Chronic Obstructive Pulmonary Disease

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Contents 1 Chronic Obstructive Pulmonary Disease 1.1 EPIDEMIOLOGY AND ETIOLOGY 1.2 PATHOPHYSIOLOGY 1.3 PATIENT EVALUATION 1.3.1 History 1.3.2 Physical Examination 1.4 DIAGNOSIS 1.4.1 Laboratory Studies and Diagnostic Procedures 1.4.2 Differential Diagnosis 1.5 MANAGEMENT 1.5.1 Nonpharmacologic Therapy 1.5.2 Lung Transplantation and Lung Volume Reduction Surgery. 1.5.3 Smoking Cessation. 1.5.4 Preventive Measures. 1.5.5 Airway Clearance. 1.5.6 Optimizing Functional Ability. 1.5.7 Pharmacologic Treatment 1.5.8 Anticholinergics (Parasympatholytics). 1.5.9 Beta-adrenergic Agonists. 1.5.10 Theophylline. 1.5.11 Systemic Corticosteroids. 1.5.12 Inhaled Corticosteroids and Other Antiinflammatory Agents. 1.5.13 Mucolytics and Expectorants. 1.5.14 Antibiotics. 1.5.15 α1-Protease Inhibitor Replacement. 1.5.16 Relief of Dyspnea. 1.5.17 Prevention of Influenza and Pneumococcal Pneumonia. 1.5.18 Supplemental Oxygen Therapy. 1.5.19 Components of Oxygen Prescription 1.6 Oxygen flow. 1.7 Routine delivery devices. 1.8 Oxygen-conserving delivery devices. 1.9 Equipment systems. 1.9.1 Follow-up Evaluations. 1.9.2 Air Travel 1.10 REFERENCES

[edit] Chronic Obstructive Pulmonary Disease

Ralph M. Schapira

Lynn F. Reinke

The term chronic obstructive pulmonary disease (COPD) refers to a spectrum of pulmonary disorders that have the common feature of impaired expiratory airflow, termed airways obstruction. COPD is diagnosed by a permanent reduction in the ratio of the forced expiratory volume in 1 second (FEV₁) to forced vital capacity (FVC). Clinically, the major disorders recognized as part of the spectrum of COPD are emphysema and chronic bronchitis. The many definitions of chronic bronchitis and emphysema have led to confusion among physicians. Chronic bronchitis is defined functionally as a disease characterized by cough and mucus hypersecretion (phlegm production) for at least 3 months of the year for 2 consecutive years, with airways obstruction defined by spirometry. Some authors use "simple chronic bronchitis" to differentiate those patients with mucus hypersecretion who do not have airways obstruction, so simple chronic bronchitis is not part of the spectrum of COPD. In contrast to chronic bronchitis, emphysema is an anatomic abnormality of the lung defined as abnormal permanent enlargement of the air spaces distal to the terminal bronchioles, with destruction of their walls but without obvious fibrosis. Although emphysema is an anatomic diagnosis, characteristic clinical features are associated with it. Chronic bronchitis and emphysema should not be considered isolated disorders, since most patients with COPD have clinical features of coexistent chronic bronchitis and emphysema. Clinical features of patients with predominant chronic bronchitis ("blue bloater") and predominant emphysema ("pink puffer") allow general qualitative differentiation between the two forms of COPD. Pure forms of chronic bronchitis and emphysema are exceptions. Cigarette smoking is the most important factor in the development of COPD.

Some patients with classic smoking-related COPD have clinically pronounced bronchial responsiveness manifested by episodes of wheezing and worsening of expiratory airflow superimposed on the permanent airways obstruction. This form of COPD must be differentiated from asthma, which is characterized by acute airways obstruction that remits between episodes (see Chapter 72 ). Thus, asthma is not part of the spectrum of COPD. However, some individuals with asthma develop irreversible obstruction to airflow even in the absence of smoking, a form of COPD termed chronic asthmatic bronchitis. Chronic asthmatic bronchitis can mimic the classic smoking-induced COPD with bronchial responsiveness, although clinical features can help differentiate these two entities.

