in patients who might benefit from it has not been established. In patients with atelectasis and in others who have diffi culty expectorating sputum, probably no more than 4'treatments per day are practical or tolerable. Patients with more stable condi tions, especially in the home setting, usually will require fewer treatments. In those patients who will benefit from the continuation of chest physiotherapy outside the hospital, the patient and family members should undergo a complete educational pro gram on the technique and goals ofchest phys iotherapy in the home prior to discharge. Trained respiratory care personnel, nurses, or physical therapists usually provide this in struction. Family members can be taught to administer percussion and vibration. The number of teaching sessions required before the patient and family members are compe tent will depend upon their ability to grasp the concepts and apply them during therapy. Usually several sessions will be required. VI. Breathing Exercises Breathing exercises encourage patients to in spire slowly and to expire through pursed lips (25,26). Simultaneous relaxation of the neck and upper thoracic musculature should be en couraged (26). Breathing exercises may be ef fective in increasing the patient's tidal volume, decreasing the respiratory rate, and lowering the FRC (43,44), thereby improving the effi ciency of gas exchange and reducing the work of breathing. In the acutely ill patient, the use of breath ing exercises may be helpful in aborting hyper ventilation episodes precipitated by panic or anxiety, provided the patient is familiar with the technique. Even if the patient is untrained, coaching by respiratory care personnel or other trained professionals to inhale slowly and exhale through pursed lips is helpful. Patients with stable obstructive airways dis eases may benefit from breathing exercises, both physiologically and symptomatically (43-46). They are most effective over short term use, since long-term studies show no im provement in pulmonary flows (45, 47). Breathing exercises are effective in helping the patients overcome attacks of hyperventilation precipitated by fear and anxiety and may be useful to combat the urge to hyperventilate after mild exercise. References 1. Miller WF, Plummer AL, et al. Guidelines for organization and function of hospital respiratory care services. Chest 1980; 79-83. 2. American Thoracic Society. Medical director of respiratory therapy. ATS News 1976; 2:1-3. 3. Bartlett RH, Brennan ML, Gazzaniga AB, Han son EL. Studies on the pathogenesis and preven tion of postoperative pulmonary complications. Surg Gynecol Obstet 1973; 137:925-33. 4. Bartlett RH. Respiratory therapy to prevent pul monary complications ofsurgery. Respir Care 1984; 29:667-77. 5. O'Donohue WJ Jr. Perioperative measures for lung expansion. In: O'Donohue WJ Jr, ed. Cur rent advances in respiratory care. Park Ridge, 1L: Amer Col Chest Phy 1984; 10-20. (Su 6. Sonne LJ, Davis JA. Increased exercise perfor-' mance in patients with severe COPD following uj.-' spirarory resistive training. Chest 1982: 81:436-5 27. zoc198: 7. Intermittent Positive Pressure Breathing Trij] Group. Intermittent positive pressure breathing therapy ofchronic obstructive pulmonarydisease a clinical trial. Ann Intern Med 1983; 99:612-20 28. caii off 205 8. Respiratory Care Committee of the American Thoracic Society. Intermittent positive pressure breathing (IPPB). Clin Notes Respir Dis 1979. 18:3-6. ' 29. bar lict Rft 9. O'Donohue WJ Jr. Maximum volume IPPg for the management of pulmonary atelectasis. Chest 1979; 76:683-7. 10. Anderson JB, Olesen KP, Eikard B, Jansen E, Ovist J. Periodic continuous positive airway pres sure CPAP, by mask in the treatment of atelecta sis: a sequential analysis. Eur J Respir Dis 1980 60:20-5. 30. ica ho me 31. Ro ate Ch 11. Stock MC, Downs JB, GauerPK, Cooper R& Prevention of atelectasis after upper abdominal operations. Crit Care Med 1983; 11:220. . 12. Brain JD. Aerosols and humidity therapy. Am Rev Respir Dis 1980; 122(Suppl:17-21). 13. Brain JD. Aerosols and humidity therapy. In: O'Donohue WJ Jr, ed. Current advances in respi ratory care. Park Ridge, IL: Amer Col Chest Phy 1984; 72-85. ' 32 Cl in'20' 33. It of M. 34. 14. Konig P. Spacer devices used with metered* dose inhalers. Breakthrough or gimmick? Chest 1985; 88:276-84. 15. Sackner MA, Kim CS. Auxiliary MDI aero- sol delivery systems. Chest 1985; 88(Suppl: 161S-70S). ' 16. CushleyMJ, Lewis RA, Tattersfieid AE. Com- f I I f parison of three techniques of inhalation on the airway response to terbutaline. Thorax 1983; 38: 908-13. - 17. Morris J, Milledge SS, Moszoro H. The effi cacy of drug delivery by a pear-shaped spacer and metered-dose inhaler. Br J Dis Chest 1984; 78:383-7. 18. Berenberg MJ, Baigelman W, Cupples LA. Comparison of metered-dose inhaler attached to an aerochamber with an updraft nebulizer for the administration of metaproterenol in hospitalized patients. J Asthma 1985; 22:87-92. . I [ 19. Berenberg MJ, Baigelman W, Cupples LA, Pearce L. Comparison of updraft nebulizer versus metered dose inhaler attached to an aerochamber for the administration of metaproterenol to hos pitalized patients (abstract). Am Rev Respir Dis 1985; 13I(Suppl:A95). V 20. Fanta CH, Rossing TH, McFadden ER Jr. Emergency room treatment of asthma. Relation ships among therapeutic combinations, severityof obstruction and time course of response. Am J Med 1982; 72:416-22. 21. Stein M, Cassara EL. Preoperative pulmonary evaluation and therapy for surgery patients. JAMA 1970; 211:787-90. 22. Ziment I. Perioperative pharmacologic management. Respir Care 1984; 29:652-63. .$ j * br< 35 efch 3t Pi b: J 3" fc J 3> r li st 1. 3 Ci Is. 1 4 e: R 4 R a l i k c c k 23. Darrow G, Anthonsien NR. Physiotherapy* hospitalized medical patients. Am Rev Respir D 1980; 122(Suppl:155-8). 24. Murray JF. The ketchup-bottle method..N I Engl J Med 1979; 300:1155-7. -'J 25. Sutton PP, Pavia D, Bateman JRM, Clark* SW. Chest physiotherapy: a review. Eur J RcsP* Dis 1982; 63:188-201. '' 26. Rochester DF, Goldberg SK. Techniques respiratory therapy. Am Rev Respir Dis 1980; ^ ^ICAN THORACIC SOCIETY 239 31:436-9.. j ring TrialX >reathio| l { /diseased 4 *612-20. s j Americas -s j pressure * | Jis 1979; V- me 2PPBV 1 lsis. Chest \ j 3, Jansen | way pres* j atelecta- 'I Dis 1980;' j r*' >oper RE.f' { bdominal J ' 4 rapy.AjnJ-1 erapy. In;^ s in respi-.v 'hest Phy'-_ metered:k? Chest ^ 4DI aero-|v 88(Suppb'5? ^ :>n on the * * 1983; 38:2: I : . The effi-'pacer and V 78:383-7. 5ples LA.v :tached to'i' ter for the \ spitalized.; oples LA, 105- " Dis*-' 1 VTW5 vi, Cterfceg (Suppl:!33-46^ 17 Kirilloff LH, Owens GR, Rogers RM, Maz-Jco MC. Does chest physical therapy work? Chest 1985; 88:436-44. jg Thoren L. Post-operative pulmonary complicatjons. Observations on their prevention by means of physiotherapy. Acta ChirScand 1954; 107:193-- 205. 29. Marini JJ, Pierson DJ, Hudson LD. Acute lo bar atelectasis: a prospective comparison offiberop tic bronchoscopy and respiratory therapy. Am Rev Respir Dis 1979; 119:971-8. 30. Holody B, Goldberg H. The effect ofmechan ical vibration physiotherapy on arterial oxygena tion in acutely ill patients with atelectasis or pneu monia. Am Rev Respir Dis 1981; 124:372-5. 31. Connors AF Jr, Hammon WE, Martin RJ, Rogers RM. Chest physical therapy. The immedi ate effect on oxygenation in acutely ill patients. Chest 1980; 78:559-64. 32. Mackenzie CF, Shin B, Hadi F, Imle PC. Changes in total lung/thorax compliance follow ing chest physiotherapy. Anesth Analg 1980; 59: 207-10. 33. Anthonisen P, Riis P, Sogaard-Anderson T. The value of lung physiotherapy in the treatment ofacute exacerbations in chronic bronchitis. Acta Med Scand 1964; 175:715-9. 34. Newton DAG, Bevans HG. Physiotherapy and intermittent positive pressure ventilation in chronic bronchitis. Br Med J 1978; 2:1525-8. 35. Campbell AH, O'Connell JM, Wilson F. The effect of chest physiotherapy upon the FEV, in chronic bronchitis. Med J Aust 1975; 1:33-5. 36. Graham WGB, Bradley DA. Efficacy ofchest physiotherapy and intermittent positive-pressure breathing in the resolution of pneumonia. N Engl J Med 1978; 299:624-7. 37. Cochrane GM, Webber BA, Clarke SW. Ef fects of sputum on pulmonary function. Br Med J 1977; 2:1181-3. 38. Bateman JRM, Daunt KM, Newman SP. Re gional lung clearance of excessive bronchial secre tions during chest physiotherapy in patients with stable chronic airways obstruction. Lancet 1979; 1294-7. 39. Bateman JRM, Newman SP, Daunt KM. Is cough as effective as chest physiotherapy in the removal of excessive tracheobronchial secretions? Thorax 1981; 36:638-87. 40. Feldman J, Traver GA, Taussig LM. Maximal expiratory flows after postural drainage. Am Rev Respir Dis 1979; 119:239^*5. 41. Mazzocco MC, Owens GR, Kirilloff LH, Rogers RM. Chest percussion and postural drain age in patients with bronchiectasis. Chest 1985; 88:360-3. 42. Mohsenifar Z, Rosenberg N, Goldberg HS, Koerner SK. Mechanical vibration and conventional ehest physiotherapy in outpatients with stable chronic obstructive lung disease. Chest 1985; 87:483-5. 43- Campbell EJM, Friend J. Action of breath- ln8 exercises in pulmonary emphysema. Lancet 1955; 1:325-9. ' 44- Mueller RE, Petty TL, Filley GF. Ventilation arterial blood gas changes induced by pursed "Ps breathing. J Appl Physiol 1970; 28:784-9. 43- Jones NL. Physical therapy: present state of me art. Am Rev Respir Dis 1974; 110(Suppl:132-6). Miller WF. A physiologic evaluation of the effects ofdiaphragmatic breathing training in pa^ents with chronic pulmonary emphysema. Am J Med 1954; 17:471-84. 47. Emirgil C, Sobol BJ, Normal J, el al. A study of the long-term effect of therapy in chronic ob structive pulmonary disease. Am J Med 1969; 47:367-77. CHAPTER 6 Physical Rehabilitation and Home Care I. Introduction The most common and distressing symptom in patients with COPD is dyspnea resulting in limitation ofactivity. The objectives ofpul monary rehabilitation are to control and al leviate symptoms and pathophysiologic com plications and to achieve optimal ability to carry out activities of daily living. The broad concepts and elements of pulmonary rehabili tation have been reviewed in a previous ATS statement (1). Most pulmonary rehabilitation programs include either encouragement for patient activity or a regular exercise component. Although there is general agreement that pa tients benefit from pulmonary rehabilitation programs, the specific contribution of exer cise to the improvement is not well defined. Limitation of exercise in patients with COPD is related to multiple factors includ ing; abnormal pulmonary mechanics, impair ment in pulmonary gas exchange, an abnor mal perception of breathlessness and ventila tory control, the presence of impaired cardiac performance due to cor pulmonale, poor nu tritional status, and the development of respi ratory muscle fatigue (2). Determination of the exact number of fac tors involved and their relative importance in an individual patient with COPD is difficult and often impossible. The inability to ac curately characterize the exercise-limiting fac tors in individual patients has led to confu sion and controversy in assessing the effec tiveness of various forms of therapy designed to improve exercise performance. Several physical rehabilitation techniques are utilized to increase the dyspnea-limited level of activity or to decrease the degree of dyspnea associated with the same level of ac tivity. The methods utilized include exercise reconditioning, inspiratory muscle training, breathing retraining, and energy conservation techniques. II. Patient Selection Physical rehabilitation should not be consid ered in the COPD patient until optimal med ical control of the disease has been achieved. Motivation is the most important factor in the selection of patients for physical rehabili tation. In younger patients with less than ad vanced disease, preservation of body weight and muscle mass and minimal disease in other organ systems are more likely to persist with and benefit from physical rehabilitation. It is important that patients be realistically ap prised of the effort and time involved and the limited benefits to be expected from physical rehabilitation before embarking on an exten sive program. Screening should include spirometry, ar terial blood gases, and exercise evaluation. A standard 6- or 12-min walk, cycle or tread mill testing can be used; the ventilatory limit to exercise can be estimated from the FEV,. The presence of exercise arterial desaturation should be evaluated by exercise oximetry or exercise blood gases since patients with exer cise desaturation should receive oxygen dur ing exercise if it increases exercise capacity (see Oi therapy). On the basis of these data, a prescription for the tolerable level of exer cise can be formulated. The type(s) of physi cal rehabilitation program and adjunctive therapy must be individualized to each pa tient. For some patients, there may be some psychosocial and motivational advantages to group programs. The program should be ini tiated under medical supervision. Periodic as sessment of the benefits or side effects of the program is required. Improved general fitness frequently results in improved exercise toler ance. In general, physical activity should be encouraged for patients with COPD. Whether additional benefit is derived from formal ex ercise programs is uncertain and unproved. Ilf. Comments of Rehabilitation A. Exercise Reconditioning Exercise training to improve performance in COPD patients, using methods similar to those used to improve athletic performance, was suggested in 1951 (3) and demonstrated to be effective in 1964 (4). A recent review of the numerous studies of exercise recondi tioning in COPD summarizes the potential benefits (table 1) (5). The type of exercise (stair climbing, walk ing, treadmill or bicycle ergometer) appears to be unimportant and is best determined by patient preference and cost. Although the in tensity of exercise is usually determined by patient tolerance, the minimal duration and frequency required to improve performance appears to be 20 to 30 min, 3 to 5 times per wk. Leg exercise is usually better tolerated than arm exercise. Due to ventilatory limita tion, the level of exercise tolerated by most patients will not increase cardiovascular fit ness. Many patients are not suitable candi dates for exercise training because of faradvanced lung disease; advanced age, lack of motivation, and associated diseases. The ef fects of exercise conditioning disappear rap idly with cessation of exercise. B. Inspiratory Muscle Training Measures to specifically increase the strength and endurance of respiratory muscles have received recent attention as a potential part of a physical rehabilitation program for pa tients with COPD (6-9). The efficacy of this therapy is unproved and its role is unknown at present. The physiologic basis for the improved per formance associated with either exercise reconditioning or inspiratory muscle training is not fully understood. Major factors in volved appear to be improved aerobic capac ity, increased motivation, desensitization to the sensation of dyspnea, improved muscle 240 AMERICAN THORACIC SOd^ TABLE 1 BENEFITS OF EXERCISE RECONDITIONING____________________ ACCEPTED 8ENEFITS Increased endurance and exercise tolerance. Increased maximal oxygen consumption (generally small). Increased skill in performance of a task with decreased ventilation oxygen consumption, heart rate. UNLIKELY OR UNKNOWN BENEFITS Improved survival. Improved pulmonary function tests. Lowered pulmonary artery pressure. Improved arterial blood gases. Improved biood lipids. Change in muscle 02 extraction. Change in sleep desaturation or apnea. '__________ vided at lower cost to greater numbers of smokers (22-24). The efficacy ofhypnosisha, neither been proved nor disproved. Controlled clinical trials have not demonstrated acupun^ ture to be an effective strategy (25). . , The prompt benefits of smoking cessation ' for patients with chronic obstructive pulmo nary disease are reduction of cough and spu. turn production. Ultimately, a decrease in the rate of decline of the FEV, may be seen (21) Additional major clinical benefits include a reduction in the risk of cardiovascular mor tality and in the risk of cancers of the lung, larynx, mouth, esophagus, and bladder (26). Smoking cessation should be of highest prii ority in the comprehensive care of patients with COPD. function, and improved technique of perfor mance (6, 8, 9, 12). In addition to physical conditioning, sev eral forms of adjunctive therapy may improve exercise performance in some patients. Those generally accepted to be beneficial include ox ygen, beta-2 bronchodilators, and theophyl line. As yet unproved modalities include pul monary vasodilators, nutritional manipula tion, and improved psychosocial health. C Breathing Retraining Breathing retraining consists of teaching pa tients to utilize pursed-lip breathing, expira tory abdominal augmentation, synchroniza tion of movement of abdomen and thorax, and relaxation techniques for the accessory respiratory muscles, as well as psychologi cal assurance and education about COPD. Breathing retraining appears to allow patients to recover more rapidly from dyspnea induced by exercise. Such training is a useful compo nent ofa comprehensive care program for pa tients with COPD. D. Energy Conservation A standard aspect of physical medicine and rehabilitation is instruction in work simplifi cation and the use of energy conservation devices to allow disabled patients more inde pendence and greater participation in activi ties of daily living (13). Such instruction, par ticularly in patients with advanced COPD, may result in similar benefits (14). E. Nutrition Advanced COPD is frequently associated with loss ofweight and muscle mass. This may pro duce respiratory muscle weakness and fur ther limit ventilatory capacity. Patients need to maintain sufficient protein/calorie intake to prevent malnutrition. Frequent small feed ings or use of liquid formula diets may help. Enteral or parenteral hyperalimentation has been attempted to restore muscle mass in mal nourished COPD patients but the efficacy of such therapy is unknown at present. There is a recognized hazard in administering high carbohydrate loads, which may result in in creased C02 production, requiring increased ventilation (15), although the clinical impor tance of this is uncertain. F. Smoking Cessation G. Psychosocial Management Cigarette smoking affects lung structure and function in the following ways: increased mu cous secretion due to mucous gland hyper trophy and hyperplasia leads to increased cough and sputum production; small airways demonstrate a spectrum of abnormalities from mild inflammation to airway closure; lung parenchymal changes vary from a sim ple increase in inflammatory cells to destruc tion of alveolar walls which results in cen- trilobular emphysema (16-18). A significant functional impairment is identified in 10 to 15% of smokers, and is best identified by changes in FEV,. In non smoking adults, FEV, declines at the rate of approximately 20 to 30 ml per year. In those smokers who develop significant impairment, the rate of decline is 50 to 100 ml per year (19-21). . The profoundly adverse pulmonary effects of cigarette smoking demand that smoking cessation efforts be implemented by all who care for patients with chronic obstructive pul monary disease. Physicians should assume major responsibility in this regard. Motivational factors governing smoking behavior vary. There is evidence that strongly suggests that smoking is an addictive behavior due, in large part, to nicotine. Successful smoking cessation programs are those that address the biologic, behavioral, and psychological forces responsible for smoking as specifically as possible for each individual patient. Cessation programs in clude education and counseling by the physi cian or other trained personnel, and a variety of other techniques, including provision of self-help materials, group or individual be havior modification programs, pharmaco logic management using nicotine polacrilex to minimize nicotine withdrawal, adversive conditioning using rapid cigarette smoking, hypnosis, and acupuncture. Current data indicate that 20 to 30% of those enrolling in a "successful" smoking ces sation program will not have resumed smok ing at the end of 1 yr. Using this criterion, the efficacy of counseling and nicotine pola crilex, and of adversive conditioning, have been proved. Self-help programs result in somewhat lower quit rates, but can be pro Patients with chronic obstructive pulmonary disease frequently suffer from anxiety, depres sion, and problems related to cognitive, per ceptual, and motor activity. Limitations of financial and social resources are common place. Comprehensive care requires that at tention be given to the psychosocial as well as the physiologic problems of patients with COPD. The medical history, specific psy chosocial interviews, questionnaires, and for mal testing may be used to develop a thor- . ough psychosocial assessment. Problems should be identified by evaluation of the pa tient's social, cultural, ethnic, and educational background. Employment history, current ' financial resources, and family and conunu- nity support should be identified. In addi- / tion, the patient's personality, psychosexual >. concerns, significant life events, previous and f current lifestyle, and level of disability should be assessed (27, 28). .v Individuals responsible for the psychoso cial evaluation may include the primary phy- - siciaii, pulmonary consultant, nurses, ther- . apists, and chaplains. Formal rehabilitation . programs frequently use psychologists, social workers, and psychiatrists in performing the ; psychosocial evaluation. - Effective psychosocial interventions include education, counseling, and supervised exer- cise and supportive therapy provided by the medical staff, family, and groups of similarly . afflicted patients. Motivation and the devd- opment of realistic goals are emphasized Other aspects of a psychosocial, intervention V program include community referral, vqca*; tionai counseling, psychiatric consultation. ) and the use of anti-anxiety and/or and* ; depressive medications (29, 30). ; Psychosocial interventions provide the pa* tient with improved understanding of the ;? physiologic factors responsible for symptoms ; and aid in coping with dyspnea, stress, anxh ; ety, and depression. The patient and fanw I are helped in identifying and using I community, social, financial, and health car* | resources. Successful psychosocial manaj* | ment helps the patient accept physiologic oifr * tations, optimize strengths, and clarify sonable goals and priorities. Such mter^J tion allows the patient to participate 241 'tixrs'ojp'iosis>-'' >ntro `CUpun^; I essatfonl | spu*''; ] iseinthe j sen (21)., | delude a ; i Jar mor/' * he lung,' ] der (26). J '.hestpri- I patients J Imonary . depress ive, per* -tions of? Dmmon-' that at-;-; 1 as well V nts withf ific psy-'}' and fw-yv a thor-t;.'robIemr| fthepa^| icatioo^-' cun COfQQiw ^ In addi*r' rosexualg Sousand l y should'^ .'X jychoso-/ aryphy-v es, therv ilitatioh.. ts, social., tiing the* s include'; ;ed exer4: d by the jiimilarlyV re devd-:^ hasized.^ rvention^; U, vqca-%;? or anti-gi \~*y ethepa;J > of tbe| nptorns,>, ss, anxi-^: d fam3y^ ivail' altb nanage; igiclimk nfy nterye^ actively and effectively in a therapeutic pro- _raITli When psychosocial approaches are used fffectively, the patient is provided with a sense der the direction of: (a) visiting nurse associ ation, community nursing or public health agency, (b) proprietary nursing agency, or (c) 0fcontrol and mastery of his disease, and his durable medical equipment companies. quality of life is enhanced. To summarize, physical rehabilitation is an important component of a comprehensive B. Patient Selection Selection of patients and authorization for care program for patients with COPD. In many patients, activity level can be improved or maintained, resulting in both physical and psychologic benefits. Programs must be in home health care is the responsibility of the treating physician based on medical evalua tion and information obtained by nurses, so cial workers, and other members of the health dividualized to the needs and capabilities of each patient. Investigation is needed in iden tifying and assessing specific exercise-limiting factors in patients with COPD and determin ing the optimal therapy for each factor. This would allow more appropriate prescription ofphysical rehabilitation techniques and other adjunctive therapy for the individual patient. care team. Referral to an organized home health program is necessary for patients when there is doubt that the medical care program can be carried out in the home because of lack of knowledge, motivation, or adequate family caregivers, or because of the severity of illness. Any patient requiring additional teaching or support should be considered as a candidate for home care. Examples of the IV. Home Care Home care refers to health services that are provided to individuals and families in their place of residence for the purpose of promot ing, maintaining, or restoring health, or minimizing the effects of illness and disabil ity. Services appropriate to the needs of the individual patient and family are planned, coordinated, and made available by an agency or institution, and organized for the delivery of health care through the use of employed staff, contractual arrangements, or a combi nation of administrative patterns. Home care encompasses components including but not limited to, medical care, dental care, nursing, respiratory care, physical therapy, speech ther apy, occupational therapy, social work, nutri tion, homemaker, home health aide, trans portation, laboratory services, medical equip ment and supplies (31). The goals of home care are to: (7) improve the quality of life by allowing those patients with advanced disease to remain in their own spectrum of home health needs include: (7) patients who require only periodic outpatient medical supervision; (2) patients who require the assistance of home health aides and/or homemakers and infrequent or no profes sional visits; (5) patients newly diagnosed or newly educated in a comprehensive care pro gram who require visits for 2 to 4 wk to rein force details and to help with adapting fam ily caregivers and the home environment to the patient's needs. Generally, 1 or 2 visits per wk are sufficient; (4) patients with repeated hospitalizations who need regular supervision for an indefinite period to prevent clinical de terioration and repeated hospitalizations. The number of required visits depends on the com plexity of the treatment program -- from 1 to 2 times per month to several times per wk; and (5) patients with complex treatment pro grams, such as home ventilator care. The num ber of visits required depends on the skill of the patient and family caregivers. The need may last for the rest of the patient's life. environment and be with family and friends; C Types of Services Provided in the Home (2) minimize or prevent complications that would require hospitalization; (5) detect changes in physical and psychosocial status that indicate the need for changes in manage ment; (4) provide treatment for the patient's A position paper developed by the American Lung Association describes the essential com ponents of a