BREATHING DIFFICULTIES
| CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)—Andrew Ries, MD, MPH, Associate Dean for Academic
Affairs and Professor of Medicine and Family and Preventive Medicine, University of California, San Diego, School
of Medicine
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| Introduction: many complex mechanisms involved in airflow obstruction; several modalities available for treating
COPD, but Global Initiative for Chronic Obstructive Lung Disease (GOLD) guidelines most widely accepted
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| Epidemiology: COPD increasing cause of death and disability throughout world and now 4th leading cause of death in
United States
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| Contributing factors to COPD epidemic: cigarette smoking; people living longer (serious problems due to COPD
typically develop in people in their 60s, 70s, and 80s)
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| Demographics: COPD largely related to smoking; death rates in white and black men leveled off in recent years, but dramatically
increased among women; current incidence of COPD almost equal among men and women
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| Objectives of GOLD guidelines: increase awareness worldwide about COPD; improve diagnosis, treatment, and prevention;
stimulate research; recommendations—based on sources of evidence and subdivided into 4 classes; class A
recommendation (highest) supported by randomized clinical trials and “rich body of data”
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| Definition of COPD: disease characterized by airflow limitation; not fully reversible; airflow limitation usually progressive
and associated with abnormal inflammatory response of lung to noxious particles or gases
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| Burden of COPD: underestimated worldwide; typically begins when people start smoking; at least 50% of lung reserve
must be destroyed before symptoms develop (usually takes many years)
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| Components addressed in GOLD guidelines: 1) importance of assessing and monitoring disease; 2) reduction of
risk factors; 3) management of patients with stable lung disease; 4) management of exacerbations
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| Assessment and monitoring: spirometry gold standard (only way to make diagnosis); key measurements forced expiratory
volume in 1 sec (FEV1 ) and forced vital capacity (FVC)
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| Stages of severity: class 0—people at risk (particularly smokers), may have chronic symptoms (eg, cough, sputum), but
spirometry normal; class 1 (mild disease)—associated with FEV1 /FVC ratio <70% (ratio <70% diagnostic for COPD),
FEV1 >80% of predicted value, with or without symptoms; class 2 (moderate)—FEV1 50% to 80% of predicted value,
with or without symptoms; class 3 (severe)—FEV1 30% to 50% of predicted value; patient symptomatic; class 4 (very
severe)—FEV1 <30% of predicted value
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| Stepped approach to management: 1) avoidance of risk factors, smoking cessation, and vaccination against respiratory
infections; 2) use of short-term bronchodilators prn for patients with mild disease; 3) use of ≥1 longer-acting bronchodilators
for patients with moderate-to-severe disease; 4) rehabilitation for individuals with moderate-to-severe COPD; 5) inhaled corticosteroids
for patients with more severe disease or who begin experiencing frequent exacerbations; 6) O2 therapy for patients
with very severe disease (proven to prolong survival); surgical options for select group of people with severe emphysema
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| Screening: spirometry indicated for all patients with smoking history; only 20% to 30% of smokers eventually develop
significant COPD because of genetic differences
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| Smoking cessation: most effective and cost-effective intervention to reduce risk of developing COPD or to stop its progression;
basic strategies for cessation (5 As)—ask; advise (urge smokers to quit); assess willingness to quit; assist
people ready to quit; arrange for follow-up visits
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| Overall approach to management of stable COPD: depends on severity of disease (based on spirometry); health
education—advise patients that their disease progressing for many years before symptoms develop (first symptoms usually
precipitated by another medical problem); emphasize that existing medications not shown to modify long-term decline