[edit] EPIDEMIOLOGY AND ETIOLOGY

Approximately 15 million people in the United States are believed to have COPD. In 1994, COPD ranked fourth as the estimated cause of death in the United States, accounting for 4.5% of all deaths. COPD is a common disorder seen in outpatient settings, accounting for 17 million annual office visits in a recent survey. The prevalence of COPD and hospitalization for COPD are directly related to increasing age. Males are affected much more often than females, reflecting past gender-related patterns of smoking. With the gap narrowing, however, the number of women with COPD is increasing.

Cigarette smoking is the most important risk factor for the development of COPD. The risk of developing COPD is related to the number of cigarettes smoked and the duration of smoking. Cigar or pipe smoking also increases the risk of developing COPD, but to a much lesser extent than cigarette smoking. Individual host susceptibility to the effect of smoking is believed to be a key factor in the development of COPD, since only about 15% of smokers develop COPD. Smokers who develop COPD have a much greater annual decline in the FEV₁ than do nonsusceptible smokers or nonsmokers. This rate of decline can normalize to that of nonsmokers with smoking cessation. Recent evidence suggests that passive smoking may be a risk factor in the development of COPD in nonsmokers.

People with homozygous alpha₁-protease inhibitor (α₁-PI) deficiency (usually, PiZZ phenotype) are at risk for the development of emphysema, although this condition represents fewer than 2% of patients with emphysema. Certain chronic occupational exposures, particularly to inorganic dusts (coal, cement), grain dusts, or acid fumes (sulfuric acid), may result in chronic bronchitis. The role of indoor air pollution, ambient outdoor air pollution, and recurrent childhood respiratory infections in causing COPD in the absence of smoking has not been clearly established.

[edit] PATHOPHYSIOLOGY

Emphysema is an anatomic abnormality of the acinus, the portion of the lung parenchyma supplied by and distal to a terminal bronchiole (respiratory bronchiole, alveolar ducts, alveolar sacs). Emphysema is characterized by destructive changes of the acinus. In contrast, chronic bronchitis is a functional abnormality defined by clinical criteria and associated with pathologic changes in the airways.

The pathogenesis of emphysema is controversial, although emphysema probably is caused by an imbalance between proteinases and antiproteinases in the lung. Neutrophils are believed to be a major source of proteinases, such as elastase. Cigarette smoking causes a chronic inflammatory response in the lung characterized by a migration of neutrophils. The neutrophils in the lung release elastase, which overwhelms the local natural antiproteinase activity, resulting in the destruction of lung elastin. Cigarette smoke may inactivate α₁-PI, a major antiproteinase found in the epithelial lining fluid of the lung. In addition, some people with α₁-PI deficiency develop emphysema on the basis of inadequate antiproteinase protection. The resulting proteinase-antiproteinase imbalance in the lung leads to the destruction of elastin, an integral component of the structural framework of the lung parenchyma. Loss of elastin is associated with air space enlargement and reduction in the elastic recoil of the lung. Forms of emphysema include centriacinar emphysema, the type strongly associated with cigarette smoking. It predominantly involves the respiratory bronchiole, is irregular in severity, and most often involves the upper lobes. In contrast, panacinar emphysema is characteristic of α₁-PI deficiency but may be seen in patients who do not have this disorder. The entire acinus is uniformly enlarged and destroyed. Why some smokers develop emphysema and others do not is not known.

In contrast to emphysema, which involves the pulmonary parenchyma (acinus), the pathologic lesions of chronic bronchitis involve the airways. Morphologic changes in chronic bronchitis include hypertrophy of the submucosal glands and goblet cells of the large airways, clinically manifested as mucus hypersecretion and cough. In addition, infiltration of the submucosa by chronic inflammatory cells is common. Involvement of the small airways (bronchioles) is manifested by the abnormal presence of mucus-secreting cells, frequently accompanied by chronic inflammation. Smooth muscle hyperplasia and edema may also be present in the airways. The mucus hypersecretion seen in chronic bronchitis may be complicated by bacterial colonization and infection, potentially aggravating the underlying chronic inflammation.

Chronic bronchitis is believed to represent the airway epithelial response to chronic irritation by tobacco smoke or other agents. The pathogenesis of chronic bronchitis is less well understood than that of emphysema. In animal models the induction of airway injury by irritant gases, proteinases, and acids results in the pathologic changes in the airways seen in chronic bronchitis.