home care program (36). These include evaluation, education, observation, primary diagnosis and foster adherence to the sexual counseling, consultation, psychosocial therapeutic program; and (5) foster a posi support, monitoring of respiratory equip tive and independent attitude. ment, direct patient care, and household help. A small number of studies document the Not all services are required by all patients benefits of home health care (32-34), but more and the types of services required by patients work needs to be done to confirm that con with COPD must be individualized. Dupli tinuing care at home will, in fact, decrease cation of services is both unnecessary and ex hospital admissions and length of hospital . pensive. Although home care is most com stay, and reduce overall cost of care. monly instituted upon hospital discharge, such care may be initiated in the absence of A- Qualifications oftheHome Care Provider a hospital admission. In hospitalized patients, The skills required of the home health care the plan of care should be determined and team are outlined in a position paper by the communicated to the home care team prior ATS (35). In addition, if durable medical to discharge to assure a smooth transition equipment is required, the vendor should pro- from hospital to home. The physician, nurs 'ride 24-h coverage by a respiratory care prac ing staff, and other allied health professionals titioner, rapid response to correct problems need to work collaboratively to develop a of equipment malfunction, and adequate feasible plan of care. The discharge planner, hack-up equipment. generally a nurse or social worker, needs to The home care programs may be: (7) be aware of the patient early in the hospital hospital-based, or (2) community-based, un course. Equipment requirements need to be assessed before discharge and, preferably, the hospitalized patient should be able to see and use the equipment that will be available in the home. The process of discharge planning should begin at the time of admission (37). A care plan needs to be developed for each patient. The standards for nursing care out lined by the ATS Section on Nursing (38) and guidelines developed by the California Tho racic Society Nursing Section (39) may be used along with standards of home care outlined by the American Association for Respiratory Care (40) as a basis for the development of this plan. V. Home Mechanical Ventilation Because the care ofventilator-assisted patients in the hospital setting is extremely expensive, there is great interest in identifying those ventilator-assisted patients who can be man aged safely in the home. At present, the prin cipal role for mechanical ventilation in the home is in the management of patients with ventilatory failure due to neuromuscular dis ease. Patients with severe chronic obstructive pulmonary disease are rarely suitable candi dates for mechanical ventilation at home be cause of complicating and frequently unsta ble medical problems that create such strin gent demands upon caregivers' therapy, thus making management in the home unsafe and impractical. However, a select and undoubt edly very small group of patients with severe, stable chronic obstructive pulmonary disease who are unable to maintain adequate pulmo nary gas exchange on their own may be can didates for mechanical ventilation at home. They consist of an unknown number of pa tients with severe chronic obstructive pulmo nary disease who are hospitalized for acute respiratory failure, placed on mechanical ven tilation, and, who despite stabilization of their condition, cannot be weaned from total ven tilator support. It has been noted that intan gible factors such as familiar surroundings and the attention of friends and loved ones may, when coupled with respiratory muscle rest, result in increasing independence from the ventilator in some patients who could not be weaned in the hospital setting despite exhaustive attempts by skilled physicians, nurses, and respiratory therapists. The poten tial for ventilator dependency should be rec ognized and, when appropriate, patients with severe obstructive lung disease should be in formed of the possibility of permanent ven tilator dependency prior to initiating mechan ical ventilation in the hospital setting. In addition, an as yet poorly defined sub set of these ventilator-assisted patients with chronic obstructive pulmonary disease may suffer from respiratory muscle fatigue due to abnormal resistive loads, muscle weakness and, in part, to mechanical disadvantage and shortening of the diaphragm due to pulmo nary overinflation (41). When total inter mittent ventilator support is discontinued, these patients may experience increasing dysp nea, hypercapnia, and hypoxemia. The quality oflife and physical well-being ofsuch patients I nay be improved with intermittent mechanical entilatory support (42, 43). In this group, ventilation is usually provided at night with a negative pressure ventilator. Insufficient data exist with regard to the benefit of this form of partial ventilator support, and, at present, it should be considered investigational. Several reports have formulated criteria for patient selection, established guidelines for home ventilator management, and demon strated that ventilator-assisted patients can be managed safely in the home (44--51); however, there have been no large-scale, controlled clin ical trials to evaluate the health and/or eco nomic benefits and risks ofsuch management. A. Patient Selection Consideration of mechanical ventilation in the home setting is indicated when a compe tent respiratory care team is unable to wean a patient with COPD from total ventilator support after several attempts over a period of weeks. The patient's health status must be stable such that no major therapeutic or di agnostic interventions are contemplated within a 30-day period ofdischarge from the hospital. The patient should maintain an ar terial oxygen tension of greater than 60 mm Hg with an inspired oxygen concentration of less than 40'Fo. The patient should not dem onstrate wide fluctuations in arterial oxygen or carbon dioxide tensions. The patient should have an active cough and gag reflex, and should not require frequent endotracheal suc tioning. A secure tracheostomy tube should be present, except in those patients managed with a negative pressure ventilator. The pa tient should be free of active infection, and should not be subject to frequent or recur rent infections. Any comorbid medical con ditions should be stable, and should not re quire frequent therapeuticinterventions. The candidate for mechanical ventilation in the home should express a desire to be discharged to home on a ventilator, and a willingness to cooperate with the respiratory care team in order to acquire the information and skills required of a ventilator-dependent patient at home. Care of a ventilator-assisted patient in the home often creates significant physical and emotional stress for the patient, family, and caregivers. Patients and their caregivers must be fully aware of this potential prior to deciding to participate in a home ventilator program. A psychosocial evaluation should confirm that the patient and caregivers are aware of and understand the demands and stresses associated with maintaining a ven tilator-dependent patient in the home, and that coping resources are adequate to meet these demands (52). B. Caregivers Within the circle of family and friends, caregivers must be identified who are avail able and express the willingness and physical, emotional, and cognitive ability to provide care. A support network of family, friends, and neighbors should be available to provide additional assistance when needed. Individ uals identified as caregivers must demonstrate a commitment to participate in an educational program, and devote sufficient time and energy to develop, utilize, and demonstrate the skills necessary to care for a ventilatorassisted patient at home. Caregivers must learn, master, and dem onstrate those skills that will enable them to provide total patient care. The skills required include the ability to: (!) administer medica tions in a correct and timely manner and familiarity with the actions of and side ef fects of such medications; (2) assemble and disassemble ventilator circuits; (5) adjust ven tilator settings and alarms; (4) clean, main tain, and troubleshoot equipment; (5) use a hand resuscitator; (6) administer breathing treatments; (7) continue weaning efforts; (8) administer supplemental oxygen when neces sary; (9) set up, use, and clean suction ap paratus; (10) perform tracheostomy care and suctioning; (IT) clean, change, and plug tra cheostomy tubes when indicated; (12) main tain proper tracheostomy cuff inflation when applicable; (13) provide clapping, vibration, and postural drainage as well as cough as sistance; (14) position patients correctly and assist with transfers, strengthening and range of motion exercises; (IS) understand and in struct in energy conservation techniques; (16) measure vital signs and recognize changes in vital signs and other signs and symptoms of respiratory distress; (17) recognize signs and symptoms of respiratory infection; (18) per form proper skin care; (19) feed the patient or administer enteral feedings if necessary; (20) perform required bladderand bowel care; (21) communicate effectively with the patient; (22) contact the local emergency systems; and (23) perform cardiopulmonary resuscitation. C Resources A suitable and safe home environment with sufficient space and appropriate hygienic and electrical requirements is necessary. Doorways and halls must permit access and mobility of the patient and equipment. Required resources include a primary phy sician, medical and pharmaceutical suppliers, home health agencies, an emergency trans port system, and a reasonably proximate hos pital and emergency room. Sufficient finan cial resources to cover the total costs of environmental modification, equipment, sup plies, and paid caregivers must be available. Prior to beginning the process of patient and caregiver education, administrative ap proval for home management of a ventilatorassisted patient must be obtained from thirdparty providers. The physical home environ ment and availability of required resources must be evaluated by members of the respi ratory care team, and plans for modifications in doorways, electrical outlets, hygiene facil ities, and access must be made as necessary. D. Planning for Discharge The process of transferring a ventilatorassisted patient with chronic obstructive pul monary disease from the hospital to home' requires the involvement and cooperation of an experienced respiratory care team, work, ing with community health agencies, dura ble medical equipment suppliers, state and local agencies including the phone company utility companies, fire department, and emer gency medical services. Although the program for discharging a ventilator-assisted patient to home should be structured and the team experienced, the specific educational routine and plans for each patient must be individu alized and tailored to the patient's unique needs. .- During the process ofpreparing the patient for discharge, the full resources of the respi ratory care team must be devoted to an ongo ing process of rehabiiitation in which the pa tient's potential for independence in activi ties of daily living are maximized. Ideally, patients will be able to breathe independently for periods throughout the day. In practice, the degree of ventilator dependence ranges from ventilatory support 24 h a day to a re quirement for nighttime ventilation only." The respiratory care team leader may be a pulmonary nurse specialist, discharge coor dinator, or qualified respiratory therapist. This individual should coordinate the activi ties of the team and meet with the patient, members of the team, and home caregiveh to establish specific goals, develop training schedules, and insure that supply and equip ment needs are met. Team conferences to evaluate and accept potential candidates',-! plan the treatment program, and to measure progress are required. Documentation of training activities and patient progress is.es* sential. A physician must be willing to accept responsibility for overall supervision and peri odic follow-up care of the patient, and should approve all plans for medications, ventilator care, and nursing care. The physician should periodically assess the need for continued ven tilator assistance. The physician should be willing to make home visits if necessary. If office visits occur, appropriate transportation must be prearranged. . ,-rJ The members of the respiratory care team possess a variety of skills. Where resources vary, there may be overlapping functions of health care personnel. The skills of the fol lowing personnel may be required depending on individual patient needs: (1) primary pby* sician, (2) nurse, (J) respiratory therapist, W physical therapist, (S) occupational therapist* (6) social service worker, (7) psychologist/ psychiatrist, (5) durable medical equipment vendor, and (P) home health agency. Prior to discharge, the patient and care givers may make several brief excursions out* side the hospital, perhaps spending some time at home. At the completion ofa training pro* gram, the caregivers must have demonstinted ifcompetencies in all required care of the P*T tient to the satisfaction ofthe respiratory??1* team. A checklist should document theq^ onstration of required abilities and the ?'?JvM ability of necessary equipment and resouf^ Prior to discharge of the patient, jHEHICAN THORACIC SOCfcTY 243 hon*|r, on 00- ivorlc^*' dura e ani? `Pany,-? eraer;.:r Jgram*1 atienj : tea Jutioe ividu- miq.u/e ) atient' i respi-; I ongo, | he pa-. .; | activi-/ I ieaUy,; dently - | action * ranges';-/ o a re-'/ only.'/v iay bej : coor-/' rapist/: activi-;;/ J atiea jgivers/ aining'i equipj^ ices tor* ites,'; leasuiion of| ;s is es* ?, access . id peri:/-' should itilator % should/ ed veh// mid be sary. If;/ irtatioa'v' ^yjpjxient and supplies must be delivered to the home. Respiratory care and nursing personnel will accompany the patient home, and make fre quent home visits during the first 1 to 2 wk following discharge. Thereafter, the attend ing physician and respiratory care team will periodically evaluate the patient to determine if modifications of the medical, nursing, or ventilator program are necessary. References 1. American Thoracic Society. Pulmonary Re habilitation. Am Rev Respir Dis 1981; 124:663-6. 2. Loke J, Mahler D, Man P, Wiedemann H, Matthay R. Exercise impairment in chronic obstruc tive pulmonary disease. Clinics in Chest Medicine 1984; 5:121-43. 3. Barach A, Bickerman H, Beck G. Advances in the treatment of nontuberculous pulmonary dis ease. Bull NY Acad Med 1952; 28:353-84. 4. Pierce A, Taylor H, Archer R, Miller W. Re sponses to exercise training in patients with em physema. Arch Intern Med 1964; 113:28-36. 5. Hughes RL, Davison R. Limitations of exer cise reconditioning in COPD. Chest 1983; 83:241-9. 6. Leith D, Bradley M. Ventilatory muscle strength and endurance training. J Appl Physiol 1976; 41:508-16. 7. Peress L, McClean P, Woolf C, Zamel N. Re spiratory muscle training in severe chronic obstruc tive puimonary disease. Am Rev Respir Dis 1979; 119(Suppl:157). 8. Belman MJ, Mittman C, Weir R. Ventilatory muscle training improves exercise capacity in chronic obstructive pulmonary disease patients. Am Rev Respir Dis 1980; 121:273-80. 9. Pardy R, Rivington R, Despas P, Macklem P. The effects ofinspiratory muscle training on exer cise performance in chronic airflow limitation. Am Rev Respir Dis 1981; 123:426-33. 10. Sonne L, Davis J. Increased exercise perfor mance in patients with severe COPD following in spiratory resistive training. Chest 1981; 79:393-8. 11. Chen H, Dukes R, Martin B. Inspiratory train ing in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1985; 131:251-5. 12. Belman M, Wasserman K. Exercise training and testing in patients with chronic obstructive pul monary disease. Basics of R.D. 1981; 10:1-6. 13. Leslie L. Training for functional independence. In: Krusen's handbook of physical medicine and rehabilitation. Philadelphia: W. B. Saunders, 1982; 501-7. 14. Falconer J. Pulmonary rehabilitation. In: Adult rehabilitation: a team approach for therapists. Boston: Little, Brown, 1982; 199-223. 15. Askanazi J, Nordenstrom J, Rosenbaum SH, elal. Nutrition for the patient with respiratory fail ure. Anesthesia 1981; 54:373-7. 16. U.S. Department of Health and Human Ser ies, Public Health Service. The health conse quences of smoking--chronic obstructive pulmo nary disease--a report of the Surgeon General. Washington, D.C.: U.S. Government Printing Of fice, 1984 (DHEW Publication No. [PHS) 84-50205). American Thoracic Society. Cigarette smok es and health. Am Rev Respir Dis 1985; 132: 1133-6. 18. JanoffA. Biochemical links between cigarette smoking and pulmonary emphysema. J Appl Phys iol: Respir Environ Exercise Physiol 1983; 55(2):285-93. 19. Burrows B, Knudson RJ, Cline MG, Lebowitz MD. Quantitative relationships between cigarette smoking and ventilatory function. Am Rev Respir Dis 1977; 115:195-205. 20. Clement J, Van de Woestijne KP. Rapidly decreasing forced expiratory volume in one second or vital capacity and development of chronic air flow obstruction. Am Rev Respir Dis 1982; 125:553-8. 21. Buist AS, Sexton GJ, Nagy JM, Ross BB. The effect of smoking cessation and modification on lung function. Am Rev Respir Dis 1976; 114:115-22. 22. Davis AL, Faust R, Ordentlich M. Self-help smoking cessation and maintenance programs: a comparative study with 12-month followup by the American Lung Association. Am J Public Health 1984; 74:1212-7. . 23. Jarvis MJ, Raw M, Russell MAH, Feyerabend C. Randomized controlled trial of nicotine chew ing gum. Br Med J 1982; 285:537-40. 24. Hall RG, Hall SM, Sachs DPL, Benowitz NL. Two-year efficacy and safety of rapid smoking ther apy in patients with cardiac and pulmonary dis ease. J Consulting Clin Physiol 1984; 52:574-81. 25. Lamontage Y, Annable L, Gagnon M. Acu puncture for smokers; lack oflong-term therapeu tic effect in a controlled study. CMA J 1980; 122: 787-90. 26. Schuman LM. The benefits of cessation of smoking. Chest 1971; 59:421-7. 27. Kim HT, Knecht PA, Hiscox DE, Glaser ED. Psychosocial factors and puimonary patients. In: Hodgkin JE, Zorn EG, Connors GL, eds. Pulmo nary rehabilitation--guidelines to success. Boston: Butterworth, 1984; 207-38. 28. Dudley DM, Glaser EM, Jorgenson BN, Lo gan DL. Psychosocial concomitants to rehabilita tion in chronic obstructive pulmonary disease. I. Psychosocial and psychological considerations. Chest 1980; 77:413-20. 29. Dudley DM, Glaser EM, Jorgenson BN, Lo gan DL. Psychosocial concomitants to rehabilita tion in chronic obstructive pulmonary disease; II. Psychosocial treatment. Chest 1980; 77:544-51. 30. Dudley DM, Glaser EM, Jorgenson BN, Lo gan DL. Psychosocial concomitants to rehabilita tion in chronic obstructive puimonary disease. III. Dealing with psychiatric disease (as distinguished from psychosocial or psychophysiologjc problems). Chest 1980; 77:677-84. 31. Statement of Assembly of Outpatient and Home Care Institutions, AHA; Council of Home Health Agencies and Community Health Services, NLN; NationalAssociation ofHome Health Agen cies; National Council for Homemaker-Home Health Aide Services, Inc NLN:1973. 32. ChemiackRM, HadordRG,SvanhillE. Home care of chronic respiratory disease. JAMA 1969; 208:821-4. 33. South Hills Health System; Home Health Agency Public Health Service Grant 03-H-001:327373 Final Report, December 1981 (unpublished paper). 34. Loma Linda University Medical Center. Tes timony before the committee on labor and human resources. UnitedStates Senate, March4,1981, AAR Times. 35. American Thoracic Society. Skills of the health team involved in out-of-hospital care for patients with COPD. Am Rev Respir Dis 1986; 133:948-9. 36. American Lung Association, Home Health Care. ALA, 1740 Broadway, New York, NY 10019 (unpublished paper). 37. Arneth LM, Mamon S. Determining patient needs after discharge. Nursing Management 1985; 16:20-4. 38. American Thoracic Society Section on Nurs ing. Standards ofcare for patients with COPD. ATS News 1981; 7:31-8. 39. California Thoracic Society. Guidelines for nursing care of the pulmonary patient, 1984 (un published paper). 40. American Association of Respiratory Care. Standards for respiratory home care. An official statement by the American Association of Respi ratory Care, 1979 (unpublished paper). 41. Rochester DF, Braun NMT. Determinants of maximal inspiratory pressure in chronic obstruc tive pulmonary disease. Am Rev Respir Dis 1985; 132:42-7. 42. RochesterDF, BraunNMT, LaineS Diaphrag matic energy expenditure in chronic respiratory fail ure. Am J Med 1977; 63:223-32. 43. Garay SM, Tbrino GM, Goidring RM. Sus tained reversal of chronic hypercapnia in patients with alveolar hypoventilation syndromes. Am J Med 1981; 70:269-74. 44. Feldman J, Tuteur PG. Mechanical ventila tion: from hospital intensive care to home Heart Lung 1982; 11:162-5. 45. Roselle S, D'Amico FJ. The effect of home respiratory therapy on hospital readmission rates of patients with chronic obstructive pulmonary dis ease Respir Care 1982; 27:1194-9. 46. Fischer DA, Prentice WS. Feasibility of home care for certain respiratory-dependent restrictive or obstructive lung disease patients. Chest 1982; 82:739-43. 47. Sivak ED, Cordasco EM, Gipson WT. Pul monary mechanical ventilation at home: a reason able and less expensive alternative Respir Care 1983; 28:42-9. 48. Splaingard ML, Frates RC, Harrison GM, et al. Home positive-pressure ventilation: twenty years' experience Chest 1983; 84:376-82. 49. Gilmartin M, Make B. Home care of the ventilator-dependent person. Respir Care 1983; 28:1490-7. 50. Make B, Gilmartin M, Brody JS, Snider GL. Rehabilitation ofventilator-dependentsubjects with lung diseases. Chest 1984; 86:358-65. 51. Hughes RL. Home is the patient. Chest 1984; 86:344-5. 52. Committee ofRespiratory Care Section ofthe American College ofChest Physicians. Guidelines for the care of ventilator-assisted individuals in the home and at alternate community sites. Chest 1986; 90(Suppl:IS-37S). This statement was developed by a Task Group appointed by the ATS Scientific Assembly on Clinical Problems. Members of the Task Group were: David R. Dantzker, M.D., Chairman Susan K. Pingleton, M.D., Chairman-- Scientific Assembly on Clinical Problems Chronic Obstructive Airways Diseases John A. Pierce, M.D., Chairman Dennis E. Niewqehner, M.D. William M. Thurlbeck, M.D. A. Sonia Buist, M.D. 244 Asthma k S. Kronenberg, M.D., Chairman Daniel J. Stechschulte, M.D. Jeffrey M. Drazen, M.D. Pharmacologic Therapy Ronald B. George, M.D., Chairman Irwin Ziment, M.D. Joseph H. Bates, M.D. Respiratory Care Alan L. Plummer, M.D., Chairman David J. Pierson, M.D. Walter J. O'Donohue, M.D. Oxygen Therapy Nicholas R. Anthonisen, M.D., Chairman A. Jay Block, M.D. Paul Kvale, M.D. Thomas L. Petty, M.D. AMERICAN THORACIC SOClETy* Home Care and Rehabilitation Gerald R. Kerby, M.D., Chairman Philip M. Gold, M.D. Mary E. Gilmartoj NOTICES ADVANCES IN SECTIONAL IMAGING e Department of Radiology, University of California, San Diego School of Medicine is presenting the following postgraduate course: "Advances in Sectional Imaging," September 10-12, 1987, at the US. Grant Hotel, San Diego, California. The Program Director is Robert F. Mattrey, M.D. The guest faculty includes Matthew D. Rifkin, M.D.; Thomas Jefferson University Hospital, Philadelphia, Pennsylvania; and Elias A. Zerhouni, M.D.; Johns Hopkins, Balti more, Maryland. The faculty from the University of California, San Diego School of Medicine is Giovanna Casola, M.D.; Robert Edelman, M.D.; John Forsythe, R.D.M.S.; Paul J. Friedman, M.D.; Barbara B. Gosink, M.D.; John R. Hesselink, M.D.; George R. Leopold, M.D.; Robert F. Mattrey, M.D.; Thomas R. Nelson, Ph.D.; Dolores H. Pretorius, M.D.; David J. Sartoris, M.D.; and Eric van Sonnenberg, M.D. The registration fee for the course is $375.00 for physicians and $275.00 for residents, fellows, or technologists. The course is accredited for 14 hours in Category I. To receive more information, please contact: Dawne Ryals, Ryals & Associates, P.O. Box 920113, Norcross, GA 30092-0113; (404) 641-9773. BOARD REVIEW IN CRITICAL CARE MEDICINE Board Review in Critical Care Medicine (ACLS Option). October 7-11,1987--Portland, Oregon. School of Medicine, Oregon Health Sciences University, CME-GH., OHSU, Portland, OR 97201; (503) 225-8700. CARDIOPULMONARY UPDATE '87 The Heart & Lung Institute at St. Vincent's Medical Center in Jack sonville, Florida will hold a seminar at the Marriott at Sawgrass, Ponte Vedra Beach, Florida on current topics of interest to the pul monologist, cardiologist, oncologist, and internal medical physi cian. The registration fee is $225.00, payable by Sept. 10, 1987. For further information, please contact: Alberta Hipps, Adm. Direc tor, Heart & Lung Institute, P.O. Box 2982, Jacksonville, FL 32203; phone: (904) 387-7563. . 12th INTERNATIONAL CONFERENCE ON LUNG SOUNDS The 12th International Conference on Lung Sounds will be held in Paris, France at the Institut D'Electronique Fondamentale, Wed nesday through Friday, September 16-18, 1987. Call for abstracts: Papers for presentation during the Conference will be selected by the Program Committee. Abstracts should not exceed 200 words in length and should be submitted by July 1,1987. Notifications of acceptance will be mailed out by July 15, 1987. Abstracts may relate to any aspect of lung sounds; examples are studies ofmechanisms of production, clinical implications, physio logical correlations, methods for recording, analysis or representa tion. ' . : Registration: Registration fee is $100 per person. Checks should be made payable to: International Lung Sounds Association. ' Correspondence: All abstracts and questions regarding arrange ments should be addressed to: Robert G. Loudon, M.B., Ch.B. '. University of Cincinnati Medical Center Pulmonary Disease Division 231 Bethesda Ave. . Cincinnati, OH 45267-0564 ; PRACTICAL SPIROMETRY COURSE The course "Practical Spirometry" will beheld August 19-20,1987, in Atlanta, Georgia and October 8-9,1987 in Chicago* Illinois. Spon sored by: Mayo Pulmonary Services. For further information, please contact: Ginnie Allie, Mayo Pulmonary Services, 432 Plummet Mayo Clinic, Rochester, MN 55905; or call toll free 1-800-533-1653 (Minnesota residents, 1-800-562-1767). . 'siol American Thoracic Society (st- - 28:877-*,. The Qntj ^nrvaie*. 1984; It MEDIC -5- SECTION OF THE AMERICAN LUNG ASSOCIATION STANDARDS FOR THE DIAGNOSIS AND CARE OF PATIENTS release of e Jungt j 6. .. asargjkiiii a release sbit lunp. WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) AND ASTHMA1 a 7KJS Official Statement of the American Thoracic Society was adopted by the ATS Board of Directors, November 1986. D, etoLAinces PGI, heiial cefli. ;ger J, ]: ndin D, a 1981; 240: y MA.Prw lary hype-_ diair 1982; DC, H* 3f PGDjC*'sin thew* 7-50. m OL.. cells Mlffectscfif?*1 >onseto>? 1978; and throS* ] .ary dradfcj j rinaiol 198CT ring pul; . Columb J, for theki^-i lambs. 