of lung function and that currently, pharmacotherapy directed at controlling symptoms and reducing complications
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 | Bronchodilators: central to symptomatic management (evidence class A); give on prn basis for people with mild disease;
regular therapy indicated for those with more chronic and persistent symptoms; principal agents include selective β2 -agonists
(given by inhalation), anticholinergic agents, and (in some cases) theophylline and combination agents; regular treatment
with long-acting bronchodilators more effective; combining classes of bronchodilators better strategy overall;
patients with severe disease often on regular and long-acting drugs (eg, β2 -selective agent and anticholinergic)
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| Corticosteroids: results of various clinical trials variable; regular use with inhaled agents appropriate for symptomatic patients
with moderate to severe COPD with repeated exacerbations; avoid systemic oral steroids as routine management
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| Rehabilitation: includes exercise training; should include individually tailored multidisciplinary program involving various
health care providers
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| O2 administration: documented to improve survival in patients with significant hypoxemia
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| Management of specific stages: stage 0 (symptoms, but normal spirometry)—avoidance of risk factors; mild—prn
use of short-acting bronchodilators; moderate—consider adding ≥1 long-acting inhaled bronchodilators and starting
patient on rehabilitation program; severe—consider adding inhaled corticosteroid for exacerbations on regular basis;
very severe cases and chronic respiratory failure—treat complications; give O2 if appropriate, and consider surgical
options and referral to specialist
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| Exacerbations: educate patient about underlying causes (often infections) and appropriate treatment strategies; strategies
include high doses of bronchodilators and corticosteroids (for short period) and antibiotics
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| Patients with respiratory failure: initiate noninvasive positive pressure ventilation with bilevel positive airway pressure
(BiPAP) or continuous positive airway pressure (CPAP)
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| Questions and answers: components of pulmonary rehabilitation—education (key); instruction on respiratory physiotherapy
techniques and breathing retraining; dyspnea management; physical activity; dealing with psychologic, emotional, and
social aspects; need to worry about exacerbations in COPD patients on long and short-acting bronchodilators—
yes; they require more intensive therapies; efficacy of montelukast (Singulair) for treating COPD—data lacking to support
use
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| ASTHMA —Gerald W. Frank, MD, PhD, Associate Clinical Professor of Medicine, the David Geffen School of Medicine
at the University of California, Los Angeles
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| Epidemiology: asthma growing problem; nearly 20 million Americans asthmatic; death rate 3 per 10,000 cases; prevalence
and mortality rates higher in blacks than in other racial groups; among children, asthma accounts for 13 million
physician visits annually, is third leading cause of hospitalizations and most common chronic illness responsible for
school absenteeism; in Kaiser Hospital study in Portland, women asthmatics reported more symptoms, poorer quality of
life, and greater use of medications than men, although no differences in FEV1 between men and women
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| Definitions and concepts: Thoracic Society definition 50 yr ago—presence of widespread narrowing of airways that alters
in severity, either spontaneously or as result of therapy; classic paradigm—extrinsic asthma (usually childhood onset
with clear allergic history) vs intrinsic asthma (usually adult onset without clear allergic history); asthma essentially defined as
reversible bronchospasm; current concept—asthma is bronchospasm (potentially reversible within minutes with treatment)
with tenacious secretions and airway inflammation (not easily reversible)
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| Differential diagnosis: COPD—most patients have both chronic bronchitis and emphysema and smoking history; hypersensitivity
pneumonitis—Farmer’s lung prototype; chest x-ray typically shows pulmonary edema or (in advanced