The final common pathway of the pathologic changes in COPD is chronic airflow obstruction. In emphysema the loss of radial support produced by a decrease in elastic recoil results in airflow obstruction. In chronic bronchitis, the obstruction to airflow is believed to result from chronic inflammatory changes and muscle hyperplasia of the airways. In addition to airway obstruction, major abnormalities of gas exchange can occur in COPD. Ventilation/perfusion ( / ) relationships are altered by destruction of pulmonary parenchyma (emphysema) and airway abnormalities (chronic bronchitis). The changes in / relationships are highly complex but can result in hypoxemia and hypercapnia. It is speculated that the degree of hypoxemia and hypercapnia is related 2to such factors as severity and pattern of / mismatch, ventilatory drive response, and breathing pattern. The predominance of parenchymal abnormalities (emphysema) or airway inflammation (chronic bronchitis) as well as the level of alveolar ventilation help characterize a patient as having predominant emphysema or chronic bronchitis. In addition, patients with COPD who develop hyperinflation (predominant emphysema) have mechanically impaired muscles of respiration and respiratory muscle dysfunction. These changes increase the work of breathing, leading to respiratory muscle fatigue and potential respiratory failure. Hypoxemia results in pulmonary arterial hypertension and right ventricular failure.

[edit] PATIENT EVALUATION

[edit] History

COPD is typically a disease of older smoking or exsmoking adults (more than 20 pack-years), usually over age 50. The diagnosis of COPD is suggested by the history and confirmed by the criterion standard, spirometry. The cardinal symptom of COPD is progressive dyspnea, frequently accompanied by cough and phlegm production and episodes of wheezing. The cough usually precedes or accompanies the onset of dyspnea. Phlegm is whitish gray and expectorated in the morning but may continue intermittently during the day. A history of productive cough with relatively less prominent dyspnea suggests predominant chronic bronchitis.

In contrast, patients with predominant emphysema usually give a history of minimal productive cough but with marked dyspnea. Asthmatic bronchitis, a form of COPD, is suggested by a history of typical paroxysmal asthma, especially occurring at rest or during sleep, with no or minimal smoking history. Changes in the quality of expectorated sputum, from whitish gray and mucoid to purulent, suggest acute bacterial bronchitis. The wheezing in some patients with COPD may be from bronchospasm or from the flow of air through inflamed and narrowed airways. A history of wheezing predicts a beneficial response to inhaled bronchodilators. A family history of COPD suggests α₁-PI deficiency, particularly if the onset is during the fourth or fifth decade of life. Hemoptysis in patients with COPD usually results from acute bacterial bronchitis or pneumonia, but an underlying lung cancer must always be considered. A patient who presents with progressive dyspnea and a history of asthma, particularly a nonsmoker, may have asthmatic bronchitis. A detailed occupational history, including exposure to dusts and fumes, should be obtained.

Patients with predominant chronic bronchitis tend to remain relatively comfortable at rest but develop hypoxemia, which leads to pulmonary arterial hypertension and subsequent right ventricular failure (cor pulmonale). Their failure to complain about respiratory problems may be misleading. In contrast, patients with predominant emphysema tend to complain of dyspnea, even at rest. Patients with COPD may have complaints not directly related to the pulmonary system. The history, particularly in patients with severe COPD, may reveal easy fatigability, weight loss, and decreased appetite. Patients with COPD may have sleep disturbances and neuropsychiatric abnormalities such as depression, poor concentration, and memory impairment. A history of peripheral edema suggests cor pulmonale.

[edit] Physical Examination

Patients with predominant chronic bronchitis are usually of normal body weight or obese. The physical examination may reveal cyanosis and peripheral edema caused by right ventricular failure (blue bloater). The respiratory rate is usually normal, with no use of the accessory muscles of respiration. Chest percussion note is usually resonant, and auscultation may demonstrate wheezes and coarse rhonchi that may change in location and intensity after a cough. Physical findings compatible with allergic rhinitis or nasal polyps may be noted in patients with asthmatic bronchitis.