1 Contents Chapter 1............................Chronic Obstructive Pulmonary Disease Chapter 2..................................................Asthma Chapter 3......................Pharmacologic Therapy Chapter 4............................................0, Therapy Chapter 5..............Respiratory Care Modalities Chapter 6........................Physical Rehabilitation . and Home Care CHAPTER 1 Chronic destructive Pulmonary Disease i. introduction Thirty years ago, British and North Ameri can terminology for the same major lung con dition differed: The clinical term "emphy sema" in the United States was equivalent to "chronic bronchitis" in Great Britain. Gener ations of British physicians had recognized chronic bronchitis as a potentially disabling and even lethal affliction that was associated with cigarette smoking and dusty working en vironments (1). Attention in the United States somehow '.- id been directed more to the pro found structural changes of emphysema that were first described by Laennec (2). The mor bidity and mortality due to these diseases in creased during the 20th century on both sides of the Atlantic. Improved physiological techniques were ap plied after World War II thal rapidly advanced understanding of pulmonary pathophysioliy (3-6). The significance of reduced expi ratory airflow was widely appreciated. The first Aspen Conference in 1958 had interna tional representation, and appointed a com mittee on terminology, which agreed unani mously fi. . :mphysema must be defined mor phologically (7). British workers met in 1959 to discuss terminology, and published com prehensive suggestions (8) for an orderly tranJJhon to the newly recommended terminol^The term "chronic non-specific lung dis*^se" was devised, but proved too awkward *?) It also included a category of "obstrucl|ve lung disease" that could occur either with 0r without reversibility, and with or without Chronic Airways Obstruction Chronic obstructive pulmonary disease (COPD) end asthma are the ma)or causes of pulmonary disability In the United States, with at least 10 million Americans suffering from COPD and up to 5W of the population afflicted with asthma. Over the past 20 years, major strides have been made in our understanding of the pathophysiology of these two disorders, although there are still large gaps in our knowledge. While a number of position papers and statements have been promulgated by the American Tho racic Society concerning various aspects ot the diagnosis and treatment of COPD and asthma, it was felt that a review of the overall topic was timely. This statement represents the combined efforts of a Task Group appointed by the Scientific Assembly on Clinical Problems of the American Thoracic Society to accomplish this task. Clearly, we could not cover every aspect of this bread topic nor even provide a detailed review of those areas addressed. We elected instead to concentrate on clinically relevant topics and to provide sufficient data to bt useful as a guide as well as to Include selected, but in no way exhaus tive, references. The first two chapters define the entitles and set forth recommendations for diag nosis, hospital admission, and discharge. The remaining four chapters critically review the various facets ot therapy. We have noted controversial areas and those where conclusive experimental data are not yet available. In these situations, the committee often decided to taka a position on one side or the other baaed upon the beat available information. emphysema. The present recommendations continue along this line of reasoning. Chronic obstructive pulmonary disease (COPD) is defined as a disorder character ed by abnormal tests of expiratory flow that uo not change markedly over periods of sev eral months observation. The qualification is intended to distinguish'COPD from asthma. The airflow obstruction may be struc tural or functional. Specific causes of airflow obstruction such as localized disease of the upper airways, bronchiectasis, and cystic fibrosis are excluded. Bronchial hyperreac tivity may be present in patients with COPD as measured by an improvement in airflow following the inhalation of beta-adrenergic agents or worsening after inhalation of methachoiine or histamine (10). Three disorders are incorporated in COPD: emphysema, peripheral airways disease, and chronic bronchitis. Of these, only emphysema is further classified. Any individual patient may have one or all of these conditions, but the dominant clinical feature in COPD is al ways impairment, or limitation of expiratory airflow. II. Definitions A. Emphysema The American Thoracic Society previously defined emphysema as an anatomic altera tion of the lung, characterized by an abnor mal enlargement of the airspaces distal to the terminal non-respiratory bronchiole, accom panied by destructive changes of the alveolar walls (11). This definition was reconsidered and modified by a recent workshop of the National Heart, Lung and Blood Institute. Our committee recommends adoption of the concepts and definitions published by that group in 1985 (12). Emphysema is defined as "a condition of the lung characterized by abnormal perma nent enlargement of the airspaces distal to the terminal bronchiole, accompanied by de struction of their walls, and without obvious fibrosis." Destruction in emphysema is de- ' This project was supported by a grant from Boehringer Ingelheim Pharmaceuticals. Inc 1 Reprints may be requested from your state or local (ung associations. 225 226 American thoracic fined as nonuniformity in the pattern of re spiratory airspace enlargement so that the or derly appearance of the acinus and its com ponents is disturbed and may be lost. It is recognized that emphysema, depend ing on its severity, may be diagnosed in a va riety of ways, including naked eye examina tion, by examination of an inflation-fixed lung slice using a dissecting microscope (sub-gross examination), or by light microscopic exami nation of thick (200 to 400 urn) or thin (4 to 6 pim) stained and mounted sections. Emphysema is recognized as a subcategory of respiratory airspace enlargement which in cludes: Respiratory Airspace Enlargement 1. Simple Airspace Enlargement a) congenital b) acquired 2. Airspace Enlargement with Fibrosis 3. Emphysema a) centriacinar b) panacinar c) distal acinar In simple airspace enlargement the pattern of the acinus is retained with no evidence of destruction. Congenital airspace enlargement occurs in Down's syndrome or congenital lo bar overinflation, whereas acquired forms of respiratory airspace enlargement include com pensatory overinflation and the uniform re spiratory airspace enlargement in the aging ''mg. It is still possible that the airspace en- rgemem of age is not due to age alone, but e to the combination of age and environ mental conditions. However, the changes oc cur in nearly all subjects and it has been sug gested that these changes are therefore "nor mal." The term "aging lung" is preferable to the term "senile emphysema." A spectrum of airspace enlargement is usu ally associated with fibrosis of the lung. There is generally no difficulty recognizing honey combed interstitial pulmonary fibrosis or air space enlargement associated with fibrosis in granulomatous lesions such as tuberculosis, sarcoidosis, or eosinophilic granuloma. Three subtypes of emphysema are recog nized: a) Centricinar emphysema. This is also re ferred to as proximal acinar emphysema be cause the proximal part of the acinus (respi ratory bronchiole) is dominantly involved. There are 2 subdivisions of this form of em physema. The first is classically associated with cigarette smoking and airflow obstruc tion, and is also referred to as centrilobular emphysema. Inhalation of coal dust and other mineral dust also results in dilatation of re spiratory bronchioles with accumulation of dust-laden macrophages in and around respi ratory bronchioles, and has been referred to - focal emphysema. However, in those ex- ed to coal dust, the term coal pneumoconiis preferable. i panacinar emphysema. In this subtype, 11 components of the acinus tend to be in-olved about equally. It is the form of em physema commonly associated with alpha- 1-antiprotease deficiency (13). It may also oc cur in the bases of the lung in patients with centrilobular emphysema, and as an inciden tal finding in older subjects. c) Distal acinar emphysema. In this sub type the distal part of the acinus, alveolar ducts and sacs, are predominantly involved. Because of the association of this form with the secondary interlobular septa, it is also known as paraseptal emphysema; the distal acinus also abuts on pleuras. vessels, and air ways, and the emphysema may be worse in these regions. Additional types of emphysema have been suggested, but considerable overlap exists even with the types already described, and there seems to be little reason for further subdivi sions. When emphysema becomes severe, it is difficult to classify, and expert pathologists often disagree on the classification of such emphysematous lungs. Emphysema severity as assessed morpho logically is the single best correlate with an index ofairflow obstruction such as the forced expiratory volume in one second (FEV,) (14-16). Patients who have significant physi cal impairment due to COPD usually exhibit emphysema of at least moderate severity when examined postmortem. Occasionally, such pa tients have only minimal emphysema (17), and, rarely, it is absent (18). B. Peripheral Airways Disease A variety of morphologic abnormalities have been identified in the peripheral airways of patients with COPD. These include inflam mation of the terminal and respiratory bron chioles, fibrosis of airway walls with narrow ing, and goblet cell metaplasia of the bronchiolar epithelium (19). The distribution and severity of these changes varies considerably among individuals. Structure-function corre lations suggest that these lesions contribute to airflow obstruction in severe COPD, but that their importance is secondary to that of emphysema (14-16). In persons at risk for de veloping COPD (e.g., cigarette smokers), pathological changes in the peripheral airways appear to precede the development of emphy sema (20). It has been suggested that inflam mation and other changes in the peripheral airways may be responsible for subtleabnormalities in pulmonary function tests that are not associated with physical impairment and that these physiological and pathological ab normalities may represent "early, ot preclinical" COPD (15,21). It is emphasized that these relationships remain unconfirmed by long term studies, and that their clinical relevance remains uncertain. C Chronic Bronchitis Chronic bronchitis, as previously defined, refers to "the condition of subjects with chronic or recurrent excess mucus secretion into the bronchial tree." Chronic was defined as "occurring on most days for at least three months of the year for at least two successive years" (8). The excess secretion should not be brought about by other diseases such as bronchiectasis or tuberculosis. Excess miK secretion was empirically recognized */?* production of any sputum, whether expT rated or swallowed, and in most instances*^ turn production is accompanied by chroS cough. Although not explicitly stated in tS ' definition, it was generally held that exS mucus production is an important cause of airflow obstruction (19), and "chronic brt chitis has been commonly used to mean ev piratory airflow obstruction." Many patients with COPD have excess spy. turn production as well as hyperplasia ofU* mucus glands of the trachea and large broachi. Both abnormalities have been linked etio logically to cigarette smoking. However, avail, able evidence indicates that these effects of cigarette smoke are independent of those which cause airflow obstruction. Numerous structure-function correlative studies have failed to identify a dose relationship betweea airflow obstruction and mucus gland hyper, plasia (6, 8, 22, 23). More importantly, lon gitudinal population studies have failed to identify an independent effect of cough and excess sputum production upon the develop ment of airflow obstruction (1, 24, 25). 11). Diagnosis A. Clinical Assessment A complete history and physical examination should be performed during the initial assess ment of each patient suspected of having COPD, and repeated on those occasions when the condition of the patient changes (eg., hos pitalization). Limited histories and physical examinations should be performed at inter vals to evaluate the course of the disease and 1 the response to therapy. Characteristically, COPD affects middle^., aged and older persons. The dyspnea due to, COPD cannot be reliably distinguished fro, that due to other causes, and is frequent^ associated with cough, wheezing, sputum;, production, and recurrent respiratory infec tions. Occasionally, dyspnea is the onlysymp* tom of COPD. In this situation it is insidious^ in onset and progressive in severity. Long-tens], cigarette use is the principal identified causey of COPD, but these disorders do not occur,; exclusively in cigarette smokers and tbe majority of smokers do not develop clinical^ manifested lung disease (26). Inhaled tons*/; encountered in the workplace or in the env| ronment pose additional risk factors for tbf/. development of COPD and a history of sueh%' exposures should be sought. The inherited^ deficiency of plasma alpha-l-antiproteas* renders the patient more susceptible to the . damaging effects of cigarette smoke and; predisposes to the early development ofe COPD (13, 27, 28). Physical examination of patients ^th^ COPD may reveal signs of lung overinflatioi* increased respiratory muscle effort, altered* breathing patterns, and abnormal breath* sounds. Wheezes, especially on forced ratory and diminished breath sounds, may detected by auscultation. One or more of thes i i 1 r it 2 c 1 v. d $ a ii c tl P S' tl b It P 0: a, d< si tr ti. b) m. n> c. sh ex S'fo te di th, 30 th. sii in m;. an ere um ity oarf? jrnEWCA* THOBACtC SOCIETY 227 nucr as tby *ironic in this excess use of brot> an ex- 1 I < I 1 ) physical signs are usually present in patients uh advanced COPD, but the changes on physical examination may be sufficiently sub tle as to be overlooked even in the presence of moderate airflow limitation. The need for com 'tative services may arise anytime the cone -on of the patient deteriorates. Laboratory Tests l Roentgenographic examination. A plain chest roentgenograph in posterior-anterior ssspuofthe brondetio. avai]. ects of those nerous s have ctween hype;iy, ioniled to and lateral projections is necessary for the evaluation of patients with suspected COPD since the presence of regional hyperlucency and vascular attentuation confirm the exis tence ofemphysema. With severe emphysema, overinflation ispresent often, and bullous le sions are fairly common. It is pertinent, how ever. that roentgenographic studies have limr sensitivity for the detection of emphy sema, and that the correlation of roentgeno graphic abnormalities with the severity of air flow obstruction or of anatomic emphysema is imperfect. Specialized studies such as com eh and puted tomography are not usually necessary rveiop- in patients with uncomplicated COPD. 25). 2. Pulmonary function testing. Spirometric evaluation establishes the diagnosis of COPD. Testing should be performed by methods, and > with instrumentation, that conform to stan - f dards established by the American Thoracic inatr Society (29). The spirometric abnormalities asse assc ? ted with COPD consist of a reduction h in if.. forced expiratory volume in one sec is . ond (FEV,) and in the ratio of the FEV, to .g., hos- the forced vital capacity (FVC). Many other >hysical parameters may be calculated from the spiro it inter* gram (30, 31). but there is no evidence that ase and they provide useful diagnostic information middle-'--1 a due to .. ed from -1 beyond that contained in the FEV, and FVC. it is desirable to perform spirometry in all patients who have unexplained dyspnea and/ or in whom COPD is suspected. It has been quently sputum { advocated that all individuals at risk for developing COPD (e.g., habitual cigarette y infee-j smokers) be screened regularly by spirome y symp- $ isidiouJj ng-term ; try detect mild abnormalities with the ra tionale that severe disease might be prevented by smoking cessation and early treatment ;d causey1 ot occur; and the v finicaliy . d toxins 'w_ :he envi--M s for the * | ; of such ;' nherited > ( protease le to the 3 oke and * men' * measures. The efficacy of such programs has not been demonstrated. Repeat spirometric testing following medi cations (e.g., bronchodilators, corticosteroids) should be performed to determine to what extent the disease is reversible and to provide guidelines for rational therapy. The failure of forced expiratory flows to improve acutely af ter bronchodilator inhalation does not pre clude a long-term beneficial response to ei ther bronchodilators or corticosteroids (10, 30, The response of spirometric tests to the inhalation of bronchoconstrictor sub stances (e.g., methacholine) have been useful its in asthma but their use in the diagnosis and nfl* tnanagement of COPD has not been defined, *nd a role seems unlikely. 1 P.vathj^. COPD is frequently associated with an in :ed expi' l crease in total lung capacity and residual vol se,omfathyebs1ee - ume, and a reduction in the diffusing capac ity for carbon monoxide (Dlco) (33). The measurement of lung volumes and of the Dlco may be helpful in the initial evaluation of patients suspected of having COPD. In sub sequent follow-ups, forced expiratory spirom etry alone usually suffices to demonstrate the response to therapy, or to explain symptom atic deterioration. COPD is also associated with abnormali ties in lung mechanics (e.g., compliance, air flow resistance), and abnormalities of vari ous tests of ventilation distribution (e.g., the single breath nitrogen washout test) have been described. The clinical relevance of these tests in the diagnosis and evaluation of COPD is unsettled, and their routine use is not recom mended. A reduction in exercise tolerance is com monly found in COPD, and routine evalua tion of exercise capacity is unnecessary. Such an evaluation may be indicated, however, when considering the need for supplemental oxygen therapy or when looking for additional causes of disability in patients whose exer cise tolerance seems out of proportion to the limitation of airflow. Any impairment in the efficiency of oxy gen uptake or carbon dioxide elimination by the lung can be detected by analysis of the arterial blood. COPD is characteristically as sociated with hypoxemia of varying severity and, in advanced stages, with hypercarbia. The efficacy of supplemental oxygen for pa tients with a defined degree of hypoxemia has been established. Arterial blood oxygenation should be assessed directly by measurement of Poj or indirectly by oximetry in all patients with moderately severe airflow limitation (e.g., FEV, below 1.5 L) at the time of initial evalu ation, and subsequently, at appropriate in tervals. The adequacy of therapy in those pa tients receiving oxygen should be documented by repeated analyses. In patients hospitalized for respiratory insufficiency, frequent mea surements of arterial blood gases may be necessary to assess the adequacy of ventila tion and oxygenation, and to monitor acidbase balance. The methodology for measur ing arterial blood gases and for performing ear oximetry should conform to accepted lab oratory standards. 3. Additional laboratory tests. The need for other laboratory investigations in patients with COPD is defined largely by special cir cumstances and by complicating clinical con ditions. The detection of secondary erythrocytosis from periodic measurements of hemo globin or hematocrit levels suggests chronic hypoxemia and represents an indication to as sess the need for oxygen therapy. Addition al details about nocturnal hypoxemia are provided in the section on oxygen therapy. The presence or evolution of changes on the electrocardiogram consistent with right ven tricular enlargement suggests the need for ar terial blood gas analyses and supplemental oxygen. Many patients with severe COPD experi ence recurrent illnesses characterized by in creased cough and expectoration of purulent sputum. Although suspected of being infec tious in origin, the precise etiology of these episodes remains speculative. In the absence of clinical or radiographic signs of pneumo nia, bacterial or viral cultures of sputum usu ally provide little useful information. In a very small percentage of cases, COPD is associated with and is thought to result from a severe deficiency in the plasma level of alpha-l-antiprotease. Deficiency of this inhib itor permits the early development of panacinar emphysema (13, 27, 28, 34). This genetic disorder should be suspected in patients w ho develop severe COPD at a relatively young age, especially if they have affected siblings or parents, and have smoked sparingly or not at all. The diagnosis can be made by mea surement of the serum alpha-l-antiprotease levels specifically, or by determining that the tiny sharp peak in the alpha 1-globulin re gion of the plasma electrophoretogram is ab sent. Quantitation of the alpha 1-globulin fraction as usually reported from the auto mated densitometer readout of the serum pro tein electrophoretogram is worthless for di agnosing the deficiency since it is virtually always normal. Specific phenotype determi nations are desirable but not essential. At the present time, replacement therapy has not been completely assessed, and is not gener ally available. Thus, the practical implication of establishing this diagnosis, aside from admonishing against smoking, relates to its possible use in genetic counseling. Modestly reduced levels of alpha-l-antiprotease, asso ciated with the heterozygous deficient pheno type, do not pose a clear-cut risk of prema ture COPD (35). IV, Indications for Hospital Admission The principal indications for hospitalization of the patient with COPD include: (/) acute exacerbation of symptoms such as markedly increased dyspnea, cough, and sputum pro duction that have not responded to adjust ments in ambulatory care, (2) acute respiratory failure characterized by respiratory distress, hypercarbia, or worsening hypoxemia, (3) acute cor pulmonale with dependent edema, further impairment of exercise capacity, and hypoxemia, (4) complications of COPD such as acute bronchitis or pneumonia, (5) the per formance of invasive diagnostic procedures on the lung such as bronchoscopy, transbronchial biopsy, or needle aspiration of nodules, (6) the need for surgery or other procedures chat require significant amounts of analgesics, or anesthesia, and (7) diseases that might not require hospitalization by themselves, but that in the presence of severe COPD represent a significant risk to the patient. A continuing program of education is an important hospital function. Whenever pos sible the patient must know the schedule of each medication and understand its purpose. Guidelines for clinical response in the hospi tal include improvements in symptoms and signs, as well as in the results of spirometr> and arterial blood gas analyses. r 228 AHER1CAN TMORACtC S0C^^ Discharge Criteria iieria for hospital discharge rest with iramovement to the point that the patient is able to care for his personal needs and manage his medication, or that these requirements can be arranged for outside the hospital. References L Fletcher C, Peco R, Tinker C, Speizer FE. The natural history of chronic bronchitis and emphy sema. Oxford: Oxford University Press, 1976. 2. Laennec RTH. A treatise on diseases of the chest. Translated from the French by John Forbes. London: T. and C. Underwood, 198). 3. Otis AB, Fenn WO, Rahn H. Mechanics of breathing in man. J Appl Physiol 1950; 2:592-607. 4. Harvey RM. Ferrer Ml, Richards DW Jr, Cournand A. Influence of chronic pulmonary disease on the heart and circulation. Am J Med 1951; 10:719-38. 5. Fry DL, Ebert RV, Stead WW, Brown CC. The mechanics of pulmonary ventilation in normal sub jects and in patients with emphysema. Am J Med 1954; 16:80-97. 6. Bates DV. Chronic bronchitis and emphysema: the search for their natural history. In: Macklem PT, Permutt S. eds. The lung in transition between health and disease. New York: Marcel Dekker, 1979; 1-13. 7. Aspen Conference Report of committee on def inition of emphysema. Am'Rev Respir Dis 1959; ?9(Part II):114. I. Ciba Guest Symposium Report. Terminology, definitions and classification of chronic pulmonary emphysema and related conditions. Thorax 1959; 14:286-99. 9. Fletcher CM. Pride NB. Definitions ofemphy sema, chronic bronchitis, asthma, and airflow ob struction: 25 years on from the Ciba Symposium. Thorax 1984; 39:81-5. 10. Ramsdell JW, Nachtwey FJ, Moser KM. Bron chial hyperreactivity in chronic obstructive bron chitis. Am Rev Respir Dis 1982; 126:829-32. II. American Thoracic Society. Definitions and classification of chronic bronchitis, asthma, and pulmonary emphysema. Am Rev Respir Dis 1962; 85:762-8. 12. National Heart, Lung, and Blood Institute, Division of Lung Diseases Workshop Report. The definition of emphysema. Am Rev Respir Dis 1985; 132:182-5. 13. Carrel! RW, Jeppsson JO, Laurell CB, et al. Structure and variation of human alpha-1antitrypsin. Nature 1982; 298:329-34. 14. Mitchell RS, Stanford RE, Johnson JM, Sil vers GW, Dart D, George MS. The morphologic features of the bronchi, bronchioles, and alveoli in chronic airway obstruction: a ciinicopathologic study. Am Rev Respir Dis 1976; 114:137-45. 15. Cosio M, Ghezzo H. Hogg HC, el al. The re lations between structural changes in small airways and pulmonary function tests. N Engl J Med 1977; 298:1277-81. 16. Nagai A, West WW, Thurlbeck WM. The Na tional institutes of Health Intermittent positivepressure breathing trial: Pathology studies II. Corre lation between morphologic findings, clinical find ings, and evidence of expiratory-airflow obstruc tion. Am Rev Respir Dis 1985; 132:946-53. 17. Hentel W, Longfield AN, Vincent T, Ftlley GF, Mitchell RS. Fatal chronic bronchitis. Am Rev Respir Dis 1963; 87:216-27. 18. Simpson T, Heard B, Laws JW. Severe irre versible airways obstruction without emphysema. Thorax 18:361-70. 19. Thurlbeck WM. Chronic airflow obstruction in lung disease. In: Major problems in pathology. Vol. V. Philadelphia: W. B. Saunders, 1978. 20. Niewoehner DE, Kleinerman J, Rice DB. Pathologic changes in the peripheral airways of young cigarette smokers. N Engi J Med 1974; 291:755-8. 21. Wright JL, Lawson LM, Pare PD, Kennedy S, Wiggs B, Hogg JC. The detection of small air ways disease. Am Rev Respir Dis 1984; 129:989-94. 22. Thurlbeck WM. Aspects of chronic airflow obstruction. Chest 1977; 72:341-9. 23. Thurlbeck WM. Chronic airflow obstruction: correlation of structure and function. In: Petty T. ed. Chronic Obstructive Pulmonary Disease. 2nd ed. New York: Marcel Dekker. 1985; 129-203. 24. Bates DV. The fate of the chronic bronchitic: a report of the ten-year follow-up in the Canadian Department of Veterans Affairs coordinated study of chronic bronchitis. Am Rev Respir Dis 1973; 108:1043-65. 25. Sharp JT, Paul O, McKean H, Best WR. A longitudinal study of bronchitic symptoms and spirometry in a middle-aged, male, industrial popu lation. Am Rev Respir Dis 1973; 108:1066-77. 26. Buis; S, Ducic S. Smoking: evaluation of studies which have demonstrated pulmonary func tion changes. In: Macklem PT, Permutt S, eds. The lung in transition between health and disease. New York: Marcel Dekker. 1979; 271-86. 27. Tobin MJ, Cook PJ, Hutchinson DDS. Al pha 1-amitrypsin deficiency: the clinical and phys iological features of pulmonary emphysema in sub jects homozygous for Pi type Z: a survey by the British Thoracic Association. Br J Dis Chest 1983; 77:14-27. 