cases) pulmonary fibrosis; vocal cord dysfunction syndrome—diagnosis made by examining vocal cords at time of attacks;
does not respond to normal asthma treatment
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| Asthma syndromes: occasional or mild intermittent asthma (usually precipitated by exposure to particular allergen);
persistent asthma; severe asthma; exercise-induced asthma; hyperreactive airway syndrome (presents as chronic cough);
occupational asthma; nocturnal asthma (manifestation of more severe asthma); allergic bronchopulmonary aspergillosis
(very severe form of asthma); allergic granulomatosis (Churg-Strauss disease; vasculitis affecting lungs); reactive airways
dysfunction syndrome (can follow toxic exposure)
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| Diagnosis: history—inquire about exposure to allergens and reactivity to aspirin and nonsteroidal anti-inflammatory drugs
(NSAIDs); ask about atopic symptoms, food allergies, skin allergies, family history of allergy, smoking history, rhinitis,
gastroesophageal reflux disease (GERD), relationship of workplace to asthma attacks, and exercise-induced asthma
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| Occupational asthma: usually response to animal or plant proteins, but can be response to organic chemicals (eg, isocyanates);
symptoms may have delayed onset (typically at home in evening), but should clear during vacations and weekends
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| Physical examination findings: wheezes (typically high pitched, worse on exhalation; in stridor, wheeze worse on inhalation);
prolonged exhalation; “quiet” lung (may be ominous sign of air movement insufficient to generate wheeze); features
of severe asthma—use of accessory muscles; confusion; somnolence; pulsus paradoxus; wheezing on
inhalation and exhalation
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| Chest x-ray: with asthma—hyperinflation, large lung volume, flattened diaphragm, and decreased vascular markings;
with allergic bronchopulmonary aspergillosis—mucoid impaction and “gloved-hand sign”
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| Pulmonary function: characterized by obstruction, decreased FEV1 /FVC ratio, reversibility (hallmark of asthma; FEV1
improves with inhaled bronchodilator), and airway hyperreactivity (FEV1 decreases in response to methacholine or
histamine test); comments—peak expiratory flow rate (PEFR) routinely varies with circadian rhythm (lower in morning
than in evening); circadian difference exaggerated in asthma
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| Pathophysiology: several inflammatory cells in lung (eg, eosinophils, mast cells, T lymphocytes) contribute to symptomatology;
these cells release histamine, leukotrienes, prostaglandins, tryptase, eosinophilic cationic proteins, and several cytokines;
symptomatology begins with bronchospasm, leading to hypoxia, thickening mucus, and other problems
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| National Institutes of Health (NIH) guidelines for managing asthma: mild intermittent asthma (stage 1)—
symptoms occur <2 times/wk, exacerbations brief, nighttime symptoms seldom occur, patients generally asymptomatic with
normal lung function between exacerbations; circadian variability in PEFR <20%; mild persistent asthma (stage 2)—
symptoms occur >2 times/wk, but not daily; exacerbations may begin to affect activity; nighttime symptoms occur >2 times/
mo; pulmonary function still within normal limits, but circadian variability abnormal; moderate persistent (stage 3)—
symptoms occur daily; exacerbations occur >2 times/wk; disease affects activity; nighttime symptoms occur at least 1 time/
wk, mild pulmonary obstruction present, and circadian variability of PEFR continues to widen; daily use of short-acting β-agonists;
severe persistent—symptoms continuous; exacerbations and nighttime symptoms frequent; activity limited; worsening
pulmonary function
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| Management: drugs used for treating asthma divided into relievers (act rapidly and treat acute episodes) and controllers
(act slowly and treat underlying predisposition that causes acute symptoms)
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| β-adrenergic agents: primary relievers; older nonspecific agents include epinephrine, isoproterenol, and isoetharine; specific
β2 agents include albuterol, terbutaline, metaproterenol, and pirbuterol; long-acting agents (controllers) include salmeterol
and formoterol; delivery systems—subcutaneous for epinephrine and terbutaline; oral for delayed-released
tablets (albuterol [Repetabs]); inhalation route for most newer agents (eg, nebulizers, metered-dose inhalers [MDIs],