In contrast, patients with predominant emphysema are frequently asthenic with weight loss. Tachypnea, the use of accessory muscles of respiration, retraction of the lower intercostal spaces with inspiration, and the use of pursed lips during expiration are common. Cyanosis is uncommon until the disease becomes very advanced because the increased FEV₁ maintains a sufficient oxyhemoglobin saturation and prevents hypercapnia (pink puffer). The chest percussion note is usually resonant. Auscultation reveals diminished breath sounds.

A useful bedside diagnostic test for COPD is the forced expiratory time (FET), measured by timing a full exhalation of the vital capacity during chest auscultation. In a large clinical study^[1] evaluating the FET, sensitivity and specificity of FET at a value of 6 or more seconds for the diagnosis of airways obstruction was 74% and 75%, respectively. The FET is most useful in patients older than 60.

[edit] DIAGNOSIS

[edit] Laboratory Studies and Diagnostic Procedures

Pulmonary function testing (spirometry) is the only criterion standard to demonstrate an obstructive ventilatory defect, the hallmark of COPD.^[2] An obstructive defect is defined by a FEV₁/FVC ratio below the subject's predicted value. Alternatively, some pulmonary function laboratories use a percentage of FEV₁ or FVC (less than 70%) to define obstruction. Once airway obstruction has been documented from the FEV₁/FVC ratio, the severity of the obstructive abnormality can be graded by the patient's percentage of predicted FEV₁: down to 70%, mild; less than 70% to 60%, moderate; less than 60% to 50%, moderately severe; less than 50% to 34%, severe; and less than 34%, very severe. Patients with COPD have an irreversible obstructive impairment, as demonstrated by a persistently abnormal FEV₁/FVC ratio, although the FEV₁ and FVC may vary between bouts of wheezing or pulmonary infection and clinical stability during optimal therapy. Any changes in spirometry, either improvement or worsening, should be viewed cautiously unless serial tests show a consistent trend. In contrast, asthmatic patients have a reversible obstructive impairment, with normalization of the FEV₁/FVC ratio between clinical episodes of asthma. Spirometry can also be used to determine other parameters, such as the forced expiratory flow between the time 25% to 75% of the FVC is exhaled (FEF_25-75). A decrease in the FEF_25-75 is not used to diagnose an obstructive airways defect but does suggest obstruction of the small airways (less than 2 mm). Survival estimates of patients with COPD can be predicted based on the FEV₁. The 5-year survival begins to decrease at a FEV₁ of 1.15 to 1.5 L. At ranges of FEV₁ of 0.75 to 1.15 L, 5-year survival decreases to 66% and is even lower in this group if chronic hypercapnia is present.

The functional ability of a patient with COPD is more precisely defined by a formal pulmonary exercise evaluation than by the FEV₁ alone. Functional impairment of patients with COPD varies for any given FEV₁, although in general, functional ability decreases as the FEV₁ decreases. Exercise testing can also differentiate among limitations caused by gas exchange, ventilation, or cardiovascular abnormalities. Many patients with COPD are limited because of cardiovascular deconditioning and not by a gas exchange or ventilation impairment. An exercise test is not routinely recommended unless a major medical intervention is planned, for example, a lung resection in a patient when postoperative respiratory disability is a concern.

Spirometry in patients who demonstrate an obstructive defect typically includes measurement of the FEV₁ and FVC immediately after administration of an inhaled bronchodilator, the bronchodilator response. A widely used definition of a significant bronchodilator response is both a 12% increase and an absolute increase of 200 cc in the FEV₁ or FVC. Although not clinically proved, patients with a significant response are believed to derive the greatest benefit from inhaled bronchodilators and corticosteroids. The lack of a significant bronchodilator response, however, does not preclude clinical benefit, since the one-time administration of a bronchodilator during spirometry does not necessarily predict response with regular use. Therefore, inhaled bronchodilators should not be withheld from patients who do not exhibit a significant bronchodilator response. Some laboratories no longer perform a test of bronchodilator response in a patient with an established diagnosis of COPD, since the clinical practice is to prescribe a bronchodilator regardless of response. Finally, normalization of the FEV₁/FVC percentage after administration of a bronchodilator strongly suggests asthma.