28. Janus ED, Phillips NT, Carrell RW. Smok ing, lung function and alpha 1-antitrypsin defi ciency. Lancet 1985; 1:152-4. 29. American Thoracic Society. Snowbird work shop on standardization of spirometry. Am Rev Respir Dis 1979; 119:831-8. 30. Knudson RJ, Burrows B, Lebowitz MD. The maximal expiratory flow-volume curve: its use in the detection of ventilatory abnormalities in a popu lation study. Am Rev Respir Dis 1976; 114:871-9. 31. Knudson RJ, Lebowitz MD. Comparison of flow-volume and closing volume variables in a ran dom population. Am Rev Respir Dis 1979; 116: 1039-47. 32. Eaton ML, Green BA, Church MS, McGow an T, Niewoehner DE. Efficacy of theophylline in "irreversible" airflow obstruction. Ann Intern Med 1980; 92:758-61. 33. Bates DV, Macklem PT, Christie RV. Respira tory function in disease. 2nd ed. Philadelphia: W. B. Saunders, 1971. 34. Larsson C. Natural history and life expectancy in severe alpha 1-antitrypsin deficiency, Pi Z. Acta Med Scand 1978; 204:345-51. 35. Bruce RM, Cohen BH, Diamond EL, et al. Collaborative study to assess risk of lung disease in Pi MZ phenotype subjects. Am Rev Respir Dis 1984; 130:386-90. bronchial tree to a variety of stimuli. The rna? jor symptoms of asthma are paroxysms of dyspnea, wheezing, and cough, which may vary from mild and almost undetectable to severe and unremitting (status asthmatic^). The primary physiological manifestation of this hyperresponsiveness is variable airways obstruction. This can take the form of spon taneous fluctuations in the severity of obstruc tion, substantiai improvements in the severity of obstruction following bronchodilators or corticosteroids, or increased obstruction caused by drugs or other stimuli. Histologi cally, patients with fatal asthma have evidence of mucosal edema of the bronchi; infiltra tion of the bronchial mucosa or submucosa with inflammatory ceils, especially eosino phils; and shedding of epithelium and ob struction of peripheral airways with mucus ' II. Diagnosis The diagnosis of asthma can occasionally be confusing because of its overlap with COPD. In addition, the diagnosis of asthma is occa sionally confused with other causes of air way obstruction such as tumors, foreign bod ies, laryngospasm, or even cardiogenic pul monary edema. Patients with COPD may have significant reversibility after treatment and patients with asthma may develop air flow obstruction with little to no reversibil ity. The separation of these overlap patients is often arbitrary and difficult, and from a clinical standpoint probably not important ' * unless the diagnosis has therapeutic impliestions, i.e., the bronchospasm results from a specific and avoidable etiologic agent. . a A. Clinical Assessment ^ The symptoms of episodic cough, wheezing, and dyspnea suggest a diagnosis of asthma. The history should explore these symptoms'^ in detail including; (/) family and personal history of allergic disease, (2) age at onset of symptoms, and frequency and severity of at tacks, (J) known provocative stimuli (table 1), and (4) prior pharmacologic and immuno- logic therapy. Initial symptoms may be a vague heavy feeling or tightness in the chest accon>*` panied in the allergic patient by rhinitis and conjunctivitis. The patient may complain of a nonproductive cough followed by wheez ing and dyspnea. Although initially non-, productive, the cough frequently does become, productive of a viscous, mucoid sputum that, may contain casts of the distal airways or mif appear purulent. A subset of patients with ; asthma are characterized by recurrent ofchronic nonproductive cough without any. overt wheezing (1). .__ In the asymptomatic patient, the examin**- tion of the chest may be normal, although examination ofthe eyes, ears, nose, and flu** may reveal concomitant serous otitis med* CHAPTER 2 Asthma 1. Definition Asthma is a clinical syndrome characterized by increased responsiveness of the tracheo- conjunctivitis, rhinitis, nasal polyps, p nasal sinus tenderness, and signs of postn drip, including pharyngeal mucosal lympho* hyperplasia. In mild asthma, wheezing only be detected on forced expiration. increasing degrees of severity, wheezing Si X^FTf AMERICAN THORACIC SOCIETY 229 e ma-v ns ma Die . ' ^ on rways spon- struc- ` ' verity lators iction ' ologi- \ dence r rilira- I acosa isinod ob- acus. I -Ily be OPD. occa-. >f airlbod-*- Jc pul- ' may I tment p airrsibil- w tients^ rom 3rta -ring, v i thma. moms': J. sonal.] set of vj ofat-^l (taWe'^J iuno-.`-~J vague"i | :com-V ' .s 2nd I sin of c / mi emaVi TABLE 1 STIMULATORS OF BRONCHOCONSTRICTION A. Nonspecific 1. Exercise 2. Col<3 air 3. Environmental pollutants and irritants - Pharmacologic agents, i.e., histamine, cholinergic agonists ? .Reflux esophagitis 8. Specific 1. Aspirin and all nonsteroidal anti-inflammatory drugs (NSAlD's) 2. Occupational antigens a. ingested antigens - 5. Beta-adrenergic antagonists be heard on quiet expiration and on inspira tion. The findings of severe airways obstruc tion include restlessness, agitation, orthopnea, tachypnea, breathing through pursed lips with a pr ' mged expiratory phase, using accessory muiv.cs of respiration, diaphoresis, coughing, audible wheezing, and difficulty speaking. In the acutely ill asthmatic, the abatement of wheezing may occur with increasing severity of airways obstruction and must not be taken as a clinical sign of improvement. The evalua tion of the blood pressure may reveal that the patient has a widened pulse pressure, and a pulsus paradoxus (10 mm Hg or greater) may be present. The latter sign is a relatively reli able indicator of the severity of the asthma, the FEV, almost always being less than 40% predicted in this situation (2). The presence of fc r is indicative of an infectious compli cation such as pulmonary infection. The tho rax is often hyperinflated. Patients with asthma and persistent sinusi tis and nasal polyposis with or without mid dle ear disease frequently benefit from an evaluation by an otorhinolaryngologist. Ag gressive management of sinusitis and correc tion of upper airway obstruction may improve the asthmatic condition. Patients with poorly controlled asthma requiring hospitalization should be evaluated by a specialist in pulmo nary disease or allergy. The accurate recogni tion r f the importance of allergic disease in the as.nmatic syndrome may require consul tation with a physician skilled in testing for allergic diseases. fl Laboratory Tests _ l Pulmonary function tests. Spirometric studies of pulmonary function are valuable both in the diagnosis of asthma and in as sessing the severity of the disease and the re sponse of therapy (3). Spirometry and peak flow measurements are also useful on a regu lar basis during outpatient management. All meat1 -ible parameters of pulmonary function may be within normal limits when the patient with asthma is in remission. If the diagnosis is suspected, bronchial provocation testing utilizing a cholinergic agonist, histamine, cold air, or specific antigens or industrial agents may demonstrate significant airways obstruc tion with a quantifiable stimulus known to be tolerated by a normal individual (4). Induced airways obstruction may be severe and delayed for up to 24 h. Hospitalization may be war ranted when this approach is taken (see Indi cations for Hospital Admission). When preexisting airways obstruction is noted, bron chial provocation is contraindicated. The typical abnormalities noted with spi rometry in the asthmatic patient include a reduction in FEV,, peak expiratory flow rate, FEV,/FVC ratio, and an increase of 15% or greater in the FEV, in response to a bronchodilator. (Patients with asthma may not im prove their FEV, in response to bronchodilators during episodes ofsevere airways obstruc tion.) Abnormalities in lung volumes include a decreased vital capacity, an increase in func tional residual capacity, total lung capacity, and especially in the residual volume; how ever, it is not necessary to measure lung volumes in order to make the diagnosis of asthma. 2. Arterial blood gases. The measurement of arterial blood gases may be helpful in de termining the severity of disease in the hos pitalized patient. Hypercapnia and respira tory acidosis implies severe disease with FEV, of less than 15% of predicted (5). Under these circumstances, frequent monitoring of arterial blood gases is essential in patient manage ment. Signs and symptoms of hypoxemia, such as cyanosis, are unreliable and should not be substituted for actual blood gas deter minations. With milder bronchospasm, the arterial blood gases usually reflect a respira tory alkalosis, with a near normal Poj and a widened alveolar-arterial oxygen gradient. In these milder cases the Pos'and Pco, are relatively insensitive indicators ofairways ob struction (6). Normalization of the pH and Pco2 in the face of a failing Po usually indi cates worsening obstruction with an FEV, less than 25% of predicted. 3. Blood leukocytes. Peripheral eosinophilia is common in both allergic and nonaliergic forms of asthma; consequently, this parame ter cannot be used as a differentiating point between the two. Values of 5 to 15% of the total white blood cell count are common. To tal eosinophil counts provide a more accurate measure of peripheral eosinophilia. Although leukocytosis may suggest the presence of infection, leukocytosis with marked eosinophilia (greater than 3,000 per cubic mm) should raise the possibility of another diag nosis, such as Loffler's syndrome, the hypereosinophilic syndrome, allergic bronchopul monary aspergillosis, or Churg-Strauss aller gic granulomatous angiitis. 4. Sputum. Grossly purulent sputum may reflect eosinophilia rather than PMNs as sociated with infection. In this situation, mi croscopy may document eosinophilia, Curschmann's spirals, and Charcot-Leydon crys tals, all consistent with the diagnosis of asthma. 5. Electrocardiography. The electrocar diogram is of little value in the diagnosis or management of asthma. ECG changes are usually noted only in severe acute attacks of asthma, are nonspecific in nature, and include sinus tachycardia and rarely ventricular strain pattern and right axis deviation. 6. Radiology. The chest radiograph is not helpful for the diagnosis of asthma or for de termining the severity of the acute attack (7). It may be helpful in evaluating potential com plications of asthma, such as rib fractures, pneumothorax, pneumomediastinum, atelec tasis, and pneumonia. Paranasal sinus films may be of use in evaluation of the patient thought to have concomitant allergic rhinitis and sinusitis. 7. Measurement of serum IgE. A large proportion of the allergic asthmatic popula tion has normal IgE levels, and many condi tions other than asthma are associated with elevated IgE levels. Therefore, the usefulness of obtaining a serum IgE measurement in pulmonary conditions other than allergic bronchopulmonary aspergillosis has not been established. 8. Detection ofIgE antibody. Tests to de tect antigen-specific IgE are indicated when the asthma is thought to be due to an iden tifiable and avoidable substance. Bronchial provocation testing with specific antigens (8) can also be used to demonstrate bronchial reactivity and is useful in the evalu ation of (/) the asthmatic patient with inter mittent episodes of asthma who presents for evaluation in the asymptomatic stage, and (2) a patient with suspected occupational asthma, since the use of skin testing in occupational asthma is complicated by a lack of specific antigens and the nonspecific irritating effect of the available antigens on the skin. Immediate-type hypersensitivity skin test ing remains the most important tool for the detection of IgE antibody and confirms the clinical suspicion of an allergic component to the patient's asthma as elicited by the his tory. Skin tests, which are done by prick, scratch, or intradermal methods, must be in terpreted in the light of a well-taken history, as false positive results may occur. A diagno sis of specific allergy should rarely be made in the absence of a correlating positive his tory. Skin testing is safe, sensitive, and use ful for the evaluation of allergy to inhalant aeroallergens that may be a trigger in airways obstruction. The RAST (Radioallergosorbent test) as say or ELISA (enzyme linked immunosorbent assay) permit the in vitro evaluation and semi quantitation ofantigen-specific IgE antibod ies in serum (9). These tests correlate well with clinical provocation testing and are free of r 230 AMERICAN THORACIC ***** the risk of systemic reactions. They may be useful when the patient is currently receiving forms of symptomatic therapy that alter the interpretation of skin tests. Disadvantages in clude expense, a lag in the time from testing to the availability of results (at least 48 h), a lesser availability of potential antigens that may be utilized compared with skin testing, a decreased sensitivity, and the potential mis use of these assays by physicians not engaged in the evaluation of patients with allergic dis ease. 111. Indications for Hospital Admission A. Diagnosis In general, the diagnosis of asthma or asth matic syndromes can be firmly established in outpatients. However, when inhalational challenge testing with environmental allergens or occupational substances are to be ad ministered and there is reason to believe a late response (one which occurs 4 h or later after inhalation) may occur, hospitalization may be required to firmly and safely establish a diagnosis (7, 10). The hospital facilities are used in this circumstance to confirm and quantitate obstructive airways dysfunction at a time of day that may preclude testing as an outpatient. Another indication for hospi talization is to establish a diagnosis of asthma when diagnostic challenge testing is planned in patients with possible or probable com plicating medical illnesses, such as cardiac dis ease, where close monitoring of cardiopul monary status is advisable. & Treatment l. Treatment oftheprimary disorder. Hospi talization for the treatment of asthma is in dicated for the acute onset of symptoms or physiological changes that are so severe as to preclude successful initial management as an outpatient or in an emergency room (1-5, 7). This indication is more likely to occur in pa tients in whom the diagnosis of asthma had not been previously established, in patients who have not previously required treatment, or in patients whose treatment requirements have recently changed. Another indication is exacerbation of symptoms in individuals who are undergoing therapy as outpatients but in whom the control of symptoms or physio logical changes is such that outpatient man agement is no longer feasible. Rather than defining specific physiological or clinical cri teria for admission, the criteria should be the failure or probable failure ofoutpatient man agement as judged by the physician (11-16). Hospitalization is recommended for initi ation of therapy in asthmatic subjects with serious complicating medical conditions such as cardiac disease or pregnancy (17), depend ing on the severity of the asthmatic condi tion or the underlying medical complication. Hospitalization may be indicated for the f purpose of removing the patient in exacerba tion from an unfavorable environment when there is substantia] reason to believe that the environment is contributing to the patient's condition. 2. Treatment of complications of the pri mary disorder. In addition to treatment of the asthmatic condition itself, a number of complications may arise that require hospi talization. These include serious infectious complications such as acute bronchitis, pneu monia, or sinusitis. Hospitalization is also in dicated for treatment of pneumothorax and pneumomediastinum. Hospitalization may be indicated for the treatment of iatrogenic com plications of the primary disorder, including medication overdose or severe adverse reac tion to medication, and complications of stan dard treatment, including severe side effects from steroid therapy, both acute, such as hyperglycemia or fluid retention, and chronic, including opportunistic infections, ocular, and skeletal complications. In the case of pa tients with status asthmaticus requiring treat ment with mechanical ventilation, there may be complications of the mechanical ventila tion, including disorders of the trachea or per sistent bronchopleural fistula, which may re quire prolonged hospitalization or readmis sion (18). 3. Treatment ofasthma in association with other disorders. Hospitalization may be in dicated prior to elective surgery or invasive diagnostic tests for the asthmatic subject who has required chronic treatment (19). The du ration of the in-hospital treatment would be proportional to the severity of the patient's disease and the likelihood of the surgery to result in respiratory insult, but usually would be 2 to 5 days. Asthma may be a factor that contributes to prolonged hospitalization in patients with non-pulmonary medical or sur gical disease. The combination of asthma with other forms of pulmonary disease may also extend the duration of required hospitaliza tion beyond that of the simple disorder; the duration of additional hospitalization will vary with the severity of the patient's asth matic condition. IV. Discharge Criteria In patients admitted to the hospital for the purpose of establishing a diagnosis ofasthma, discharge is indicated when the diagnosis has been established, the diagnostic procedure has been completed, appropriate treatment be gun, and the patient's conditiofris stable. In those cases in which a diagnosis cannot be established but in which asthma has been reasonably excluded as a diagnostic possibil ity, discharge would be indicated depending upon the patient's overall condition. In patients admitted for the treatment of asthma as a primary diagnosis, discharge is indicated when a stable treatment regimen using oral or inhaled medications has been both established and demonstrated effective for 24 to 48 h after withdrawal of intravenous medications. Further, these patients should have documented clinical and physiological improvement (comparing the time oftheir ad mission to discharge) consistent with them pursuing activities of daily life. Subsequent monitoring of spirometry or peak flows af ter discharge is important in the patient's rou tine management. When complications oftk. disease are the indication for admission, then appropriate diagnosis and treatment of'these complications should be instituted prior to discharge. This does not necessarily mean that the treatment must be completed, but rather it must be demonstrated that an outpatient regimen is sufficient for the condition dia*. i nosed. In patients with pneumothorax and \ pneumomediastinum, the associated radio- ! graphic changes must be demonstrated to haw = improved or stabilized with implementation ' of a stable medical regimen. In circumstances in which complications arising from medica tions were the indication for admission, these complications must be shown to be resolving or to have resolved prior to discharge. In cir cumstances where the patient was admitted for other disorders but in which asthma oc curs in association with those disorders, the recovery from the primary disorder, or elec tive surgery, must have progressed to the point where discharge is usually considered; at that time the asthmatic symptoms must be under control using oral or inhaled medications that can be administered by the patients or their families. In all hospitalized patients with asthma, definite plans for follow-up care are an essential part of the management. References 1. Corrao WM, Braman SS, Irwin RS. Chronk cough as the sole presenting manifestation ofbron chial asthma. N Eng! J Med 1979; 300:633-7. : 2. Rebuck AS, Pengelly LD. Development of pulsus paradoxus in the presence of airways ob struction. N Engl J Med 1973; 288:66-9. 3. Gold WM. Clinical and physiologic evaluatios of asthma. Chest 1985; 87(Suppl:30S-2S). r 4. Gershel JC, Goldman HS, Stein REK, Shelo* SP, Ziprkowski M. The usefulness of chest radio graphs in first asthma attacks. N Engl J Med 1983; 309:336-9. 5. Tai E, Read J. Blood gas tensions in bronchial asthma. Lancet 1967; 1:644-6. 6. McFadden ER Jr, Lyons HA. Arterial-blood gas tension in asthma. N Engl J Med 1968; 278: 1027-32. 7. Pepys J, Hutchcroft BJ. Bronchial provocation tests in etiologic diagnosis and analysis of asthma- Am Rev Respir Dis 1975; 112:829-59. . 8. Hargreave FE, Dolovich J, Boulet LP. Inhala tion provocation tests. Semin Respir Med 1983; 4:224-36. ' 9. Wide L, Bennich H, Johansson SGO. Diagno sis of allergy by an in vitro test for allergen anti bodies. Lancet 1962; 2:1305-7. f. 10. Pratter MR, Irwin PS. The clinical value of pharmacologic bronchoprovocation challenge- Chest 1984; 85:260-5. > U. McFadden ER Jr, Kiser R, deGroot WJ. Acute bronchial asthma: relations between clinical and physiologic manifestations. N Engl J Med 1973! 288:221-5. & 12. Banner AS, Shah RS, Addington WW. RaPilJ prediction of need for hospitalization in acute asthma. JAMA 1976; 235:1337-8. 13. Kelsen SG, Kelsen DP, Fleegler BF, Jones RC. Rodman T. Emergency room assessment and treat* ment of patients with acute asthma: adequacy o* the conventional approach. Am J Med 197 r THORACIC SOCIETY 231 >nic on-' elov 5*/ >.dio- j 983; *-V ;hiai -J v*i] lood qyj 278: y, t622-8. _ , Fischl MA, Pitchenik A, Gardner LB. An in\ predicting relapse and need for hospitalization patients with acute bronchial asthma. N Engl j Med 1981: 305:783-9. 15. Arnold AG, Lane DJ. Zapata E. The speed of onset .ind severity of acute severe asthma. Br jDis Chest'1982: 76:157-63. 1$. Centor RM, Yarbrough B. Wood JP. Inabil ity to predict relapse in acute asthma. N Engl J Med 1994; 3)0:577-9. 17, Turner ES, Greenberger PA, Patterson R. Management of the pregnant asthmatic patient. Ann Intern Med 1980; 93:905-48. Ifi. Kingston HG, Hirshman CA. Perioperative management of the patient with asthma. Anesth Analog 1984: 63:844-55. 19. Westerroan DE. Benetar SR, Potgreter PD, Fer guson AD. Identification of the high risk asthmatic patient. Experience with 39 patients undergoing veniilai'vti for status asthmaticus. Am J Med 1979: 66:565-72. CHAPTER 3 Pharmacologic Therapy l. Introduction The use of pharmacologic agents is an im portant part of the management of patients with obstructive airways diseases, both dur ing exacerbations and during interim periods ofstability. This section will discuss the prin cipal pharmacologic agents and their use in the therapy of asthma and COPD. The infor mation in this chapter is based upon current medical knowledge, and, where controversy exists, upon accepted medical practice. The authors recognize that the following recom mendations may need to be revised as new information appears. ii. Therapeutic Agents /. Beta-adrenergic agonises. The sympathomi metic bronchodilators are the keystone of therapy in patients with obstructive airways disease. Because they can improve mucociliary clearance and serve prophylactically to pro tect against bronchospasm produced by vari ous stimuli, they may be of value even if they do not result in improvement of spirometric responses on pulmonary function testing. Aerosol formulations provide the optimal therapy for chronic outpatientuse (I). In most patients, the metered-dose inhaler (MDI) is preferred, whereas for inpatient therapy pow ered nebulizers are often used (see Respi ratory Care Modalities, Chapter 5). Oral preparations are falling into disfavor, since they are no more effective than aerosols in most patients and they cause more side ef fects (2). Appropriate oral dosages are diffi cult to establish in individual patients, since variables in bowel absorption and first-pass metabolism may markedly reduce the frac tion of the drug that enters the circulation m an active form. Aerosol dosages are easier to titrate, result in a more rapid onset of bronchodilation than oral preparations, and achieve a comparable peak response and per sistence of effect with a decreased incidence of tremor, nervousness, and palpitations. Fur thermore, aerosol bronchodilator delivery is more effective than oral dosing in the pro phylaxis of exercise-induced bronchospasm. Although many patients are unable to use the MDI optimally, repeated instruction results in a satisfactory outcome in the ma jority of cases (3). There is a small group of patients who fail to learn to use their MDI effectively, and for them the addition of a large volume reservoir or spacer can be ad vantageous (4). Optimal use of an MDI results in not more than 30% of the dose being deposited in the lung, while as much as 85% is deposited in the oropharynx. The use of a large volume reservoir may increase the amount deposited in the lungs to 15%, while reducing the oropharyngeal deposition to 5%. In contrast, a typical powered nebulizer unit will result in about 10% of the initial dose being depos ited in the lung, whereas only about 10% will be deposited in the mouth and pharynx; about 80% of the dose remains in the apparatus or is lost in the atmosphere (5). The actual amounts deposited will be determined by the apparatus used, the breathing technique, and the length of the treatment session, and there fore considerate variability in the effective dosage can result. The manufacturers' recommended dosages for use in powered nebulizers are compara ble to the ora! dosages, and both are many times greater than the dosage delivered by the typical 2 or 3 actuations of an MDI (table 1). Since patients using powered nebulizers or oral tablets usually tolerate these much larger dosages, it is reasonable to evaluate the effect of increasing the number of puffs from an MDI beyond the customary 8 to 12 per day up to 16 to 24, and to add a large volume reservoir, before deciding to add an oral betaadrenergic drug to the regimen or to change to a powered nebulizer. The older sympathomimetic agents ephedrine, epinephrine, and isoproterenol have been generally replaced by the newer, longer act ing, more beta-2 specific bronchodilators (ta ble 1). Metaproterenol, albuterol, terbutaline, and bitolterol are mainly used as aerosols, but oral preparations of the first 3 are available and terbutaline can be given subcutaneously. In Europe, additional agents that are in use include fenoterol, pirbuterol, clenbuterol, reproteroi, and rimiterol. Metaproterenol, al buterol, terbutaline, and bitolerol, when given as aerosols, appear to be comparable enough in potency, length of action and side effects such that when used in recommended doses, they can be used serially or interchangeably. Individual patient preference and cost may be the best determinants for selecting one for chronic use. Intravenous sympathomimetic bronchodi lators have been recommended by physicians in Europe for treating severe bronchospasm, but experience in their use is limited. Only isoproterenol is available for intravenous use in the U.S. and it is not approved by the FDA for treatment of bronchospasm. 