powdered-delivery systems); comments—medium-droplet aerosol agents best; spacers maximize fraction of medium
droplets
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| Controllers: long-acting β2 agents—include salmeterol, salmeterol-fluticasone (Advair Diskus), and formoterol; leukotriene
antagonists—zileuton first agent developed (required bid dosing); newer agents include zafirlukast (Accolate)
and montelukast (given once daily)
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| Corticosteroids: most potent controlling agents; intravenous (IV) use—methylprednisolone can be given IV in hospital
setting for short period; oral agents—include prednisone and prednisolone; intramuscular (IM) use—triamcinolone
most popular agent; caution—patients on systemic steroids should be tapered to lowest dose as soon as possible; inhaled
corticosteroids—most effective way to control asthma without side effects; MDIs effective when used bid (not
for acute attacks); patients should rinse mouth after use; can use breath-activated powder delivery system for steroids,
eg, Advair; steroid toxicities
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| Mast cell inhibitors: effective for exercise-induced asthma; agents include cromolyn and nedocromil
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| Theophylline: good bronchodilator; 300 mg/day may be helpful
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| Antihistamines: out of favor for treating asthma because of drying effect; same applies for anticholinergics (eg, atropine,
ipratropium, tiotropium)
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| Controversial treatments: magnesium; macrolides; methotrexate; inhaled furosemide (Lasix); colchicine; gold; cyclosporine;
dapsone; immunoglobulins; none of these shown effective
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| Immunotherapy (desensitization): established therapy, but benefit not long lasting; omalizumab (Xolair)—now
available; anti-IgE antibody; indicated for patients poorly controlled on inhaled steroids; reduces exacerbations; given
subcutaneously every 2 to 4 wk
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| Adjunctive therapies: treat rhinitis or GERD if present; air purifiers and removal of molds (not evidence based)
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| National guidelines: mild intermittent asthma—provide patient education and give short-acting β-agonists; mild
persistent—give β-agonist (reliever) almost daily, and consider use of low-dose steroid MDI, leukotriene antagonist, or
theophylline; give mast-cell inhibitor if exercise-induced asthma present; moderate persistent—give inhaled β-agonist
prn, moderate-dose steroid MDI, long-acting β-agonist, and oral albuterol; severe persistent—give high-dose inhaled
steroids, long-acting β-agonist, and possibly oral corticosteroids
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Educational Objectives
| The goal of this program is to educate the listener about chronic obstructive pulmonary disease (COPD) and asthma. After
hearing and assimilating this program, the clinician will be better able to:
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| 1. Subdivide patients with COPD into mild, moderate, severe, and very severe categories.
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| 2. Provide a stepped approach to the management of COPD, beginning with smoking cessation and avoidance of risk
factors, and progressing to the use of bronchodilators, inhaled corticosteroids, O2 therapy, and even (in very severe
situations) surgery.
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| 3. Understand the etiology of asthma.
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| 4. Recognize that reversible bronchospasm and airway inflammation are key elements of asthma.
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| 5. Treat patients with mild intermittent, mild persistent, moderate persistent, and severe persistent asthma.
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Discussed on This Program
Albuterol (salbutamol sulphate in United Kingdom); [ AccuNeb, Proventil, Proventil HFA, Proventil Repetabs, Ventolin,
Ventolin HFA, Volmax]
Atropine sulfate (several trade names)
Colchicine
Cyclosporine (cyclosporin A) [Gengraf, Neoral, Sandimmune]
Dapsone (DDS) [Aczone]
Epinephrine (several trade names)
Fluticasone propionate [Cutivate, Flovent, Flonase]
Fluticasone propionate/salmeterol
[Advair Diskus]
Formoterol fumarate [Foradil Aerolizer]
Furosemide [Lasix]
Ipratropium bromide [Atrovent]
Isoetharine HCl
Isoproterenol HCl [Isuprel]
Metaproterenol sulfate [Alupent]