Patients with predominant chronic bronchitis or asthmatic bronchitis tend to have a relatively mild reduction in diffusing lung capacity for carbon monoxide (DLco), since the principal abnormality is in the airways. In contrast, patients with predominant emphysema, a parenchymal abnormality, have a greater reduction in DLco, which tends to correlate with the anatomic extent of the emphysema. The lung volumes in predominant chronic bronchitis tend to show a normal or slightly increased total lung capacity (TLC). In predominant emphysema, however, the lung volumes often show hyperinflation, as manifested by a marked increase in TLC and residual volume (RV). The increase in RV may compromise the vital capacity. Arterial blood gas (ABG) results in patients with predominant bronchitis demonstrate marked hypoxemia and, in advanced cases or during exacerbations, hypercapnia. ABG abnormalities may be relatively modest in patients with predominant emphysema, however, demonstrating only mild hypoxemia without hypercapnia except in advanced cases. Significant ABG abnormalities in patients with COPD tend to be unusual until the FEV₁ drops below 1.25 to 1.5 L. Exercise may worsen hypoxemia in patients with COPD. Secondary erythrocytosis may ensue in severely hypoxemic patients.

Standard chest radiographs can suggest the diagnosis of emphysema. Marked overdistention of the lungs, as manifested by flattened diaphragms and an enlarged retrosternal air space, is highly suggestive of emphysema. A small and vertically oriented heart contour and hyperlucent lung fields due to oligemia are also suggestive of emphysema. Localized radiolucencies and upper lobe bullae may be visible on the chest radiograph. Lower lobe bullae are highly suggestive of emphysema associated with α₁-PI deficiency. Although the chest radiograph can provide only an approximation of the severity of emphysema, it is most useful in suggesting the presence of severe emphysema. Computed tomography (CT) and particularly high-resolution CT are much more sensitive than plain films in detecting emphysematous changes in the lung, such as small bullae. Neither the chest radiograph nor the CT scan replaces the criterion standard, spirometry.

Other helpful tests in the initial evaluation of a patient with COPD include Gram's stain of the sputum; a complete blood count and differential to identify eosinophilia, which may suggest asthmatic bronchitis; a baseline electrocardiogram to identify right atrial or ventricular abnormalities suggestive of cor pulmonale; and α₁-PI level if deficiency is suspected. Skin allergy tests and a serum IgE level should be considered in patients with suspected asthmatic bronchitis.

[edit] Differential Diagnosis

Chronic bronchitis and emphysema must be distinguished from other lung diseases that may cause obstructive ventilatory impairment on spirometry. Patients with an exacerbation of asthma may have impairment and radiographic abnormalities suggestive of emphysema. By definition, however, the airways obstruction in asthma is reversible between acute exacerbations. Patients with cystic fibrosis may have ventilatory impairment from airway inflammation and obstruction by secretions. Cystic fibrosis is differentiated from chronic bronchitis and emphysema by its numerous systemic nonpulmonary manifestations and early age of onset. Bronchiectasis, the persistent dilation and destruction of bronchi, represents the sequelae of other lung processes, such as granulomatous infections and an array of genetic defects. The spirometric results in patients with bronchiectasis vary, but those with diffuse bronchiectasis may have an obstructive ventilatory defect. The history, underlying disease process, and CT scan can help differentiate bronchiectasis from chronic bronchitis and emphysema.

[edit] MANAGEMENT

[edit] Nonpharmacologic Therapy

[edit] Lung Transplantation and Lung Volume Reduction Surgery.

Lung transplantation has been used with success in patients with severe COPD, although clinical follow-up has been limited to a few years. Single-lung transplantation is usually preferred. In 1997, for example, more than 950 lung and heart-lung transplants were performed in the United States for COPD, including α₁-PI deficiency–related COPD. Patients being considered for lung transplantation should be referred to specialized centers. The resection of large bullae may improve gas exchange and improve symptoms in selected patients with bullae of sufficient size to compress normal lung parenchyma.

Lung volume reduction surgery (LVRS) is currently limited to certain designated, specialized centers participating in a National Institutes of Health–sponsored study. LVRS, the removal of emphysematous areas of lung, can improve some measures of pulmonary function and gas exchange, decrease dyspnea, and diminish or eliminate the need for supplemental oxygen. The criteria to select patients most likely to benefit from LVRS are uncertain, however, and await the results of the LVRS national multicenter study.

[edit] Smoking Cessation.