2. Theophylline. Theophylline is usually given orally as sustained-release formulations for chronic maintenance therapy. Although the benefits of theophylline are difficult to prove in patients with COPD, its use is fa vored by most clinicians when appropriately used sympathomimetic agents fail to produce adequate bronchodilation. Twice-a-day ad ministration is generally adequate, although some patients are better controlled if the daily dose is given in 3 equal portions. Recently, some formulations have been demonstrated to provide effective airway dilation when given once a day to patients with less severe asthma. The reliability of longer-acting preparations can be ofconcern; established products should be favored, and their optimal bioavailability ensured by giving them before meals. Although some patterns respond adequately when their theophylline serum levels are as low as 5 mcg/ml, most require 8 to 20 mcg/ml. A major problem with theophylline is that some patients experience toxic symptoms while blood levels are in the therapeutic range (6). The main side effects are nervous ness and tremor resulting from the endoge nous release ofcathecholamines that theoph ylline causes, and gastrointestinal symptoms. When a patient begins to use theophylline, a relatively low dosage schedule should be selected; the theophylline serum level can be checked after a few days, and the dosage ad justed appropriately to maintain adequate bronchodilation without associated side ef fects. Therapeutic serum levels of theophyl line on stable doses ofa sustained-release oral TABLE 1 SYMPATHOMIMETIC AGENTS Drug Epinephrine (1:1000 solution) Isoproterenol isoetharine Metaproterenol Albuterol Terbutaline Bitolterol Recommended Dosage per Treatment Subcutaneous (m() MDI (mg) Nebulizer* (mg) Oral (mg) 0.1-0.5 - '- - 0.25-0.5 - 0.32-0.9 0.16-0.39 0.66-1.02 1.3-1.95 0.16-0.27 0.4-0.6 0.37-1.11 2.5-22 0.63-3.8 1.25-5 10-15 - - - 5-20 1-4 1.25-5 - Duration Of Action (0) 1-2 1-2 2-3 3-4 4-6 4-6 4-6 * Dosages vary wwly. These are typical treatment Meet, usually given at Intervals ot 3-6 h. 1 j | ! ! \ , ' 232 w AMERICAN THORACIC theophylline preparation occur for about 8 to 12 h in most adults (7). The dosage of oral theophylline for the av erage nonsmoking, reasonably healthy adult is 10 to 12 mg/kg/day (e.g., 400 mg twice a day). Smokers may require up to 50% larger dosages, whereas hypoxemic patients or those with liver insufficiency may require a 25 to 50% reduction in dosage. If cimetidine therapy is given, the serum level of theophyl line may be rapidly increased by as much as 30 to 50%; the related agent ranitidine has little effect on serum theophylline levels (8). Many drugs (eg., erythromycin) and other en vironmental conditions (e.g., diet, hydrocar bon exposure, illness) affect theophylline clearance, and a serum level determination is indicated when a serious environmental or health change alters the control of the bronchospasm. Aminophylline contains about 80% the ophylline solubilized by the addition of ethylenediamine. The latter can rarely cause hyper sensitivity reactions in susceptible patients. Aminophylline or theophylline can be given intravenously in critically ill patients, as is dis cussed later. 3. Anticholinergics. Atropine was used for many years for the management of asthma, but with the availability of potent beta-ad renergic agonists its use declined in the U.S. In recent years there has been an increased interest in inhaled atropine sulfate, especially for patients with chronic bronchitis associated with bronchospasm, although its use as a bronchodilator is not approved by the FDA (9). Atropine is usually given by powered nebulizer, often in combination with a betaadrenergic agent. Its side effects include tachy cardia, dryness of the oral mucosa, blurred vision, urinary obstruction, and constipation. Ipratropium bromide, a quaternary ammo nium derivative of atropine, is bronchoselective when delivered by inhalation (10). It is relatively free of systemic side effects because it is minimally absorbed into the systemic cir culation and does not cross the blood-brain barrier. It has been shown to be an effective bronchodilator in patients with COPD and in selected patients with asthma both alone and when used concomitantly with beta-2 agonists and theophylline (10). When ad ministered via MDI aerosol, the recommended dose is 2 puffs (40 meg) 4 times daily. 4. Cromolyn. Cromolyn is neither a bronchodiiator nor an antagonist of anaphylactic mediators. However, it has been shown to in hibit histamine release from mast cells (11, 12). Cromolyn is poorly absorbed when given orally and must be given by inhalation, ei ther as a powder or as an aqueous solution available for nebulization and more recently as an MDI. Its advantages are its lack of tox icity and its effectiveness in preventing asthma when used properly, especially in younger pa tients. A trial period of 4 to 6 wk may be re quired to determine its usefulness. Cromo lyn has been found to be effective in prevent ing exercise-induced bronchospasm (EIB) and for this condition its preventive effects are im mediate (13). Because of its irritating effects on the airways, the powder form of cromo lyn should not be used in acute asthma attacks. 5. Corticosteroids. Corticosteroids are use ful in the management of acute exacerbations of most cases of asthma and for a minority of cases of chronic airways obstruction (14, 15). They may be given orally or intravenously during acute attacks along with bronchodi lator agents. Both oral and inhaled corti costeroids may prove beneficial in prevent ing acute asthma attacks, and oral therapy can help improve airflow in some patients with COPD. Response should be monitored with objective tests such as FHV, or peak flows, and therapy should be continued only if sig nificant improvement occurs (13). Oral cor ticosteroids are associated with significant toxicity when administered chronically, but alternate-day dosing (in which the entire twoday dose is given once in the morning on alter nate days) can be effective in asthma with fewer side effects (16). It is important to use bronchodilators concomitantly in an effort to re duce or discontinue steroid administration. 6. Mucolytics and expectorants. The most troublesome area in pulmonary pharmacol ogy is the treatment of abnormal mucus (17). Sympathomimetic bronchodilators and the ophylline offer the advantage of stimulating mucociliary clearance, and these drugs are in dicated for any obstructive disease syndrome that is accompanied by impaired mucokinesis. There is also evidence that corticosteroid therapy can improve mucokinesis in bronchitis and asthma. Inhaled atropine does not ad versely affect clearance, although systemic an ticholinergic and antihistamine therapy can impair mucociliary clearance. Oral expectorants are popularly used in over-the-counter preparations, e.g., guaifene sin, terpin hydrate, ammonium and other, salts, iodide and ipecac The only topical mucolytic available is n-acetylcysteine, which can be given by aerosol or instillation. The value of inhaled expectorants and mucolytic agents has not been demonstrated in objec tive studies (18). 7. Antibiotics. Although antibiotics have been used extensively for years t'etreat acute exacerbations of chronic bronchitis, as well as for prophylaxis in stable chronic bronchi tis, their value for either purpose has not yet been established (19-22). Bacterial infection or colonization of the trachea, bronchi, and small airways has been shown not to influence the natural history of COPD. It has been demonstrated repeatedly that the large air ways of most of these patients are colonized by the same aerobic bacteria that are found in the oropharynx (23, 24). Two organisms, Hemophilus influenzae and Streptococcus pneumoniae, have been cultured from spu tum and transtracheal aspirates more fre quently and in greater numbers from patients with acute exacerbations of chronic bronchi tis. The H. influenzae strains are almost al- ways nonencapsulated and therefore canC. be typed with specific antiserum, altiw? they can be studied biochemically and p!*2 into "biotypes." Clinicians have prescribe short-term antimicrobial therapy directed cifically against these 2 organisms. The of such short-term treatment is difficult u assess, although the few carefully controlled and properly designed studies reported this far have failed to show any clear-cut benefit A few patients undoubtedly have repeated aacerbations due to bacterial infection and do benefit clearly from antimicrobial therapy; the clinician has little trouble identifying thee relatively uncommon individuals. Prophylac. tic therapy has not been shown to arrest de terioration of pulmonary function overtime or to decrease symptoms. If antimicrobial therapy is to be used in the patient with COPD, the microbial agents of most concern are H. influenzae and S. pneu moniae. The role of other bacteria that colo nize the bronchial tree is unknown, and in vestigators give them little or no place of im portance as this condition is understood at present. Since the value of antimicrobial tbr- \ apy for most patients is doubtful, any drug chosen for this purpose must be economical and nontoxic The most suitable agents are ampicillin, amoxicillin, tetracycline, erythro- *] mycin, and trimethoprim-sulfamethoxazole If antimicrobial therapy is to be given, an eo- j pirical choice is usually made without knovd-' edge of results from Gram stain of sputum,5 sputum culture, or studies for antimicrobial resistance. ,v i 8. Vaccines. Influenza vaccine has beenes-1 tablished to be of great value in reduction of | mortality and morbidity during epidemics of j influenza. Most deaths from influenza result from bacterial pneumonia which leads to re spiratory failure, although influenza viral pneumonia is well documented. The adminis tration ofinfluenza vaccine is associated with a protection rate of 60 to 80%. Complications from the vaccine directed against Influenza A and B are relatively mi nor: 2% develop febrile reactions and mus cle aching that may last for a few hours, while hypersensitivity reactions can be seen in per sons allergic to egg protein. The severe reac tions observed following the mass vaccina tion for swine influenza in 1976 have not been noted with the vaccine containing types A and B. Since the mortality rate for pneumococcal pneumonia among persons over 60 yr of age has remained unchanged over the past 30 yr. attempts have been made to control this in fection with a vaccine containing purified cap sular polysaccharide from 23 pneumococcal | serotypes. The vaccine is immunogenic m healthy, ambulatory, elderly persons, although its efficacy in preventing pneumococcal pneu monia in debilitated patients with COPD has not been established. The U.S. Public Health Service recommends use of the vaccine in all persons over 50 years of age and in patients with chronic disease including cardiopulm<>: U&OCAM THORACIC SOCIETY 233 tea spejf# le vaiue^ 'cult tos itrollcdf ed thuj'f benefit^ atedoc^' and do^ herapyfj' ng these*1; 'phyiac- r rest de-j$ *er time** J, been es-| ction of^ emics of^ za result! ds to re-J za vjraJ i idminis-' Lted with^| directed^ vely mijg nd mus-j? rs, while " n in perere reac vaccina* not been types A lococcal . r of age ist 30 yh ! this in* tied cap* lococcal genic in alth' ;alr DPI, c in.. ^ patient opubnOj oary disorders. A single dose of the vaccine is judged to be sufficient, but experience is limited and the duration of protection after primary vaccination has not been determined. ^ Amantadine. Amantadine hydrochloride is a tricyclic amine that inhibits an early state 0f replication of the Influenza A virus. A num ber of controlled trials have demonstrated the prophylactic effectiveness of amantadine against the development of clinical illness in naturally-occurring and experimentally-in duced Influenza A infection. Estimates of ef ficacy range from 50 to 90%. Side effects in clude mental changes, ataxia, tremors, and convulsions, especially in the elderly. The recommended adult dose is 100 mg twice daily. ]n patients over age 65, renal excretion is de creased and daily dosage should be decreased to 100 mg after an initial loading dose of 200 mg. 10. Immunotherapy. Controversy persists concerning the use of immunotherapy in pa tients with allergic asthma and hay fever (25, 26). The repeated injection of extracts from substances that cause positive immediate skintest reactions results in the production of "blocking" antibodies, which may decrease the late, but not the early, IgE mediated al lergic response (27). Major problems with im munotherapy today include the lack of stan dardization of allergen extracts and dose, the lack of criteria for selection of those patients who might benefit, and the lack of objective studies to document its possible benefit in asthma (26). Pending the results of these in vestigations, it seems reasonable to employ immunotherapy for selected patients with epi sodic wheezing associated with rhinorrhea and conjunctivitis following exposure to known allergens (e.g., animal danders, rag weed pollen), provided contact with these al lergens is unavoidable. 111. Drug Therapy of Asthma /. Therapy of the acute attack. Management of the acute asthma attack is dependent upon the severity of the airway obstruction and the response to initial therapeutic maneuvers. Severity ofthe attack is determined by objec tive measurements, such as the FEV, or peak flow (28). The initial therapy of the acute at tack includes the administration of oxygen ajtd bronchodilator agents (29). Beta-2 spe cific agents administered via a metered-dose inhaler or powered nebulizer are advised, par ticularly in older patients and those with car diovascular problems. Larger doses than those used in stable asthmatics may be required. In young, otherwise healthy asthmatics, sub cutaneous epinephrine or terbutaline give tesults that are comparable to inhaled betaadrenergic agents. In patients who have severe obstruction and tave not responded to inhaled beta-adrenergic Agents, theophylline should be added to the tegimen. If intravenous aminophyliine or theophylline is selected, an initial loading dose followed by a continuous drip is preferred TABLE 2 MAINTENANCE DOSAGES OF IV AMINOPHYLLINE AND THEOPHYLLINE* Aminophyline Theophylline Calculated (img/kg/h) Typical Dose (mg/day) Calculated (mg/kg/day) Typical Dose (mg/day) Nonsmokers Smokers Cimetidme use Cor pulmonale Hepatic insufficiency 0.5-0.7 0.9 0.3-0.4 0.2S-0.3 0.2-0.25 900 1.300 600 500 450 0.4-0.6 0.75 0.25-0.3 0.2-0.25 0.18-0.2 800 1,100 500 400 350 Recommenced loading doses ot patients who nave not been on maintenance oral tnerapy are ammoonyiime. $-7 mgikg, or theopnyfline. <-6 mg/kg. (table 2). If the patient has been on oral methylxanthines at home, a serum theophyl line level should be obtained and the initial loading dose decreased or eliminated. Serum levels should be maintained within the ther apeutic range of 8 to 20 meg/mi and an im mediate reduction made if nausea, vomiting, severe nervousness, or cardiac arrhythmia de velop. Peak serum theophylline levels should be determined on 2 or 3 occasions when initiating therapy to obtain an estimate of daily requirements. Thereafter, they need not be repeated unless there is a change in the pa tient's status or new therapeutic agents are added. Severely ill patients may require fre quent determinations due to rapid changes in their clinical state. Corticosteroids should be administered promptly if the patient has had frequent re cent attacks, if steroids have been required in the recent past, or if the attack is severe and does not respond rapidly (within 30 to 60 min) to sympathomimetic and theophyl line therapy. In such cases, corticosteroids are given intravenously along with the bronchodilator agents; their onset of effect is not seen for 3 to 6 h, even with parenteral therapy (30). The dosage of corticosteroids for the acute asthma attack is still controversial; however, a loading dose of intravenous hydrocortisone of 4 mg/kg followed by 0.5 mg/kg/h or an equivalent dose of methylprednisolone (0.8 mg/kg initially followed by 0.1 mg/kg/h) is probably adequate for the initial therapy (30). As soon as flow rates improve, the patient may be switched to oral prednisone or methylprednisolone. The initial maintenance doses should be about 40 mg of prednisone per day or its equivalent; tapering should occur as rap idly as possible while the patient is monitored to avoid relapse. Weaning should be complete within about 2 wk and if this is not possible, a long-term maintenance regimen may be necessary. If attempts at weaning from cor ticosteroids fail, the lowest effective main tenance dose should be given, with repeated attempts at lowering the dose. Inhaled cor ticosteroids should be substituted if possible; if not, aiternate-day therapy should be tried. Inhaled atropine, given by powered neb ulizer in doses of 0.025 to 0.035 mg/kg, may be given at intervals of 4 to 6 h if the acute attack does not respond to the above meas ures. The atropine may be combined with a beta-adrenergic agent. Inhaled corticoste roids, cromolyn, and n-acetylcysteine are in effective and may increase bronchospasm dur ing the acute asthmatic attack. Sedatives are also hazardous and should not be given dur ing an acute attack unless mechanical venti lation is required. 2. Preventive and long-term therapy. Ef fective management of patients with asthma is designed to prevent acute attacks. In the patient with mild, exercise-induced asthma, most agents have been shown to be effective, including the inhaled beta-adrenergic ago nists, oral sustained-release theophylline and cromolyn. The easiest and most convenient way of preventing exercise-induced asthma is by administration of a beta-2 adrenergic agonist from a metered-dose inhaler shortly before engaging in exercise. Inhaled cromo lyn is also effective in preventing exerciseinduced asthma (18). For more severe asthma (exercise-induced or otherwise troublesome), oral sustained-release theophylline twice daily may be combined with an inhaled betaadrenergic agent taken at regular intervals of 4 to 6 h. If long-term corticosteroid therapy is re quired, the dosage should be tapered to the lowest possible maintenance dose. At this time, patients should be tried on alternateday therapy, although this may be less effec tive. Inhaled corticosteroids (beclomethasone, triamcinolone, or flunisolide) may be ad ministered with the goal of eliminating oral steroids. The inhaled agents do not have sig nificant systemic effects, and their major side effects are sore throat and oral candidiasis. This is avoided by using an aerosol spacer and rinsing the mouth and throat with water af ter each inhalation. When switching from oral to inhaled corticosteroids, it is important to observe the patient for the development of adrenal insufficiency, especially during periods of stress; an overlap period is advised. Non-asthmatic symptoms such as rhinorrhea and arthralgias may appear if they were sup pressed by systemic steroid therapy. In patients with asthma inadequately con trolled by other therapy, a trial of inhaled cromolyn is indicated using either a spinhaler, MDI, or powered nebulizer. Cromolyn pow der by inhalation often causes bronchospasm r 234 AMERICAN THORACIC SOCtEJ^ 1 and preceding the cromolyn with a betaadrenergic agent is generally advisable; when cromolyn is given by MDl, bronchospasm is uncommon, and this is the preferred method of administration. IV. Drug Therapy of Chronic Obstructive Pulmonary Disease (COPD) Many patients with COPD have a bronchospastic component, and these patients usu ally respond to appropriate bronchodilator therapy (14, 31, 32). While inhaled betaadrenergic agents are often effective, the ad dition of oral sustained-release theophyllines and/or an inhaled anticholinergic agent may be beneficial in some patients. For many years, corticosteroids were con sidered to be contraindicated for patients with COPD; however, investigators have recently shown that there is a subgroup of these pa tients who may benefit from oral corticoste roid therapy. These are usually patients who respond to inhaled beta-adrenergic agonists, but some patients with less reversible disease occasionally derive significant benefit from corticosteroid therapy (11). A therapeutic trial consists of determining baseline flow rates on optimum bronchodilator therapy, then ad ministering a dose of 32 mg of oral methylprednisolone or its equivalent once daily for 2 to 3 wk. Following this, flow rates are again determined and if no- objective benefit is demonstrated by spirometry or peak flow, the corticosteroids should be discontinued. If there is significant improvement, the steroid dose is tapered as rapidly as possible until a maintenance dose is determined. At this time the patient may be changed to alternate-day therapy or an attempt may be made to sub stitute an inhaled corticosteroid; however, these methods of steroid administration are not effective in all patients with COPD who respond to oral steroids (33). In acute exacer bations of COPD, the addition of intravenous corticosteroids has been shown to be of ben efit (34). Benefits of long-term corticosteroids must be weighed against the multiple and var ied.side effects of these agents. The prevention of acute attacks of bronchi tis includes influenza immunization in the fall of each year utilizing that antigenic combina tion recommended by the U.S. Public Health Service. This action will reduce death and morbidity from pneumonia and from influ enza-induced exacerbations of bronchitis. Amantadine is recommended *'or short term prophylaxis during presumed influenza A outbreaks for high-risk patients who have not been immunized, and in situations where the vaccine may be ineffective, as in patients who may show a poor antibody response to vaccination. It should be given throughout the epidemic period for patients who cannot be immunized, but should not be a substitute for vaccination for most patients. In an out break, nonimmunized patients should be vac cinated and treated with amantadine for 2 wk. The usual dose is 200 mg/day given in 2 di vided doses. For the patient who is hospitalized with an acute exacerbation of bronchitis, antimicro bial therapy is almost always given even though many of these episodes are induced by viral infection. When the patient is to re ceive intravenous drugs, ampicillin and/or amoxicillin are the drugs of choice. If allergy to penicillin is a concern, alternative agents include erythromycin, cephalosporin, tri methoprim-sulfamethoxazole, chloramphen icol, and tetracycline. The duration of treat ment must be individualized since these pa tients usually show a prolonged recovery period. For the patient with less severe dis ease who develops a sudden worsening of the bronchitis with increased cough and sputum production with or without fever, leukocyto sis, change in sputum volume and sputum purulence, symptomatic care, and rest are in dicated. Some physicians treat these patients with oral antibiotics for 1 to 2 wk, but there is little evidence to prove that this approach produces a more favorable outcome than symptomatic care and rest. References 1. Skidmore IF. Drugs acting on adrenoceptors. In: Buckle DR, Smith H, eds. Development of anti asthma drugs. London: Butterworths, 1984. 2. Pops VT. Clinical pharmacology of adrener gic drugs. J Asthma 1984; 21:183-207. 3. Shim C, Williams MH Jr. The adequacy of in halation of aerosol from canister nebulizer. Am J Med 3980; 69:891-4. 4. Sackner MA, Kim CS. Auxiliary MDI aerosol delivery systems. Chest 1985; 88(Supp! 2:161S-70S). 5. Newman SP. Aerosol deposition considerations in inhalation therapy. Chest 1985; 88(Suppi 2: 152S-60S). 6. Weinberger M, Hendeies L. Methylxanthines. In: Weiss EB, Segal MS. Stein M, eds. Bronchial asthma. Mechanisms and therapeutics. 2nd ed. Bos ton: Little, Brown and Company, 1985. 7. Goldstein RS, Allen LC, Thiessen J J, Michalro K, Dayneka N, Woolf CR. Daily maintenance dose ofa long-acting theophylline from a single theophyl line serum level. Chest 1986; 89:103-8. 8. Brenn KJ, Bury R. Desmond PV. Effects of cimetidine and ranitidine on hepatic drug metabo lism. Clin Pharmacol Therap 1982; 31:297-300. 9. Gross NJ. Skorodin MS. Anticholinergic, antimuscarimc bronchodilators. Am RevRespir Dis 1984; 129:856-70. 10. Pakes GE. Anticholinergic drugs. In: Buckle DR, Smith H, eds. Development of anti-asthma drugs. London: Butterworths, 1984. 11. George RB, Payne DK. Anticholinergics, cromolyn, and other occasionally useful drugs. Clin Chest Med 3984; 5:685-93. 12. Cox JSG. Disodium cromoglycate (FPL670). A specific inhibitor of reaginic antibody-antigen mechanism. Nature 1967; 216:1328-9. 13. Morton AR, Turner KJ, Fitch KDi Protection of exercise-induced asthma by pre-exercise cromo lyn sodium and its relationship to serum IgE lev els. Ann Allergy 1973; 31:265-71. 14. Mandella LA, Manfreda J, Warren CPW, Anthonisen NR. Steroid response in stable chronic ob structive pulmonary disease. Ann Intern Med 1982; 96:17-21. 15. Sahn SA. Corticosteroid therapy in chronic obstructive pulmonary disease. Pract Cardiol J9<. ]l(No. 8);J50-6. 1 16. Blair GP, Light RW. Treatment of chronic ob. structive pulmonary disease with corticostero:d Chest 1984; 86:524-8. 17. Ziment I. Hydration, humidification and mucokinetic therapy. In: Weiss EB, Segal MS, Stein M, eds. Bronchial asthma. Mechanisms and ther apeutics. 2nd ed. Boston: Little Brown and Com pany, 1985. 1 18. Brain J. Aerosol and humidity therapy. Am Rev Respir Dis 1980; 122(Suppl:I7-21), 19. Ziment 1. Prophylactic and therapeutic man agement of chronic obstructive pulmonary disease In: Ziment I, ed. Practical pulmonary disease. Ne* York: John Wiley and Sons, 1983. 20. Leeder SR. Role of infection in the cause and course of chronic bronchitis. J Infect Dis 1975 131:731-42. ' 21. McHardy VU, Inglis JM, Calder MA, Crofton JW. A study of infective and other factors in ex acerbation of chronic bronchitis. Br J Dis Chest 1980; 74:228-38. 22. Tager I, Speizer FE. Role of infection in chronic bronchitis. N Engl J Med 1975; 292:563-71. - 23. Haas H, Morris JG. Samson S, Kilbourn JR, Kim PJ. Bacterial flora of the respiratory tract in chronic bronchitis. Comparison of transtracheal, ftberbronchoscopic and oropharyngeal sampling methods. Am Rev Respir Dis 1977; 116:41-7. ; 24. Irwin RS, Erickson AD, Pratter MR, et el. Prediction of tracheobronchial colonization in cur rent cigarette smokers with chronic obstructive bronchitis. J Infect Dis 1982; 145:234-41. > 25. Lichtenstein LM. An evaluation of the role i of immunotherapy in asthma. Am Rev Respir Dis 1978; 117:191-7. 26. Lichtenstein LM. A reevaluation of immuno therapy in asthma. Am Rev Respir Dis 1984; 129. 657-9. 27. Behrens BL, Marsh WR, Henson PM, Lar sen GL. Passive transfer of the late pulmonary re sponse in an animal model. Relationship of ia- munologic status to pulmonary physiologic changes (abstract). Am Rev Respir Dis 1983; 127 (Suppl:A65). j ' 28. George RB. Some recent advances in the man agement of asthma. Arch Intern Med 1982; 142: 933-5. :'J 29. Hopewell PC, Miller RT. Pathophysiologyand management of severe asthma. Clin Chest Med 1984; 5:623-34. j* . 30. Collins JV, Clark TJH, Brown D, Townsend J. The use of corticosteroid in the treatment ofacute asthma. Quart j Med 1975; 174:259-73. 31. Lertzman MM, Cherniack RM. Rehabilitate of patients with chronic obstructive pulmonaryda* ease. Am Rev Respir Dis 1976; 114:1145-65. 32. Filuk RB, Easton PA, Anrhonisen NRsponses to large doses of salbutamol and theophyl line in patients with chronic obstructive pulmonary -disease. Am Rev Respir Dis 1985; 132:871-4. 33. Shim CS, Williams MH Jr. Aerosol t** clomethasone in patients with steroid-respons* chronic obstructive pulmonary disease. Am J M 1985; 78:655-8. 