Methotrexate (amethopterin; MTX) [Methotrexate LPF, Rheumatrex Dose Pack, Trexall]
Methylprednisolone [Medrol]
Montelukast sodium [Singulair]
Omalizumab [Xolair]
Pirbuterol acetate [Maxair Inhaler, Maxair Autohaler]
Prednisolone (several trade names)
Prednisone (several trade names)
Salmeterol xinafoate [Serevent Diskus]
Terbutaline sulfate [Brethine]
Theophylline (several trade names)
Tiotropium bromide [Spiriva, Spiriva HandiHaler]
Triamcinolone (several trade names)
Zafirlukast [Accolate]
Zileuton [Zyflo]
Suggested Reading
Allen TW: Return to play following exercise-induced bronchoconstriction. Clin J Sport Med 15:421, 2005; Alvarez GG
et al: A systemic review of risk factors associated with near-fatal asthma. Can Respir J 12:265, 2005; Barr RG: Methylxanthines
for exacerbations of chronic obstructive pulmonary disease: metaanalysis of randomized trials. BMJ 327:643, 2003;
Barreiro TJ, Perillo I: An approach to interpreting spirometry. Am Fam Physician 69:1107, 2004; Blaiss MS: Asthma
disease management: a critical analysis. Ann Allergy Asthma Immunol 95(5 Suppl 1):S10, 2005; Brenes G: Anxiety and
chronic obstructive pulmonary disease: prevalence, impact, and treatment. Psychosom Med 65:963, 2003; Chavannes N et
al: Effects of physical activity in mild to moderate COPD: a systemic review. Br J Gen Pract 52:572, 2002; Courtney AU et
al: Childhood asthma: treatment update. Am Fam Physician 71:1959, 2005; Frazier SC: Implications of the GOLD Report
for chronic obstructive lung disease for the home care clinician. Home Health Nurse 23:109, 2005; Geddes EL et al: Inspiratory
muscle training in adults with chronic obstructive pulmonary disease: a systematic review. Respir Med 99:1440,
2005; Higgins JC: The “crashing asthmatic.” Am Fam Physician 67:997, 2003; Hilleman DE: New treatment options
for COPD. J Manag Care Pharm 11(6 Suppl A):S12, 2005; Holmes RL, Fadden CT: Evaluation of the patient with
chronic cough. Am Fam Physician 69:2159, 2004; Huggins JL: Allergen immunotherapy. Am Fam Physician 70:689,
2004; Hunter MH, King DE: COPD: Management of acute exacerbations and chronic stable disease. Am Fam Physician
64:603, 2001; Irani AM: The challenge of mild persistent asthma. Ann Allergy Asthma Immunol 94:517, 2005; Kemp
JP, Kemp JA: Management of asthma in children. Am Fam Physician 63:1341, 2001; Lomas DA: Chronic obstructive
pulmonary disease: introduction. Thorax 57:735, 2002; Mallin R: Smoking cessation: integration of behavioral and drug
therapies. Am Fam Physician 65:1107, 3002; Mintz M: Asthma update: Part I. Diagnosis, monitoring, and prevention of
disease progression. Am Fam Physician 70:893, 2004; Mintz M: Asthma update: Part II. Medical management. Am Fam
Physician. 70:1061, 2004; Monninkhof E et al: Self-management education for patients with chronic obstructive pulmonary
disease: a systematic review. Thorax 58:394, 2003; Murphy KR: Asthma: versatile treatment of a variable disease. J
Asthma 42:149, 2005; Ngoc PL et al: Cytokines, allergy, and asthma. Curr Opin Allergy Clin Immunol 5:161, 2005;
Petty TL: Benefits and barriers of the widespread use of spirometry. Curr Opin Pulm Med 11:115, 2005; Ram FS et al:
Noninvasive positive pressure ventilation for treatment of respiratory failure due to severe acute exacerbations of asthma. Cochrane
Database Syst Rev (1)CD004360, 2005; Sin DD et al: Contemporary management of chronic obstructive pulmonary
disease: scientific review. JAMA 290:2301, 2003; Somand H, Remington TL: Tiotropium: a bronchodilator for
chronic obstructive pulmonary disease. Ann Pharmacother 39:1467, 2005; Tovar JM, Gums JG: Monitoring pulmonary
function in asthma and COPD: point-of-care testing. Ann Pharmacother 38:126, 2004; Viegi G, Di Pede C: Chronic obstructive
lung diseases and occupational exposure. Curr Opin Allergy Clin Immunol 2:115, 2005; Walters JA et al: Oral
corticosteroids for stable chronic obstructive pulmonary disease. Cochrane Database Syst Rev (3)CD005374, 2005.
Faculty Disclosure
In adherence to ACCME guidelines, the Audio-Digest Foundation requests all lecturers to disclose any significant financial relationship
with the manufacturer or provider of any commercial product or service discussed. For this issue, the faculty reported
nothing to disclose.
Dr. Ries was recorded June 24, 2005, at Family Medicine Update: 2005, sponsored by the San Diego Academy of
Family Physicians, held in Coronado, California. Dr. Frank spoke June 1, 2005, at the annual Family Practice Refresher
Course, sponsored by the David Geffen School of Medicine at the University of California, Los Angeles. The
Audio-Digest Foundation thanks the speakers and the sponsors for making this program possible.
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