Most patients (85%) with COPD are current or former cigarette smokers. Several investigations have clearly shown that smoking cessation will slow the annual decrement of FEV₁ to the level of a nonsmoker. In addition, the nonpulmonary benefits include improved cardiovascular status and a reduced risk of developing lung cancer. Comprehensive, multidisciplinary smoking cessation programs using nicotine replacement therapy, which includes nicotine chewing gum, nicotine transdermal patches, nasal spray, and an oral inhaler, have lead to long-term cessation rates as high as 50%. Nicotine gum, now available over the counter in 2-mg and 4-mg strengths, has been shown to improve smoking cessation rates when used in appropriate candidates. The gum helps to maintain a blood and tissue level at about that of a pack-a-day smoker and can be gradually decreased or stopped abruptly. Disadvantages include a bitter taste, which may lead to noncompliance, and improper chewing patterns, which result in poor absorption of the nicotine. Another method for nicotine replacement is the transdermal patch. The patch is available in three doses, which are tapered over 2 to 3 months during the smoking cessation program. Some physicians initiate therapy with a low-dose patch in patients with coronary artery disease. The patches' advantages over nicotine gum include (1) easy use and once-daily replacement and (2) a steady, unchanging dose of nicotine, unlike the boluses provided by gum. Studies have demonstrated that the nicotine patches double the quit rate achievable by various levels of behavioral modification used alone. Nicotine nasal spray delivers nicotine through the nasal mucosa. It is the fastest absorbed form of nicotine currently available and reduces cravings within minutes. The nicotine oral inhaler is the newest nicotine product on the market. It has a similar appearance to a cigarette but delivers nicotine into the mouth, not the lungs. It mimics the hand-to-mouth behavior of smoking and may be used as an adjunct tool along with other replacement therapies. The antidepressant bupropion (Zyban) is as effective as the nicotine patch in smoking cessation.^[3] Patients who received 200 or 300 mg of bupropion per day had a quit rate at 1 year of 22.9% and 23.1%, respectively. The pill should be started at least 1 week before the target quit date and is contraindicated in patients with eating or seizure disorders.

Smoking results from many factors, such as learned behaviors, environmental influences, and chemical dependence. Therefore, in addition to temporary nicotine replacement, smoking cessation programs must address these various issues to achieve long-term success. Physician support and involvement are important in making smoking cessation efforts successful.

[edit] Preventive Measures.

Exposure to occupational or environmental air pollutants may trigger an exacerbation of COPD, especially if the patient has asthmatic bronchitis. Assisting the patient to identify specific sensitivities and providing strategies to avoid these triggers may minimize exacerbations. Days with severe air pollution can exacerbate COPD.

[edit] Airway Clearance.

The clearance of excessive secretions, particularly in patients with predominant chronic bronchitis, can result in significant subjective benefit.^[4] Multiple approaches can be implemented to promote and maintain airways relatively free of excessive secretions. Most patients with COPD cough ineffectively, resulting in increased energy expenditure without adequate sputum expectoration to clear the airways. The simple combination of deep breathing and coughing is frequently overlooked as an effective method of airway clearance. One cough technique that may facilitate airway clearance is forced exhalation, which is especially valuable for patients with a weak or uncontrolled cough. This technique involves combining slow deep breaths, with 5 to 10 seconds of breath holding to increase intrathoracic pressure, then coughing on exhalation. Most patients find this cough technique easy to learn and effective for clearing secretions felt or heard in the large airways.

Another technique to aid in airway clearance is chest physiotherapy (CPT), which includes postural drainage and chest percussion and vibration either by hand or mechanical device. CPT allows gravity and applied external force to the chest wall to facilitate drainage of the dependent portions of the lung, thus improving airway clearance. Both postural drainage and CPT should always be followed with cough techniques to clear the airways. CPT can cause bronchospasm and worsening hypoxemia and should be performed by respiratory therapists or nurses who are well trained in its application.