34. Albert RK, Martin TR, Lewis SW. Control# . clinical trial of methylprednisolone in patients " chronic bronchitis and acute respiratory insug I ciency. Ann Intern Med 1980; 92:753-8. TOUCAN THORACIC SOCIETY 235 5 ii. . ':n ifn- aj n- nd on 1 ;) *! * i m1 a!, n* el. itivt olt Dis )*0- 29: rt.fa- 150 !27 an- sad * led ;ad uk ion I dis- - I i ) CHAPTER 4 02 Therapy i. introduction Supplemental oxygen is one of the most com mon modalities used in treating patients with obstructive lung disease. The ultimate goal of such therapy is to prevent hypoxic tissue damage. In patients with obstructive lung dis ease, hypoxic tissue damage results primarily from arterial hypoxemia, which is efficiently treated with 0, therapy. When other diseases complicate obstructive lung disease, tissue hypoxia may result from other causes of in adequate O, delivery to tissues, e.g., reduc tions in cardiac output or hematocrit. Inade quate 0, delivery in these situations obviously should be treated by maneuvers aimed at the basicabnormalityand is not efficiently treated by 0: ;:'.erapy, and will not be considered fur ther in this report. Arterial hypoxemia is one of the most ominous manifestations of ob structive lung disease and is at present the only acceptable indication for O, therapy. The im mediate goal of Oj therapy, therefore, must be to increase arterial oxygenation to accept able levels. In general, Oj therapy in obstructive iung disease is used in 2 situations: in acutely ill hospitalized patients, and in chronically ill patients who are not in-the hospital. '1. O2 Therapy for Acutely ill Patients A. General Guidelines As noted above, the indication for Oj ther apy is significant arterial hypoxemia. Arterial oxygenation is usually assessed by measur ing the partial pressure of Oj in arterial blood (Pao,), and when Paoj < 60 Torr, hypoxemia sufficient to treat with oxygen is present. The goal of Oj therapy should be to increase Pao, to at least 60 Torr, equivalent to an arterial Oj saturation of approximately 90%. On the other hand, increasing Paoj beyond 65 Torr is associated with relatively minor further in creases in arterial Oj content (1,2), therefore, little'purpose is usually served by increasing Pao, to values greater than 80 Torr, and O, doses that do so should generally be avoided. The Oj dose that will increase Pao, to 65 to 80 Torr in a given patient with obstructive lung disease can vary greatly, depending on the severity of the initial hypoxemia and the pre cise nature of the physiological disturbance. Attaining the correct dose is best done by trial and error, i.e., starting at a given dose (see below), measuring the Paoj and adjusting the dose accordingly. It should be noted that in Patients with severe COPD, it can take 20 to 30 min for a steady state to be achieved after a change in the inspired gas mixture, so that arterial blood should usually not be sampled at shorter intervals after changes in O, dose. & O, Therapy and COj Retention In some patients with COPD, Os therapy and the associated increase in Pao, produce CO, retention, or an increase in arterial CO, ten sion (Paco,) (3-5). This is a potentially seri ous problem in that CO, retention may pro duce coma. There is at present no good way to predict whether or not a given patient will develop a rising Paco, with O, therapy, though it generally occurs in very sick patients with Pao, of < 40 Torr and with an elevated Paco, while breathing room air, and very rarely oc curs in asthmatics (5-7). It follows that the only accurate way to assess the effect of O, therapy on Paco,, as well as its effect on Pao,, is to measure Pao, and Paco, repetitively. In patients who demonstrate increases in Paco, with O, therapy, the latter should be used with caution. CO, produces central nervous sys tem disturbances by changing brain pH, so that the level of Paco, that produces clini cally significant complications depends, in turn, on brain bicarbonate levels. CO, nar cosis, therefore, cannot be predicted on the basis of the Paco,, since no fixed level of Paco, may be defined as "too high," and CO, narcosis can only be diagnosed by careful serial clinical observations. In hypoxemic pa tients who develop CO, retention with O, ther apy, the physician should attempt to increase the Pao, without causing an increase of Paco, sufficient to cause drowsiness or stupor. Of ten it is possible to produce clinically signifi cant increases in Pao, that do not reach the ideal goal of 65 Torr, but are not associated with disturbances of consciousness. It must be recalled that severe hypoxemia causes death, whereas the disturbances associated with severe CO, retention are not usually le thal. In severe hypoxemia the first priority must be to increase Pao,. If excess O, is given, and the patient develops signs and symptoms thought to represent CO, narcosis, the in spired O, concentration should be reduced, but not to room air since abrupt cessation of all O, therapy can produce fatal hypox emia. If adequate oxygenation cannot be achieved without progressive hypercapnia, mechanical ventilation may be required (3, 5,6). C O3 Therapy in Emergency Situations The above discussion has assumed that the diagnosis of obstructive lung disease is clearly established and that measurements of Pao, and Paco, are readily available. These as sumptions do not always apply; patients are frequently encountered who are in respiratory distress for reasons that are not entirely clear, and, irrespective of diagnosis, O, therapy is frequently undertaken without prior knowl edge of arterial blood gases. It is reasonable to treat all patients in respiratory distress with O, before the results of blood gas analyses are known. If such patients clearly do not have COPD, short-term O, therapy is essentially without risk, and any O, dose - up to 100% may be safely employed. If, however, COPD is a diagnostic possibility, high-dose O, ther apy carries the risk ofCO, narcosis and should be avoided. The lower the O, dose, the lower the risk of CO, retention. Inspired concen trations of less than 40% O, are uncommonly associated with rapidly rising Paco,, and it is rare with inspired concentrations of less than 30%. Thus, when blood gas results are not available, patients suspected of having COPD should be treated with O, concentra tions of 24 to 40%. In general, it is best to start at the lower end of the dose range, and to increase the dose only when there is clini cal or laboratory evidence that this should be done. These inspired oxygen concentrations are usually achieved by nasal flows on the or der of 1 to 5 L/min (see below). Oxygen therapy without arterial blood gas measurement is acceptable only under emer gency conditions. Ideally, arterial blood should be sampled in the emergency room as O, therapy is started, and the procedure repeated some 20 to 30 min later. In acutely ill patients seen for the first time, prolonged (I to 2 h) 0, therapy without measurements of Pao, and Paco,'are acceptable only under exceptional circumstances. Though noninvasive measurements of Pao, and Paco, are available, they should not be relied upon in acute situations, or when rapid changes might be expected. D. Methods of 02 Administration In acute, inpatient situations, O, sources are readily available, as are a variety of techniques of transferring O, from the source to the pa tient (8). In general, there are 2 methods of delivering 4 40% O,. Nasal "prongs" are popular because they do not interfere with eating and conversation. The O, dose can be varied by varying O, flow, but the precise in spired concentration achieved depends on the patient's ventilation and breathing pattern, and the dose delivered at a given O, flow will show both interindividual and intraindividual variations. The inspired O, concentration in % (Fio,) can theoretically be calculated as: Fio, = 20 + 4 x O, flow (L/min). This is, how ever, only an approximation. At flows of > 4 L/min, the 02 should be humidified, although at lower flow rates this is not necessary. Al ternative methods of administration of < 40% O, are Venturi masks, which, though they in terfere with activities such as conversation and eating, supply fixed, known inspired O, con centrations ranging from 24 to 50%. Oxygen at concentrations exceeding 40% can only be administered by mask. Masks vary in design, but those employing a high flow of O, into a reservoir bag are most efficient in that they can deliver inspirates of up to 90% O,. As noted above, these systems are poten tially dangerous in patients with COPD. Hi. 02 Therapy in Chronic Lung Disease A. O: Therapy in Patients with Continuous Hypoxemia It has been conclusively shown that the sur vival of patients with hypoxemia COPD is improved by long-term O, therapy, and that this benefit is greatest if the treatment is ap plied at least 18 h/day (9-13). Thus, chroni cally hypoxemia COPD patients should, in general, be treated in this way. There is no ,.U 'T , 236 AMERICAN THORACIC *ocrfY, 'dence of benefit for long-term O, therapy ed less than 12 to 15 h/day. Benefits from home O, therapy have been demonstrated in stable patients with Pao, < 55 Torr (arterial Oj saturation, < 90Ve), and in patients with Pao, 55 to 59 Torr with evi dence of polycythemia or right heart failure when stable; it is, therefore, to this group that the treatment should be applied. Stability is best defined in terms of arterial blood gas measurements. Patients are defined as chron ically hypoxemic if, when clinically stable, they meet the above criteria during an observation period of 2 wk. Patients with Pao, of 45 to 60 Torr can usually undergo the observation period as outpatients, but sicker patients may have to be stabilized in the hospital. Patients who qualify as outlined above should receive continuous O, therapy, i-e., as close to 24 h/day as possible, and the dose should be sufficient to raise resting Pao, to 65 to 80 Torr (saturation, 91 to 95^o). The dose should be increased by I L/min while the patient is sleeping or exercising to elimi nate hypoxemic episodes during these activi ties. With such a regimen, specific studies of oxygenation during sleep and exercise are sel dom necessary. The appropriateness of the daytime resting O, dose should be assessed periodically. B. Patients with Intermittent Hypoxemia Some patients with COPD--not asthma-- who have Pao, of at least 60 Torr while awake and at rest develop more severe hypoxemia while sleeping or exercising (14). At present there are few data to indicate whether, in such patients, O, therapy during sleep or exercise are of benefit, so any standards suggested must be regarded as provisional. C. Nocturnal Hypoxemia There appears to be little question that some COPD patients who do not qualify for con tinuous home 0, therapy have episodes of se vere hypoxemia (arterial saturation, < 85V#) while sleeping. Though it is not established that such episodes are harmful, it is probably unwise to assume that they are harmless, and we believe nocturnal O, therapy can be justi fied in such patients. Detection of nocturnal hypoxemic episodes in patients who are not hypoxemic during wakefulness requires study during sleep; the criteria for patient selection for study has not yet been determined (9). COPD patients with Pao, > 60 Torr who are obese, or who have CO, retention, polycythe mia, or evidence of right heart failure, prob ably merit sleep studies. The O, dose required to eliminate severe nocturnal hypoxemia in these patients can also only be determined with accuracy by sleep study. A minimum noc turnal oxygen saturation of approximately 90Vo is a reasonable therapeutic goal. 1 It should be noted that O, therapy may not be appropriate for obstructive sleep apnea, which may coexist with COPD. In patients with nocturnal hypoxemia due to obstructive sleep apnea, therapy should be aimed at reliev ing nocturnal upper airway obstruction. D. Exercise Hypoxemia Some COPD patients-usually those with very severe airway obstruction--develop hy poxemia during exercise while maintaining Pao, > 60 Torr at rest. Home oxygen has been prescribed for use during exercise in such pa tients, though there is no solid evidence for long-term benefit. Since most of these patients spend relatively little time exercising, it is dif ficult to believe that the hypoxemia of exer cise affects survival or function at rest. Thus, the best rationale for supplemental O, dur ing exercise is that it will increase exercise toler ance and useful daily activity. However, it is not clear that arterial hypoxemia limits exer cise tolerance in all of these patients. Sup plemental O, during exercise should probably be prescribed only when it has been shown by appropriate testing to increase exercise tolerance significantly. The simplest way to measure the benefits of O, during exercise is to conduct exercise tests with the patients breathing both room air and supplemental O,. These tests are best conducted in such a way that the patient is not aware of whether O, or room air is being supplied (15). E. Methods of O, Delivery The only practical way of delivering home O, to patients is via nasal prongs (8). Recently, prongs that supply 0, only during inspira tion have been developed in an attempt to conserve gas; oxygen has also been delivered directly to the subiaryngeal trachea via a chronic transtracheal cannula. These systems have not yet been fully evaluated, and can not be recommended at present. Sources of O, suitable for use in the home vary, and each has advantages and disadvan tages. Liquid O, systems were used early in home O, therapy, and are the most versatile because of their easy portability; patients can easily carry an O, supply for shopping excur sions, etc. Liquid systems are also more ex pensive than any other, and can only be used in urban areas near a source of liquid O,. Steel cylinders containing compressed gas can be used as sources for home O,. These are available in towns large enough to have welding suppliers. They are nearly-as expen sive as liquid systems, and afford much less portability. Small steel 0, cylinders are too heavy to carry and must be moved in wheeled carts, which is frequently difficult for sick pa tients. Recently, aluminum compressed gas cylinders have become available. These are light enough to carry while containing sev eral hours of O, supply and are, in theory, an improvement over steel cylinders. How ever, the most efficient use of aluminum cylinders involves filling them from large steel cylinders in the home, which is regarded as dangerous by many municipal safety authori ties. The cheapest source of home O, is the socalled concentrator, which separates atmos pheric O, from N, and supplies the former. Though there is a substantial initial cost for these machines, they require little subsequent service and maintainance. They operate usi?, electrical power and can be used in any ho^j with electricity. Their major drawback is that they are non-portable: If the patient leavt* the home, it is either without O, or with a other portable system. Most programs sup. ply a large steel cylinder of compressed 0, along with the oxygenator, to provide against electrical failure. References J 1. Campbell EJM. Oxygen therapy in disease! 1 the chest. Br J Chest Dis 1964; 58:149-57. 1 2. Campbell EJM. Management of respiratory failure. Br Med J 1964; 2:1328. 3. Seiker HO, Hickham JB. Carbon dioxide in toxication. The clinical syndrome, its etiology and management with particular reference to the use of mechanical respirators. Medicine 1956 3$- 389-423. ' 4. Lopez-Majano V, Dutton RE. Regulation of respiration during oxygen breathing in chronic ob structive lung disease. Am Rev Respir Dis 1973 108:232-40. .' 5. Bone RC, Pierce AX, Johnson RL Jr. Con trolled oxygen administration in acute respiratory failure in chronic obstructive pulmonary Am J Med 1978; 65:896-902. * 6. Aubier M, Murciano D, Milic-Emili J, et at. Effects of the administration of O, on ventilation and blood gases in patients with chronic obstruc- ' live pulmonary disease during acute respiratory f*Bure. Am Rev Respir Dis 1980; 122:747-54. 7. Anthonisen NR. Hypoxemia and O, therapy.'' Am Rev Respir Dis 1982; 126:729-33. . 8. FulmerJD.SniderGL.ACCPNHLBlnational conference on oxygen therapy. Chest 1982; && 234-47. & < 9. Anthonisen NR. Long-term oxygen therapy. Ann Intern Med 1983; 99:519-27. 10. Levine BE, Bigelow DB, Hamstra RD. The role of long-term continuous oxygen administration in patients with chronic airway obstruction and hy poxemia. Ann Intern Med 1967; 66:639-50. * H. Abraham AS, Cole RB, Bishop JM. Reversal of pulmonary hypertension by prolonged oxygen administration in patients with chronic bronchi tis. Circ Res 1968; 23:147-57. 12. Nocturnal Oxygen Therapy Trial Group. Con tinuous or nocturnal oxygen therapy in hypoxemia chronic obstructive lung disease: a clinical trial. Ana Intern Med 1980; 91:391-8. **= 13. Medical Research Council Working PartyLong-term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic broo- cbitis and emphysema. Lancet 1981; 1:681-6. >' 14. Block AJ. Dangerous sleep: oxygen therapy, for nocturnal hypoxemia. N Engl J Med 198V 306:166-7. 15. Longo AM, Moser KM, Luchsinger PC. The role of oxygen therapy in rehabilitation of patients. with chronic obstructive pulmonary disease. A*. Rev Respir Dis 1971; 103:690-7. J ir CHAPTER 5 Respiratory Care Modalities production if.-. % liratory care modalities are valuable inctive therapy in the care of patients ructive airways diseases. Patients, fa*/-- thoracic socjety .00*** 237 aioa ; I ?I seof | 3tory | :e io- ' and r u ; 35: )n of cob- !973; * } j Coo- i itory I iease - t: el. V uioe . Itrue ' fail- L ~ rapy. ion*' rapy- I | I roie >nio ihy " ;nal \ gen 1 .chi- * .onmia \nn I ] irtr-v i -owe. | ;r0"':. I rapy.. .982; - The., | :enu | Am : / - members or other caregivers should be trained in the use of these modalities by qualiiwj practitioners, usually respiratory ther- Lists and respiratory therapy technicians un- the aegis of a medical director who has trained in the care of acute and chronic pulmonary diseases (1, 2). This section will Lver the indications and guidelines for the u$c of incentive spirometry, intermittent posi tive pressure breathing (1PPB), intermittent continuous positive airway pressure (CPAP), bland aerosol and humidity therapy, medi cated aerosol therapy, chest physiotherapy {in cluding postural drainage), chest percussion and vibration, and breathing exercises. Oxy gen therapy is discussed in Chapter 4. These modalities may be administered separately or concomitantly. - It. Measures for Lung Expansion Incentive spirometry is a technique to en courage a patient to take a sustained, deep breath, utilizing a measuring device for di rect visual feedback. It is indicated as an aid to facilitate lung expansion in hospitalized pa tients both to prevent and to treat pulmonary atelectasis. It may be particularly useful be fore and after major surgical procedures as part of a regimen to help prevent postopera tive atelectasis and other respiratory compli cations (3,4). The deep breathing maneuvers may also stimulate patients to cough and thereby aid in the removal of abnormal bron chial secretions. The frequency of use usually depends upon the clinical condition of the patient. In the initial treatment of pulmonary atelectasis, in centive spirometry may be used hourly, at least during the waking hours. With improvement of atelectasis or with prophylactic use of in centive spirometry, the frequency of therapy may be less. It is critical that patients receive instruction in the proper use of incentive spirometry from individuals trained in respi ratory care, with the emphasis on sustained maximum inhalation for 5 to 6 s, and 5 to 10 sequential deep breaths (6). Subsequent use of the incentive spirometer may be super vised by nursing personnel, but it is reason able to provide periodic follow-up assessment by respiratory care personnel to assure that incentive spirometry is being properly ad ministered and utilized. Although chronic use of hmg expansion maneuvers in the home or at other commu nity living sites may be indicated in persons with severe restrictive pulmonary dysfunction, |here is no evidence that this form of therapy is useful in patients with obstructive airways diseases. Breathing exercises with a simple in spiratory resistance device or with an incen tive spirometer may be of value as a means to increase inspiratory muscle strength and endurance (6), but studies of long-term ben efit are still lacking. The use ofthe IPPB in patients with COPD |s controversial. There is no evidence that it >s helpful or desirable for home use (7). Pos able selected indications for IPPB in the hos pital may include the following (8): (/) The management of atelectasis that has not improved with voluntary deep breathing or incentive spirometry, when it can be doc umented that the inspiratory capacity is in creased by at least 25% using IPPB (9). In these patients, IPPB should be administered by a volume-oriented technique. IPPB can not be recommended as a routine prophylac tic technique to prevent atelectasis. (2) As a measure to provide frequent peri odic deep breathing for a patient with acute ventilatory failure in an attempt to avoid in tubation or reintubation. In such circum stances, IPPB is a temporizing procedure and not meant to normalize arterial blood gases, allowing the patient time to improve by vir tue of correction of reversible factors that have precipitated the acute ventilatory failure. (3) For the delivery of aerosol medications, primarily bronchodiiators, in pateints who are unable to breathe slowly and deeply because of acute respiratory distress. It is doubtful, however, that IPPB is more effective in the delivery of nebulized bronchodiiators or in causing bronchodilatation than is a nebulizer operated by a constant pressure compressed gas source. Continuous positive airway pressure (CPAP) by mask has been used in the past for treatment of pulmonary edema. Recently, the use of intermittent CPAP by mask has been investigated in the management of pul monary atelectasis (10,11). This modality re quires further study in patients with COPD before specific recommendations for its use can be made. In particular, the possible det rimental effects of further hyperinflation on cardiac function and respiratory muscle efficiency must be evaluated. The use of in termittent mask CPAP would appear to have no place in the management of respiratory failure associated with obstructive airways diseases. III. Bland Aerosols and Humidity Therapy The use of bland aerosols and humidity ther apy in patients with obstructive airways dis ease centers primarily on humidification of the inspired gas being delivered through an artificial airway (endotracheal tube or tra cheostomy). Any patient with obstructive air ways diseases and respiratory failure who requires hospitalization and who has an ar tificial airway, either with or without mechan ical ventilation, should be provided with a heated and humidified gas source during the period of tracheal intubation, in patients with chronic obstructive airways diseases who have permanent tracheostomies, the need and method for continued humidification of the inspired gas after discharge must be individ ually assessed. Further studies are needed to determine if adequate long-term humidifica tion using a moisture-exchange device ("ar tificial nose") connected directly to the air way opening can be efficacious. Bland aerosols, utilizing either water or sa line, have not been shown to aid in the clear ance of abnormal secretions. They neither thin secretions nor enhance bronchial clearing and may precipitate bronchospasm (12,13). Room humidifiers should be discouraged because of their ineffectiveness in providing increased hu midity for the patient and because of their high rate of bacterial and fungal contamina tion. Hypertonic saline delivered by ultrasonic nebulization may be used for short periods of time to induce sputum for diagnostic studies, although there is no evidence it is su perior to coached coughing. IV. Medicated Aerosol Therapy It is well established and generally agreed that bronchodilator drugs, administered to pa tients who demonstrate symptomatic or ob jectively measured improvement, are useful both in the hospital and in the home. Advan tages of aerosol versus oral bronchodilator delivery include: more rapid, predictable on set of therapeutic effect, smaller quantity of active agent required for given degree of ob jective response, generally greater attainable response at tolerated doses, and fewer systemic side effects. Bronchodiiators may be given as aerosols via a metered-dose inhaler (MDI), with or without a variety of spacer devices (tube, col lapsible bag, cone or pear-shaped) introduced to improve the efficiency of delivery of the bronchodilator agents (14,15) in patients who are unable to use a MDI properly (16, 17). Alternatively, they may be administered with a nebulizer powered by compressed gas or by a small electrical air compressor. Patient in struction in the proper technique of using a nebulizer or an MDI with or without a spacer is essential. This may be done by respiratory care personnel, a specially trained nurse, or by a knowledgeable physician. In the hospital, aerosolized bronchodilators are usually delivered by nebulizers, al- though recent studies have demonstrated that, in patients not severely ill, the effects of metaproterenol administered by MDI plus spacer were the same as metaproterenol administered by a nebulizer (18, 19). Administration of the aerosol bronchodiiators by either MDI or nebulizer should be performed by respiratory care personnel or other trained hospital personnel for patients who are acutely ill, confused, or feeble. In the stable patient who has demonstrated proficiency in using an MDI, with or without a spacer, little supervision may be required. The frequency of administration of aero solized bronchodiiators will depend upon the severity of the illness but may be required as often as every hour in those patients with acute severe asthma (20). As the patient improves, the frequency of administration should be dictated by the duration of action of the drug administered (see Pharmacologic IkERAPY, Chapter 3). In the patient with ob structive airways disease who requires surgery, particularly of the thorax or upper abdomen, aerosolized bronchodilator agents should be started preoperativeiy and continued in the postoperative period, in order to reduce postoperative pulmonary complications (21,22). Outside the hospital, aerosolized bron- ! : : I j j ; ; j : ! I j j , I ' | i r ' , ! 1 i 11238 AMERICAN THORACIC soon? A* -hodilators are usually delivered with a nered-dose inhaler with or without a spacer. Vhen inhaled corticosteroids are required, the se of spacer devices with a MD! results in a substantially lower incidence of thrush, and fewer problems with dysphonia, than when the MD1 alone is used (14). Some outpatients, particularly those who are unable to use an MD1, derive benefit from aerosolized bronchodiiator agents delivered by a nebulizer. If the nebulizer is used on a daily basis, it may need to be powered by an air compressor since hand-bulb nebulizers may be difficult to coordinate with inhala tion. These devices are portable. Patients using a nebulizer in the home should be instructed by trained personnel in the proper use and cleaning of the equipment. Periodic servic ing and inspection of home nebulizer equip ment may be necessary for some patients. V. Chest Physical Therapy Chest physical therapy (or chest physiother apy) encompasses the use of postural drain age, chest percussion and vibration admin istered by hand or by mechanical percussion, as well as cough and deep breathing. The ra tionale for this therapy in the treatment of patients with obstructive airways diseases is the belief that gravity and applied external force to the chest wail will facilitate mobili sation and clearance of secretions from the .irways, leading to an improvement in pul monary function. In order for chest phys iotherapy to be effective in the home or hos pital, the patients must have excessive secre tions (30 cc/day or greater) that are difficult to expectorate (23-27). In the hospital setting, chest physiother apy is indicated in those patients who have great difficulty raising secretions and in those patients who develop atelectasis either post operatively (28) or under other circumstances (29, 30). Fiberoptic bronchoscopy can be ef fective in acute lobar atelectasis, but is no more effective than vigorous chest physiotherapy given by experienced personnel (27). Chest physiotherapy may be effective in acutely ill patients with obstructive lung diseases who expectorate large sputum volumes (30, 31) even if they require mechanical ventilation (30, 32). Use of chest physiotherapy has not been shown to be effective in acute exacerbations of chronic bronchitis (33-35), in patients with scant secretions receiving mechanical venti lation (31), in patients with status asthmaticus (26), or in patients who have pneumonia (36). Chest physiotherapy is indicated either in the hospital or at home in stable patients with bronchiectasis, cystic fibrosis, and chronic bronchitis who chronically produce large spu tum volumes (37-41). It is not effective in pa tients with COPD who produce less than 30 cc/day (42). To facilitate bronchodilation and mucociliary clearance, chest physiotherapy should be delivered after the administration of an aerosolized bronchodiiator (35). The frequency of administration of chest physiotherapy in patients who might benefit from it has not been established. In patients with atelectasis and in others who have diffi culty expectorating sputum, probably no more than 4 treatments per day are practical or tolerable. Patients with more stable condi tions, especially in the home setting, usually will require fewer treatments. In those patients who will benefit from the continuation of chest physiotherapy outside the hospital, the patient and family members should undergo a complete educational pro gram on the technique and goals ofchest phys iotherapy in the home prior to discharge. Trained respiratory care personnel, nurses, or physical therapists usually provide this in struction. Family members can be taught to administer percussion and vibration. The number of teaching sessions required before the patient and family members are compe tent will depend upon their ability to grasp the concepts and apply them during therapy. Usually several sessions will be required. VI. Breathing Exercises Breathing exercises encourage patients to in spire slowly and to expire through pursed Ups (25,26). Simultaneous relaxation of the neck and upper thoracic musculature should be en couraged (26). Breathing exercises may be ef fective in increasing the patient's tidal volume, decreasing the respiratory rate, and lowering the FRC (43,44), thereby improving the effi ciency of gas exchange and reducing the work of breathing. In the acutely ill patient, the use of breath ing exercises may be helpful in aborting hyper ventilation episodes precipitated by panic or anxiety, provided the patient is familiar with the technique. Even if the patient is untrained, coaching by respiratory care personnel or other trained professionals to inhale slowly and exhale through pursed lips is helpful. Patients with stable obstructive airways dis eases may benefit from breathing exercises, both physiologically and symptomatically (43-46). They are most effective over short term use, since long-term studies show no im provement in pulmonary flows (45, 47). Breathing exercises are effective in helping the patients overcome attacks of hyperventilation precipitated by fear and anxiety and may be useful to combat the urge to hyperventilate after mild exercise. References 1. Miller WF. Plummer AL, et ol. Guidelines for organization and function of hospital respiratory care services. Chest 1980; 79-83. 2. American Thoracic Society. Medical director of respiratory therapy. ATS News 1976; 2:1-3. 3. Bartlett RH, Brennan ML, GazzanigaAB, Han son EL. Studies on the pathogenesis and preven tion of postoperative pulmonary complications. Surg Gynecol Obstei 1973; 137:925-33. 4. Bartlett RH. Respiratory therapy to prevent pul monary complications of surgery. Respir Care 1984; 29:667-77. 5. O'Donohue WJ Jr. Perioperative measures for lung expansion. In: O'Donohue WJ Jr, ed. Cur rent advances in respiratory care. Park Ridge, 1L: Amer Col Chest Phy 1984; 10-20. 6. Sonne LJ, Davis JA. Increased exercise perfor mance in patients with severe COPD following jj* spiratory resistive training. Chest 1982: 81:43^.5 7. Intermittent Positive Pressure Breathing Trial Group. Intermittent positive pressure breathing therapy of chronic obstructive pulmonary disease a clinical trial. Ann Intern Med 1983; 99:612-20 8. Respiratory Care Committee of the American Thoracic Society. Intermittent positive pressure breathing (IPPB). Clin Notes Respir Dis 1979. 18:3-6. ' 9. O'Donohue WJ Jr. Maximum volume ippg for the management of pulmonary atelectasis Chest 1979; 76:683-7. 10. Anderson JB. Olesen KP, Eikard B, Jansen E, Ovist J. Periodic continuous positive airway ptej. sure CPAP, by mask in the treatment of atelecta sis: a sequential analysis. Eur J Respir Dis 1980 60:20-5. ` 11. Stock MC, Downs JB, Gauer PK, Cooper RB, Prevention of atelectasis after upper abdominal operations. Crit Care Med 1983; 11:220. 12. Brain JD. Aerosols and humidity therapy. Am Rev Respir Dis 1980; 122(Suppl:17-2l). 13. Brain JD. Aerosols and humidity therapy, in; O'Donohue WJ Jr, ed. Current advances in respi ratory care. Park Ridge, IL: Amer Col Chest Phy 1984; 72-85. - 14. Konig P. Spacer devices used with metered- dose inhalers. Breakthrough or gimmick? Chest 1985; 88:276-84. i 15. Sackner MA, Kim CS. Auxiliary MDI aero sol delivery systems. Chest 1985; 88(Suppt 161S-70S). ' 16. Cushley MJ, Lewis RA, Tattersfield AE. Com parison of three techniques of inhalation on the airway response to terbutaline. Thorax 1983; 3& 908-13. 17. Morris J, Milledge SS, Moszoro H. The effi cacy of drug delivery by a pear-shaped spacer and metered-dose inhaler. Br J Dis Chest 1984; 78:383-7. 18. Berenberg MJ, Baigelman W, Cupples LA. Comparison of metered-dose inhaler attached to an aerochamber with an updraft nebulizer for (he administration of metaproterenol in hospitalized patients. J Asthma 1985; 22:87-92. -. 19. Berenberg MJ, Baigelman W, Cupples LA, Pearce L. Comparison of updraft nebulizer versus metered dose inhaler attached to an aerochambe for the administration of metaproterenol to hos pitalized patients (abstract). Am Rev Respir Db 1985; 131(Suppl:A95). 20. Fanta CH, Rossing TH, McFadden ER Jr. Emergency room treatment of asthma. Relation ships among therapeutic combinations, severity obstruction and time course of response. Am J M*d 1982; 72:416-22. / 21. Stein M, Cassara EL. Preoperative pulmonary evaluation and therapy for surgery patients. JAMA 1970; 211:787-90. ? 22. Ziment I. Perioperative pharmacology management. Respir Care 1984; 29:652-63. -1 23. DarrowG, Anthonsien NR. Physiotherapy*9 hospitalized medical patients. Am Rev Respir IX* 1980; 122(Suppl:155-8). 24. Murray JF. The ketchup-bottle method. H Engl J Med 1979; 300:1155-7. 25. Sutton PP, Pavia D. Bateman JRM. Clart* SW. Chest physiotherapy: a review. Eur J Re*P" Dis 1982; 63:188-201. * 26. Rochester DF, Goldberg SK. Technique* respiratory therapy. Am Rev Respir Dis 198ft (S 27zc* 198 28 cal' off 205 29. ba; tic: Re- 30. tea tie me 31 Rc ait a 32 a in. 20' 33 Tf of M 34. in' br 35 efck 3< b J 3' fc 3 3 t ti S: 1. 3 c> n 7 4 e K t l i i 1 tl0Ciut thoracic society 239 4 per* >*infc 1:43' * i? V ):6i2-Mjs' 'nericaS Pressure^ ),S 197^| IPPs*"' 1 i's-Chea1 1 v7i * Jansea * I ^ypro..f fitefecu-i 3is 1980; T } ; ope: RR^ Fomina] apy-Aml ^.C The i >acer; '3:383-7^ pies LA? j :ached 102 ] er for tbejj I pitalized.; ' pies L^. er versus'..- jhamberjf 1 to hos-T, .spir Diljj r. ER Jfj Relation^ everity ofj vm J Medj ulmonarj*' :$. JAMA? lacolopfj -63- ethi niques 1980; 123 (Soppl^33_46)* A Kirilloff LH, Owens GR, Rogers RM, MazL^co MC. Does chest physical therapy work? Chest j$85; 88:436-44. y, Thoren L. Post-operative pulmonary cornpli-ijons. Observations on their prevention by means 0fphysiotherapy. Acta ChirScand 1954; 107:193- *>5. 29 Marini JJ, Pierson DJ, Hudson LD. Acute lohar atelectasis: a prospective comparison of fiberop tic bronchoscopy and respiratorytherapy. Am Rev Respir Dis 1979; 119:971-8. 30 Holody B> Goldberg H. The effect of mechan ic vibration physiotherapy on arterial oxygena tion in acutely ill patients with atelectasis or pneu monia. Am Rev Respir Dis 1981; 124:372-5. 31. Connors AF Jr, Hammon WE, Martin RJ, Rogers RM. Chest physical therapy. The immedi ate effect on oxygenation in acutely ill patients. Chest 1980: 78:559-64. 32. Mackenzie CF, Shin B, Hadi F, link PC. Changes in total lung/thorax compliance follow ing chest physiotherapy. Anesth AnaJg 1980; 59: 207-10. 33. Anthonisen P, Riis P, Sogaard-Anderson T. The value of lung physiotherapy in the treatment of acute exacerbations in chronic bronchitis. Acta Med Scand 1964; 175:715-9. 34. Newton DAG, Bevans HG. Physiotherapy and intermittent positive pressure ventilation in chronic bronchitis. Br Med J 1978; 2:1525-8. ' 35. Campbell AH, O'Connell JM, Wilson F. The effect of chest physiotherapy upon the FEV, in chronic bronchitis. Med J Aust 1975; 1:33-5. 36. Graham WGB, Bradley DA. Efficacy of chest physiotherapy and intermittent positive-pressure breathing in the resolution of pneumonia. N Engl J Med 1978; 299:624-7. 37. Cochrane GM, Webber BA, Clarke SW. Ef fects of sputum on pulmonary function. Br Med } 1977; 2:1181-3. 38. Bateman JRM, Daunt KM, Newman SP. Re gional lung clearance of excessive bronchial secre tions during chest physiotherapy in patients with stable chronic airways obstruction. Lancet 1979; 1:294-7. 39. Bateman JRM, Newman SP, Daunt KM. Is cough as effective as chest physiotherapy in the removal of excessive tracheobronchial secretions? Thorax 1981; 36:638-87. 40. Feldman J, Traver GA, Taussig LM. Maximal apiratory flows after postural drainage. Am Rev Respir Dis 1979; 119:239-45. 41. Mazzocco MC, Owens OR, Kiriiloff LH, Rogers RM. Chest percussion and postural drain age in patients with bronchiectasis. Chest 1985; 88:360-3. 42. Mohsenifar Z, Rosenberg N, Goldberg HS, Roemer SK. Mechanical vibration and conventional chest physiotherapy in outpatients with stable chronic obstructive lung disease. Chest 1985; 87:483-5. 43. Campbell EJM, Friend J. Action of breath- ln8 exercises in pulmonary emphysema. Lancet MS; 1:325-9. ` 44. Mueller RE, Petty TL, Filley GF. Ventilation 4nd arterial blood gas changes induced by pursed "PS breathing. S Appl Physiol 1970; 28:784-9. Jones NL. Physical therapy: present state of Ulan. Am Rev Respir Dis 1974; 110(Suppl:l32-6). Miller WF. A physiologic evaluation of the *fkcts of diaphragmatic breathing training in pa- with chronic pulmonary emphysema. Am J M*d 1954; 17:471-84. 47. Emirgil C, Sobol BJ, Normal J, etal. A study of the long-term effect of therapy in chronic ob structive pulmonary disease. Am J Med 1969; 47:367-77. CHAPTER 6 Physical Rehabilitation and Home Care I. Introduction The most common and distressing symptom in patients with COPD is dyspnea resulting in limitation of activity. The objectives of pul monary rehabilitation are to control and al leviate symptoms and pathophysiologic com plications and to achieve optimal ability to carry out activities of daily living. The broad concepts and elements ofpulmonary rehabili tation have been reviewed in a previous ATS statement (1). Most pulmonary rehabilitation programs include either encouragement for patient activity or a regular exercise component Although there is general agreement that pa tients benefit from pulmonary rehabilitation programs, the specific contribution of exer cise to the improvement is not well defined. Limitation of exercise in patients with COPD is related to multiple factors includ ing: abnormal pulmonary mechanics, impair ment in pulmonary gas exchange, an abnor mal perception of breathlessness and ventila tory control, the presence of impaired cardiac performance due to cor pulmonale, poor nu tritional status, and the development of respi ratory muscle fatigue (2). Determination of the exact number of fac tors involved and their relative importance in an individual patient with COPD is difficult and often impossible. The inability to ac curately characterize the exercise-limiting fac tors in individual patients has led to confu sion and controversy in assessing the effec tiveness of various forms of therapy designed to improve exercise performance. Several physical rehabilitation techniques are utilized to increase the dyspnea-limited level of activity or to decrease the degree of dyspnea associated with the same level of ac tivity. The methods utilized include exercise reconditioning, inspiratory muscle training, breathing retraining, and energy conservation techniques. , II. Patient Selection Physical rehabilitation should not be consid ered in the COPD patient until optimal med ical control of the disease has been achieved. Motivation is the most important factor in the selection of patients for physical rehabili tation. In younger patients with less than ad vanced disease, preservation of body weight and muscle mass and minimal disease in other organ systems are more likely to persist with and benefit from physical rehabilitation. It is important that patients be realistically ap prised of the effort and time involved and the limited benefits to be expected from physical rehabilitation before embarking on an exten sive program. Screening should include spirometry, ar terial blood gases, and exercise evaluation. A standard 6- or 12-min walk, cycle or tread mill testing can be used; the ventilatory limit to exercise can be estimated from the FEV,. The presence of exercise arterial desaturation should be evaluated by exercise oximetry or exercise blood gases since patients with exer cise desaturation should receive oxygen dur ing exercise if it increases exercise capacity (see O* therapy). On the basis of these data, a prescription for the tolerable level of exer cise can be formulated. The type(s) of physi cal rehabilitation program and adjunctive therapy must be individualized to each pa tient. For some patients, there may be some psychosocial and motivational advantages to group programs. The program should be ini tiated under medical supervision. Periodic as sessment of the benefits or side effects of the program is required. Improved general fitness frequently results in improved exercise toler ance. In general, physical activity should be encouraged for patients with COPD. Whether additional benefit is derived from formal ex ercise programs is uncertain and unproved. III. Comments of Rehabilitation A. Exercise Reconditioning Exercise training to improve performance in COPD patients, using methods similar to those used to improve athletic performance, was suggested in 1951 (3) and demonstrated to be effective in 1964 (4). A recent review of the numerous studies of exercise recondi tioning in COPD summarizes the potential benefits (table 1) (5). The type of exercise (stair climbing, walk ing, treadmill or bicycle ergometer) appears to be unimportant and is best determined by patient preference and cost. Although the in tensity of exercise is usually determined by patient tolerance, the minimal duration and frequency required to improve performance appears to be 20 to 30 min, 3 to 5 times per wk. Leg exercise is usually better tolerated than arm exercise. Due to ventilatory limita tion, the level of exercise tolerated by most patients will not increase cardiovascular fit ness. Many patients are not suitable candi dates for exercise training because of faradvanced lung disease, advanced age, lack of motivation, and associated diseases. The ef fects of exercise conditioning disappear rap idly with cessation of exercise. R Inspiratory Muscle TYaining Measures to specifically increase the strength and endurance of respiratory muscles have received recent attention as a potential part of a physical rehabilitation program for pa tients with COPD (6-9). The efficacy of this therapy is unproved and its role is unknown at present. The physiologic basis for the improved per formance associated with either exercise reconditioning or inspiratory muscle training is not fully understood. Major factors in volved appear to be improved aerobic capac ity, increased motivation, desensitization to the sensation of dyspnea, improved muscle 240 AMERICAN THORACIC A ft, u r it v w s g fu a u v r, -..if,li) "i TABLE 1 BENEFITS OF EXERCISE RECONDITIONING____________________ ACCEPTED BENEFITS increased endurance and exercise toierance. Increased maximal oxygen consumption (generally small). Increased skill in performance o< a task with decreased ventilation oxygen consumption, heart rate. UNLIKELY OR UNKNOWN BENEFITS Improved survival. Improved pulmonary function tests. Lowered pulmonary artery pressure. Improved arterial blood gases, improved blood lipids. Change in muscle 0, extraction. Change in sleep desaturation or apnea. ' vided at lower cost to greater numbers of smokers (22-24). The efficacy ofhypnosis neither been proved nor disproved. Controlled clinical trials have not demonstrated acupune. ture to be an effective strategy (25). The prompt benefits of smoking cessation for patients with chronic obstructive pulmo nary disease are reduction of cough and sputurn production. Ultimately, a decrease in the rate of decline of the FEV, may be seen (21). Additional major clinical benefits include a reduction in the risk of cardiovascular mor tality and in the risk of cancers of the lung, larynx, mouth, esophagus, and bladder (26). Smoking cessation should be of highest pri. ority in the comprehensive care of patieou with COPD. function, and improved technique of perfor mance (6, 8, 9, 12). In addition to physical conditioning, sev eral forms of adjunctive therapy may improve exercise performance in some patients. Those generally accepted to be beneficial include ox ygen, beta-2 bronchodilators, and theophyl line. As yet unproved modalities include pul monary vasodilators, nutritional manipula tion, and improved psychosocial health. C. Breathing Retraining Breathing retraining consists of teaching pa tients to utilize pursed-lip breathing, expira tory abdominal augmentation, synchroniza tion of movement of abdomen and thorax, and relaxation techniques for the accessory respiratory muscles, as well as psychologi cal assurance and education about COPD. Breathing retraining appears to allow patients to recover more rapidly from dyspnea induced by exercise. Such training is a useful compo nent of a comprehensive care program for pa tients with COPD. D. Energy Conservation A standard aspect of physical medicine and rehabilitation is instruction in work simplifi cation and the use of energy conservation devices to allow disabled patients more inde pendence and greater participation in activi ties of daily living (13). Such instruction, par ticularly in patients with advanced COPD, may result in similar benefits (14). E Nutrition Advanced COPD is frequently associated with loss of weight and muscle mass. This may pro duce respiratory muscle weakness and fur ther limit ventilatory capacity. Patients need to maintain sufficient protein/calorie intake to prevent malnutrition. Frequent small feed ings or use of liquid formula diets may help. Enteral or parenteral hyperalimentation has been attempted to restore muscle mass in mal nourished COPD patients but the efficacy of such therapy is unknown at present. There is a recognized hazard in administering high ' carbohydrate loads, which may result in in creased COj production, requiring increased ventilation (15), although the clinical impor tance of this is uncertain. F. Smoking Cessation Cigarette smoking affects lung structure and function in the following ways: increased mu cous secretion due to mucous gland hyper trophy and hyperplasia leads to increased cough and sputum production; small airways demonstrate a spectrum of abnormalities from mild inflammation to airway closure; lung parenchymal changes vary from a sim ple increase in inflammatory cells to destruc tion of alveolar walls which results in centrilobular emphysema (16-18). A significant functional impairment is identified in 10 to 15% of smokers, and is best identified by changes in FEV,. In non smoking adults, FEV, declines at the rate of approximately 20 to 30 ml per year. In those smokers who develop significant impairment, the rate of decline is 50 to 100 ml per year (19-21). The profoundly adverse pulmonary effects of cigarette smoking demand that smoking cessation efforts be implemented by all who care for patients with chronic obstructive pul monary disease. Physicians should assume major responsibility in this regard. Motivational factors governing smoking behavior vary. There is evidence that strongly suggests that smoking is an addictive behavior due, in large part, to nicotine. Successful smoking cessation programs are those that address the biologic, behavioral, and psychological forces responsible for smoking as specifically as possible for each individual patient. Cessation programs in clude education and counseling by the physi cian or other trained personnel, and a variety of other techniques, including provision of self-help materials, group or individual be havior modification programs, pharmaco logic management using nicotine polacrilex to minimize nicotine withdrawal, adversive conditioning using rapid cigarette smoking, hypnosis, and acupuncture. Current data indicate that 20 to 30% of those enrolling in a "successful" smoking ces sation program will not have resumed smok ing at the end of 1 yr. Using this criterion, the efficacy of counseling and nicotine pola crilex, and of adversive conditioning, have been proved. Self-help programs result in somewhat lower quit rates, but can be pro- G. Psychosocial Management Patients with chronic obstructive pulmonary disease frequently suffer from anxiety, depres sion, and problems related to cognitive, per ceptual, and motor activity. Limitations of financial and social resources are common place. Comprehensive care requires that at tention be given to the psychosocial as wdl as the physiologic problems of patients with COPD. The medical history, specific psy chosocial interviews, questionnaires, and for mal testing may be used to develop a thor- , ough psychosocial assessment Problems 3 should be identified by evaluation of the pa tient's social, cultural, ethnic, and educational background. Employment history, current financial resources, and family and commu nity support should be identified. In addi tion, the patient's personality, psychosexua! concerns, significant life events, previous and current lifestyle, and level ofdisability should be assessed (27, 28). . Individuals responsible for the psychoso cial evaluation may include the primary phy sician, pulmonary consultant, nurses, ther apists, and chaplains. Fbrmal rehabilitatioo programs frequently use psychologists, soda) workers, and psychiatrists in performing the psychosocial evaluation. Effective psychosocial interventions indude education, counseling, and supervised exer cise and supportive therapy provided by the medical staff, family, and groups of similarly afflicted patients. Motivation and the devel opment of realistic goals are emphasized. Other aspects of a psychosocial, intervention program include community referral, voca tional counseling, psychiatric consultation, and the use of anti-anxiety and/or anb- depressive medications (29, 30). -- Psychosocial interventions provide thepa tient with improved understanding of tb* physiologic factors responsible for symptom*. 3 and aid in coping with dyspnea, stress, *"* r ety, and depression. The patient and famflf J are helped in identifying and using avail*!* community, social, financial, and health resources. Successful psychosocial m****** ment helps the patient accept physiologic 1* tations, optimize strengths, and clarify**' sonable goals and priorities. Such intev tion allows the patient to participate^ ? 00XJ# WOACIC SOCIETY 241 lively and effectively in a therapeutic pro der the direction of: (a) visiting nurse associ when psychosocial approaches are used ation, community nursing or public health Actively, the patient is provided with a sense agency, (b) proprietary nursing agency, or (c) ss- -at | SUlffloJf. efcontrol and mastery of his disease, and his ^ality of life is enhanced. j0 summarize, physical rehabilitation is an important component of a comprehensive are program for patients with COPD. In many patients, activity level can be improved or maintained, resulting in both physical and psychologic benefits. Programs must be in durable medical equipment companies. B. Patient Selection Selection of patients and authorization for home health care is the responsibility of the treating physician based on medical evalua tion and information obtained by nurses, so cial workers, and other members of the health r raor- dividualized to the needs and capabilities of each patient. Investigation is needed in iden tifying and assessing specific exercise-limiting factors in patients with COPD and determin ing the optimal therapy for each factor. This would allow more appropriate prescription care team. Referral to an organized home health program is necessary for patients when there is doubt that the medical care program can be carried out in the home because of lack of knowledge, motivation, or adequate family caregivers, or because of the severity ofphysical rehabilitation techniques and other of illness. Any patient requiring additional adjunctive therapy for the individual patient. teaching or support should be considered as a candidate for home care. Examples of the usaalj IV. Home Care Home care refers to health services that are provided to individuals and families in their place of residence for the purpose of promot ing, maintaining, or restoring health, or minimizing the effects of illness and disabil ity. Services appropriate to the needs of the individual patient and family are planned, coordinated, and made available by an agency or institution, and organized for the delivery of health care through the use of employed staff, contractual arrangements, or a combi nation of administrative patterns. Home care encompasses components including but not limited to, medical care, dental care, nursing, respiratory care, physical therapy, speech ther apy, occupational therapy, social work, nutri tion, homemaker, home health aide, trans portation, laboratory services, medical equip ment and supplies (31). The goals of home care are to: (I) improve the quality of life by allowing those patients with advanced disease to remain in their own spectrum of home health needs include: (/) patients who require only periodic outpatient medical supervision; (2) patients who require the assistance of home health aides and/or homemakers and infrequent or no profes sional visits; (3) patients newly diagnosed or newly educated in a comprehensive care pro gram who require visits for 2 to 4 wk to rein force details and to help with adapting fam ily caregivers and the home environment to the patient's needs. Generally, 1 or 2 visits per wk are sufficient; (4) patients with repeated hospitalizations who need regular supervision for an indefinite period to prevent clinical de terioration and repeated hospitalizations. The number of required visits depends on the com plexity of the treatment program -- from 1 to 2 times per month to several times per wk; and (5) patients with complex treatment pro grams, such as home ventilator care. The num ber of visits required depends on the skill of the patient and family caregivers. The need may last for the rest of the patient's life. environment and be with family and friends; (3) minimize or prevent complications that would require hospitalization; (3) detect C Types of Services Provided in the Home A position paper developed by the American changes in physical and psychosocial status Lung Association describes the essential com that indicate the need for changes in manage ment; (4) provide treatment for the patient's primary diagnosis and foster adherence to the therapeutic program; and (5) foster a posi ponents of a home care program (36). These include evaluation, education, observation, sexual counseling, consultation, psychosocial support, monitoring of respiratory equip tive and independent attitude. ment, direct patient care, and household help. A small number of studies document the Not all services are required by all patients benefits of home health care (32^34), but more and the types of services required by patients work needs to be done to confirm that con with COPD must be individualized. Dupli tinuing care at home will, in fact, decrease cation of services is both unnecessary and ex hospital admissions and iength of hospital pensive. Although home care is most com stay, and reduce overall cost of care. monly instituted upon hospital discharge, such care may be initiated in the absence of 4. Qualifications ofthe Home Care Provider a hospital admission, in hospitalized patients, The skills required of the home health care the plan of care should be determined and team are outlined in a position paper by the communicated to the home care team prior ATS (33). In addition, if durable medical to discharge to assure a smooth transition ^uipment is required, the vendor should pro from hospital to home. The physician, nurs vide 24-h coverage by a respiratory care prac- ing staff, and other allied health professionals t'tioner, rapid response to correct problems need to work collaboratively to develop a ' of equipment malfunction, and adequate feasible plan of care. The discharge planner, back-up equipment. generally a nurse or social worker, needs to The home care programs may be: (7) be aware of the patient early in the hospital hospital.based, or (2) community-based, un course. Equipment requirements need to be assessed before discharge and, preferably, the hospitalized patient should be able to see and use the equipment that will be available in the home. The process of discharge planning should begin at the time of admission (37). A care plan needs to be developed for each patient. The standards for nursing care out lined by the ATS Section on Nursing (38) and guidelines developed by the California Tho racic Society Nursing Section (39) may be used along with standards of home care outlined by the American Association for Respiratory Care (40) as a basis for the development of this plan. V. Home Mechanical Ventilation Because the care of ventilator-assisted patients in the hospital setting is extremely expensive, there is great interest in identifying those ventilator-assisted patients who can be man aged safely in the home. At present, the prin cipal role for mechanical ventilation in the home is in the management of patients with ventilatory failure due to neuromuscular dis ease. Patients with severe chronic obstructive pulmonary disease are rarely suitable candi dates for mechanical ventilation at home be cause of complicating and frequently unsta ble medical problems that create such strin gent demands upon caregivers' therapy, thus making management in the home unsafe and impractical. However, a select and undoubt edly very small group of patients with severe, stable chronic obstructive pulmonary disease who are unable to maintain adequate pulmo nary gas exchange on their own may be can didates for mechanical ventilation at home. They consist of an unknown number of pa tients with severe chronic obstructive pulmo nary disease who are hospitalized for acute respiratory failure, placed on mechanical ven tilation, and, who despite stabilization of their condition, cannot be weaned from total ven tilator support. It has been noted that intan gible factors such as familiar surroundings and the attention of friends and loved ones may, when coupled with respiratory muscle rest, result in increasing independence from the ventilator in some patients who could not be weaned in the hospital setting despite exhaustive attempts by skilled physicians, nurses, and respiratory therapists. The poten tial for ventilator dependency should be rec ognized and, when appropriate, patients with severe obstructive lung disease should be in formed of the possibility of permanent ven tilator dependency prior to initiating mechan ical ventilation in the hospital setting. In addition, an as yet poorly defined sub set of these ventilator-assisted patients with chronic obstructive pulmonary disease may suffer from respiratory muscle fatigue due to abnormal resistive loads, muscle weakness and, in part, to mechanical disadvantage and shortening of the diaphragm due to pulmo nary overinflation (41). When total inter mittent ventilator support is discontinued, these patients may experience increasing dysp nea, hypercapnia, and hypoxemia. The quality oflife and physical well-being of such patients 242 AUERICAN THORACIC SOC*^ AV nay be improved with intermittent mechanical entilatory support (42, 43). In this group, entilation is usually provided at night with a negative pressure ventilator. Insufficient data exist with regard to the benefit of this form of partial ventilator support, and, at present, it should be considered investigational. Several reports have formulated criteria for patient selection, established guidelines for home ventilator management, and demon strated that ventilator-assisted patients can be managed safely in the home (44-51); however, there have been no large-scale, controlled clin ical trials to evaluate the health and/or eco nomic benefits and risks of such management. A. Patient Selection Consideration of mechanical ventilation in the home setting is indicated when a compe tent respiratory care team is unable to wean a patient with COPD from total ventilator support after several attempts over a period of weeks. The patient's health status must be stable such that no major therapeutic or di agnostic interventions are contemplated within a 30-day period of discharge from the hospital. The patient should maintain an ar terial oxygen tension of greater than 60 mm Hg with an inspired oxygen concentration of less than 40%. The patient should not dem onstrate wide fluctuations in arterial oxygen or carbon dioxide tensions. The patient should have an active cough and gag reflex, and should not require frequent endotracheal suc tioning. A secure tracheostomy tube should be present, except in those patients managed with a negative pressure ventilator. The pa tient should be free of active infection, and should not be subject to frequent or recur rent infections. Any comorbid medical con ditions should be stable, and should not re quire frequent therapeutic interventions. The candidate for mechanical ventilation in the home should express a desire to be discharged to home on a ventilator, and a willingness to cooperate with the respiratory care team in order to acquire the information and skills required of a ventilator-dependent patient at home. Care of a ventilator-assisted patient in the home often creates significant physical and emotional stress for the patient, family, and caregivers. Patients and their caregivers must be fully aware of this potential prior to deciding to participate in a home ventilator program. A psychosocial evaluation should confirm that the patient and caregivers are aware of and understand the demands and stresses associated with maintaining a ven tilator-dependent patient in the home, and that coping resources are adequate to meet these demands (52). 8. Caregivers Within the circle of family and friends, , caregivers must be identified who are avail able and express the willingness and physical, emotional, and cognitive ability to provide care. A support network of family, friends, and neighbors should be available to provide additional assistance when needed. Individ uals identified as caregivers must demonstrate a commitment to participate in an educational program, and devote sufficient time and energy to develop, utilize, and demonstrate the skills necessary to care for a ventilatorassisted patient at home. Caregivers must learn, master, and dem onstrate those skills that will enable them to provide total patient care. The skills required include the ability to: (I) administer medica tions in a correct and timely manner and familiarity with the actions of and side ef fects of such medications; (2) assemble and disassemble ventilator circuits; (3) adjust ven tilator settings and alarms; (4) clean, main tain, and troubleshoot equipment; (5) use a hand resuscitator; (6) administer breathing treatments; (7) continue weaning efforts; (8) administer supplemental oxygen when neces sary; (P) set up, use, and clean suction ap paratus; (10) perform tracheostomy care and suctioning; (11) clean, change, and plug tra cheostomy tubes when indicated; (12) main tain proper tracheostomy cuffinflation when applicable; (13) provide clapping, vibration, and postural drainage as well as cough as sistance; (/4) position patients correctly and assist with transfers, strengthening and range of motion exercises; (15) understand and in struct in energy conservation techniques; (16) measure vital signs and recognize changes in vital signs and other signs and symptoms of respiratory distress; (17) recognize signs and symptoms of respiratory infection; (18) per form proper skin care; (19) feed the patient or administer enteral feedings if necessary; (20) perform required bladder and bowel care; (21) communicate effectively with the patient; (22) contact the local emergency systems; and (23) perform cardiopulmonary resuscitation. C Resources A suitable and safe home environment with sufficient space and appropriate hygienic and electrical requirements is necessary. Doorways and halls must permit access and mobility of the patient and equipment. Required resources include a primary phy sician, medical and pharmaceutical suppliers, home health agencies, an emergency trans port system, and a reasonably proximate hos pital and emergency room. Sufficient finan cial resources to cover the total costs of environmental modification, equipment, sup plies, and paid caregivers must be available. Prior to beginning the process of patient and caregiver education, administrative ap proval for home management of a ventilatorassisted patient must be obtained from thirdparty providers. The physical home environ ment and availability of required resources must be evaluated by members of the respi ratory care team, and plans for modifications in doorways, electrical outlets, hygiene facil ities, and access must be made as necessary. D. Planning /or Discharge The process of transferring a ventilatorassisted patient with chronic obstructive pul* monary disease from the hospital to botne requires the involvement and cooperation of an experienced respiratory care team, work, ing with community health agencies, dur*.' ble medical equipment suppliers, state and local agencies including the phone company utility companies, fire department, and em! gency medical services. Although the program for discharging a ventilator-assisted patient to home should be structured and the team experienced, the specific educational routine and plans for each patient must be individu alized and tailored to the patient's unique needs. - During the process of preparing the patient for discharge, the full resources of the respi ratory care team must be devoted to an ongo ing process of rehabilitation in which thepj. tient's potential for independence in activi ties of daily living are maximized. Ideally, patients will be able to breathe independently for periods throughout the day. In practice, the degree of ventilator dependence ranges from ventilatory support 24 h a day to a re quirement for nighttime ventilation only. ,: The respiratory care team leader may be a pulmonary nurse specialist, discharge coor dinator, or qualified respiratory therapisC This individual should coordinate the activi ties of the team and meet with the patient members of the team, and home caregivers to establish specific goals, develop training schedules, and insure that supply and equip ment needs are met. Team conferences to evaluate and accept potential candidates,^* plan the treatment program, and to measure progress are required. Documentation of training activities and patient progress Is es sential. A physician must be willing to accept responsibility for overall supervision and peri odic follow-up care of the patient, and should approve all plans for medications, ventilaux care, and nursing care. The physician should periodically assess the need for continued >tatilator assistance. The physician should,be willing to make home visits if necessary. If office visits occur, appropriate transportation must be prearranged. The members of the respiratory care team possess a variety of skills. Where resources vary, there may be overlapping functions of health care personnel. The skills of the fol lowing personnel may be required depending on individual patient needs: (1) primary phy* sician, (2) nurse, (3) respiratory therapist, (4) physical therapist, (3) occupational therapist* (6) social service worker, (7) psychologist/ psychiatrist, (8) durable medical equipment vendor, and (9) home health agency. 'T.cPrior to discharge, the patient and care* givers may make several briefexcursions out* side the hospital, perhaps spending sometime at home. At the completion of a trainingP*o* gram, the caregivers must have demonsp***". competencies in all required care of thep*T tient to the satisfaction of the respiratory? team. A checklist should document the/jj* onstration of required abilities and the 5S ability of necessary equipment and resou^5 Prior to discharge of the patient, reoui** I ; jjfffQCAM THOSACJC SOCIETY 243 equipment and supplies must be delivered to the home. Respiratory care and nursing personnel will accompany the patient home, and make fre quent home visits during the first 1 to 2 wk following discharge. Thereafter, the attend ing physician and respiratory care team will periodically evaluate the patient to determine if modifications of the medical, nursing, or ventilator program are necessary. References 1. American Thoracic Society. Pulmonary Re habilitation. Am Rev Respir Dis 1981; 124:663-6. 1 Lake J, Mahler D, Man P. Wiedemann H, Matthay R. Exercise impairment in chronic obstruc tive pulmonary disease Clinics in Chest Medicine 1984; 5:121-43. y Barach A. Bickerman H. Beck G. Advances in the treatment of nontuberculous pulmonary dis ease. Bull NY Acad Med 1952; 28:353-84. 4. Pierce A. Taylor H, Archer R, Miller W. Re sponses to exercise training in patients with em physema. Arch Intern Med 1964; 113:28-36. 5. Hughes RL, Davison R. Limitations of exer cise reconditioning in COPD. Chest 1983; 83:241-9. 6. Leith D, Bradley M. Ventilatory muscle strength and endurance training. J Appl Physiol 1976; 41:508-16. 7. Peress L. McClean P, Woolf C, Zamel N. Re spiratory muscle training in severe chronic obstruc tive pulmonary disease. Am Rev Respir Dis 1979; H9(Suppl:l57). 8. Belman MJ. Mittman C, Weir R. Ventilatory muscle training improves exercise capacity in chronic obstructive pulmonary disease patients. Am Rev Respir Dis 1980; 121:273-80. 9. Pardy R, Rivington R, Despas P, Macklem P. The effects of inspiratory muscle training on exer cise performance in chronic airflow limitation. Am Rev Respir Dis 1981; 123:426-33. 10. Sonne L, Davis J. Increased exercise perfor mance in patients with severe COPD following in spiratory resistive training. Chest 1981; 79:393-8. H. Chen H, Dukes R, Martin B. Inspiratory train ing in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1985; 131:251-5. 12. Belman M, Wasserman K. Exercise training and testing in patients with chronic obstructive pul monary disease Basics of R.D. 1981; 10:1-6. 13. Leslie L. Training for functional independence, in: Krusen's handbook of physical medicine and rehabilitation. Philadelphia: W. & Saunders, 1982; 501-7. 14. Falconer J. Pulmonary rehabilitation. In: Adult rehabilitation: a team approach fortherapists. Boston: Little, Brown, 1982; 199-223. 15. Askanazi J, Nordenstrom J, Rosenbaum SH, al. Nutrition for the patient with respiratory fail ure. Anesthesia 1981; 54:373-7. If U.S. Department of Health and Human Serv*c> Public Health Service. The health conse quences of smoking--chronic obstructive pulmo*ry disease--a report of the Surgeon General. Washington, D.C.: US. Government Printing Of fice. 1984 (DHEW Publication No. (PHS) *4-50205). American Thoracic Society. Cigarette smok"8 and health. Am Rev Respir Dis 1985; 132: 1133-6. !*- JanoffA. Biochemical links between cigarette "coking and pulmonary emphysema. J Appl Phys iol: Respir Environ Exercise Physiol 1983; 55(2):285-93. 19. Burrows B, Knudson RJ, Cline MG, Lebowitz MD. Quantitative relationships between cigarette smoking and ventilatory function. Am Rev Respir Dis 1977; 115:195-205. 20. Clement J, Van de Woestijne KP. Rapidly decreasing forced expiratory volume in one second or vital capacity and development of chronic air flow obstruction. Am Rev Respir Dis 1982; 125:553-8. 21. Buist AS, Sexton Gl, Nagy JM, Ross BB. The effect of smoking cessation and modification on lung function. Am Rev Respir Dis 1976; 114:115-22. 22. Davis AL, Faust R, Ordentlich M. Self-help smoking cessation and maintenance programs: a comparative study with 12-month followup by the American Lung Association. Am J Public Health 1984; 74:1212-7. . 23. Jarvis MJ, RawM, RussellMAH, Feyerabend C. Randomized controlled trial of nicotine chew ing gum. Br Med J 1982; 285:537-40. 24. HalIRG, Hall SM, Sachs DPL, Benowitz NL. Two-year efficacy and safety of rapid smoking ther apy in patients with cardiac and pulmonary dis ease J Consulting Clin Physiol 1984; 52:574-81. 25. Lamontage Y, Annable L, Gagnon M. Acu puncture for smokers; lack oflong-term therapeu tic effect in a controlled study. CMA J 1980; 122: 787-90. 26. Schuman LM. The benefits of cessation of smoking. Chest 1971; 59:421-7. 27. Kim HT, Knecht PA, Hiscox DE, Glaser ED. Psychosocial factors and pulmonary patients. In: Hodgkin JE, Zorn EG, Connors GL, eds. Pulmo nary rehabilitation--guidelines to success. Boston: Butterworth, 1984; 207-38. 28. Dudley DM, Glaser EM, Jorgenson BN, Lo gan DL. Psychosocial concomitants to rehabilita tion in chronic obstructive pulmonary disease 1. Psychosocial and psychological considerations. Chest 1980; 77:413-20. 29. Dudley DM, Glaser EM, Jorgenson BN, Lo gan DL. Psychosocial concomitants to rehabilita tion in chronic obstructive pulmonary disease II. Psychosocial treatment. Chest 1980; 77:544-51. 30. Dudley DM, Glaser EM, Jorgenson BN, Lo gan DL. Psychosocial concomitants to rehabilita tion in chronic obstructive pulmonary disease III. Dealing with psychiatric disease (as distinguished from psychosocial or psychophysiologic problems). Chest 1980; 77:677-84. 31. Statement of Assembly of Outpatient and Home Care Institutions, AHA; Council of Home Health Agencies and Community Health Services, NLN; National Association ofHome Health Agen cies; National Council for Homemaker-Home Health Aide Services, Inc NLN:1973. 32. Chemiack RM, Hadord RG, Svanhill E. Horae care of chronic respiratory disease. JAMA 1969; 208:821-4. 33. South Hills Health System; Home Health Agency Public Health Service Grant 03-H-001:327373 Final Report, December 1981 (unpublished paper). 34. Loma Linda University Medical Center. Tes timony before the committee on labor and human resources. United States Senate, March4,1981, AAR Times. 35. American Thoradc Society. Skills of the health team involved in out-of-hospital care for patients with COPD. Am Rev Respir Dis 1986; 133:948-9. 36. American Lung Association. Home Health Cart ALA, 1740 Broadway, New York. NY 10019 (unpublished paper). 37. Ameth LM, Mamon S. Determining patient needs after discharge Nursing Management 1985; 16:20-4. 38. American Thoradc Society Section on Nurs ing. Standards ofcare for patients with COPD. ATS News 1981; 7:31-8. 39. California Thoracic Society. Guidelines for nursing care of the pulmonary patient, 1984 (un published paper). 40. American Association of Respiratory Care. Standards for respiratory home care An official statement by the American Association of Respi ratory Care 1979 (unpublished paper). 41. Rochester DF, Braun NMT. Determinants of maximal inspiratory pressure in chronic obstruc tive pulmonary disease Am Rev Respir Dis 1985; 132:42-7. 42. Rochester DF, Braun NMT, Laine S Diaphrag matic energy expenditure in chronic respiratory fail ure Am J Med 1977; 63:223-32. 43. Garay SM, Tbrino GM, Goldring RM. Sus tained reversal of chronic hypercapnia in patients with alveolar hypoventilation syndromes. Am J Med 1981; 70269-74. 44. Feldman J, Tbteur PG. Mechanical ventila tion: from hospital intensive care to home Heart Lung 1982; 11:162-5. 45. Roselle S, D'Amico FJ. The effect of home respiratory therapy on hospital readmission rates of patients with chronic obstructive pulmonary dis ease Respir Care 1982; 27:1194-9. 46. Fischer DA, Prentice WS. Feasibility of home care for certain respiratory-dependent restrictive or obstructive lung disease patients. Chest 1982; 82:739-43. 47. Sivak ED, Cordasco EM, Gipson WT. Pul monary mechanical ventilation at home: a reason able and less expensive alternative Respir Care 1983; 28:42-9. 48. Splaingard ML, Frates RC, Harrison GM. et al. Home positive-pressure ventilation: twenty years' experience. Chest 1983; 84:376-82. 49. Gilmartin M, Make B. Home care of the ventilator-dependent person. Respir Care 1983; 28:1490-7. 50. Make B, Gilmartin M, Brody JS Snider GL. Rehabilitation of ventilator-dependentsubjects with lung diseases. Chest 1984; 86:358-65. 51. Hughes RL. Home is the patient. Chest 1984; 86:344-5. 52. Committee of Respiratory Care Section ofthe American College ofChest Physicians. Guidelines for the care of ventilator-assisted individuals in the homeand at alternate community sites. Chest 1986; 90(Suppl:lS-37S). This statement was developed by a Task Group appointed by the ATS Scientific Assembly on Clinical Problems. Members of the Task Group were: David R. Dantzeer, M.D., Chairman Susan K. Pinoleton, M.D., Chairman-- Scientific Assembly on Clinical Problems Chronic Obstructive Airways Diseases John A. Pierce, M.D., Chairman Dennis E. Niewoehner, M.D. William M. Thurlbeck, M.D. A. Sonia Buist, M.D. 744 Asthma .rd S. Kkonenberg, M.D., Chairman Daniel J. Stechscjtultb, M.D. Jeffrey M. Drazbn, M.D. Pharmacologic Therapy Ronald B. George, M.D., Chairman Irwtn Ziment, M.D. Joseph H. Bates, M.D. Respiratory Care Alan L. Plummer, M.D., Chairman David J. Pierson, M.D. Walter J. O'Donohue, M.D. Oxygen Therapy Nicholas R. Anthonisen, M.D., Chairman A. Jay Block, M.D. Paul Kvale, M.D. Thomas L. Petty, M.D. AMERICAN THORACIC SOCJETT Home Care and Rehabilitation Gerald R. Kerby, M.D., Chairman Philip M. Gold, M.D,' Mary E. Gilmartin NOTICES ADVANCES IN SECTIONAL IMAGING e Department of Radiology, University of California, San Diego .nool of Medicine is presenting the following postgraduate course: "Advances in Sectional Imaging," September 10-12, 1987, at the U.S. Grant Hotel, San Diego, California. The Program Director is Robert F. Mattrey, M.D. The guest faculty includes Matthew D. Rifkin, M.D.; Thomas Jefferson University Hospital, Philadelphia, Pennsylvania; and Elias A. Zerhouni, M.D.; Johns Hopkins, Balti more, Maryland. The faculty from the University of California, San Diego School of Medicine is Giovanna Casola, M.D.; Robert Edelman, M.D.; John Forsythe, R.D.M.S.; Paul J. Friedman, M.D.; Barbara B. Gosink, M.D.; John R. Hesselink, M.D.; George R. Leopold, M.D.; Robert F. Mattrey, M.D.; Thomas R. Nelson, Ph.D.; Dolores H. Pretorius, M.D.; David J. Sartoris, M.D.; and Eric van Sonnenberg, M.D. The registration fee for the course is $375.00 for physicians and $275.00 for residents, fellows, or technologists. The course is accredited for 14 hours in Category I. To receive more information, please contact: Dawne Ryals, Ryals & Associates, P.O. Box 920113, Norcross, GA 30092-0113; (404) 641-9773. BOARD REVIEW IN CRITICAL CARE MEDICINE Board Review in Critical Care Medicine (ACLS Option). October 7-11,1987 - Portland, Oregon. School of Medicine, Oregon Health Sciences University, CME-GH., OHSU, Portland, OR 97201; (503) 225-8700. CARDIOPULMONARY UPDATE '87 The Heart & Lung Institute at St. Vincent's Medical Center in Jack sonville, Florida will hold a seminar at the Marriott at Sawgrass, Pome Vedra Beach, Florida on current topics of interest to the pul monologist, cardiologist, oncologist, and internal medical physi cian. The registration fee is $225.00, payable by Sept. 10,1987. For further information, please contact: Alberta Hipps, Adm. Direc-. tor, Heart & Lung Institute, P.O. Box 2982, Jacksonville, FL 32203;; phone: (904) 387-7563. V 12th INTERNATIONAL CONFERENCE ON LUNG SOUNDS ' The 12th International Conference on Lung Sounds will be held ; in Paris, France at the Institut D'Electronique FondamentaJe, Wed nesday through Friday, September 16-18, 1987. Call forabstracts: Papers for presentation during the Conference will be selected by the Program Committee. Abstracts should not exceed 200 words in length and should besubmitted by July 1,1987. Notifications of acceptance will be mailed out by July 15, 1987. Abstracts may relate to any aspect of lung sounds; examples are studies of mechanisms of production, clinical implications, physio logical correlations, methods for recording, analysis or representa tion. ' . ! Registration: Registration fee is $100 per person. Checks should be made payable to: International Lung Sounds Association. "v;- Correspondence: All abstracts and questions regarding arrange- ments should be addressed to: " Robert G. Loudon, M.R, Ch.E '. University of Cincinnati Medical Center ' Pulmonary Disease Division j 231 Bethesda Ave. . Cincinnati, OH 45267-0564 i PRACTICAL SPIROMETRY COURSE * The course "Practical Spirometry" will be held August 19-20,1987, in Atlanta, Georgia and October 8-9,1987 in Chicago, Illinois. Spot*-' sored by: Mayo Pulmonary Services. For further information, please contact: Ginnie Allie, Mayo Pulmonary Services, 432 Plummer. Mayo Clinic, Rochester, MN 55905; or call toll free 1-800-533-1653^ (Minnesota residents, 1-800-562-1767). .-&