Several new alternatives are available to percussion and postural drainage. The flutter valve is a hand-held mucus-clearing device that incorporates a steel ball resting in a hard plastic cone. As the patient exhales through the pipe, pressure builds in the airways and in the passage beneath the steel ball until the ball is forced to move and some gas escapes. This produces pressure oscillations that are transmitted throughout the tracheobronchial tree. In theory the oscillations dislodge mucus from the airway walls while back pressure supports smaller airways beyond the equal-pressure point; the expiratory flow helps to move the mucus toward the trachea, where it is coughed out. Although the flutter valve has been studied mainly in patients with cystic fibrosis, supporting evidence now indicates that flutter therapy is effective in patients producing more than 25 ml of sputum a day in other respiratory diseases. The main advantages of the flutter device are it is user friendly, does not require assistance from a caregiver, and is relatively inexpensive.

The ThAIRapy Vest is a high-frequency chest compression device that consists of a nonstretching inflatable vest attached by hoses to an air-pulse generator. Small volumes of gas are injected into and withdrawn from the vest at a rapid rate, pressurizing and releasing the chest with miniature hugs at frequencies from 5 to 25 Hz and generating pressures up to 53 cm H₂O. The minihugs from the vest create minicoughs in the patient, with increased mucus-airflow interaction and improved mucous rheology. Although the vest system was also developed for cystic fibrosis, any patients with excessive mucous production and difficulty clearing secretions would benefit from this therapy. An advantage of the vest is that it allows the patient to be passive, whereas the other clearance techniques require active participation. The major disadvantage is the expense of the vest system, which sells for approximately $16,000.

All these techniques can help to mobilize secretions, but deep breaths and gentle huff coughs are still required to move mucus into the central airways, where traditional cough or suction can remove it. Traditional CPT, once the predominant mucous clearance treatment, is now only one of a variety of modalities available.

[edit] Optimizing Functional Ability.

Patients with COPD have many objective and subjective barriers to living an active and productive life. Comprehensive, multidisciplinary pulmonary rehabilitation programs offer patients education, exercise training and reconditioning, proper nutrition, and psychosocial interventions to decrease anxiety and other emotional disturbances related to the effects of COPD.^[5] A recent literature review determined grades for each component of a rehabilitation program. Lower extremity and strength training was shown to improve exercise tolerance. Pulmonary rehabilitation improves dyspnea and health-related quality of life and reduces number and duration of hospitalizations. Expert opinion supports the inclusion of education and psychosocial interventions. Scientific evidence does not support the routine use of ventilatory muscle training in rehabilitation programs. Pulmonary rehabilitation may improve survival, but further research is needed, in addition to determining optimal methods for measuring outcomes and cost-effectiveness.

[edit] Pharmacologic Treatment

The aim of pharmacologic treatment of emphysema and chronic bronchitis is to improve symptoms and measurably improve lung function (Fig. 75-1). Inhaled medications (parasympatholytics, beta-adrenergic agonists (β-agonists, steroids) delivered by a metered-dose inhaler (MDI) are preferred in the pharmacotherapy of COPD, since inhalation allows direct deposition of medication in the airways and helps to minimize systemic side effects (Table 75-1). The delivery of all inhaled medications requires the use of a spacer device, which functions as a holding chamber reservoir that minimizes the need to coordinate simultaneous inhalation and depression of the MDI canister to deliver the dose. A spacer device used with an MDI provides greater drug deposition to the smaller airways, less accumulation in the oropharynx, and greater overall bronchodilator effect.

Table 75-1 Metered-dose Inhalers (MDIs) Used in Treatment of COPD

Agent	Action	Dose per inhalation (μg)
Albuterol (Proventil, Ventolin)	β2-Agonist	90
Metaproterenol (Alupent)	β2-Agonist	650
Pirbuterol (Maxair)	β2-Agonist	200
Terbutaline (Brethine, Brethaire)	β2-Agonist	200
Ipratroprium (Atrovent)	Anticholinergic (parasympatholytic)	18
Ipratropium and albuterol (Combivent)	β2-Agonist and anticholinergic	103 and 18
Triamcinolone (Azmacort)	Antiinflammatory corticosteroid	100
Flunisolide (AeroBid)	Antiinflammatory corticosteroid	250
Beclomethasone (Beclovent, Vanceril)	Antiinflammatory corticosteroid	42
Fluticasone (Flovent)	Antiinflammatory corticosteroid	44 or 110 or 220

To ensure maximal drug deposition from the MDI, the patient must be given a spacer device and educated in inhalation technique. The patient should take a slow and complete inhalation from the end of a normal tidal breath (full exhalation to RV is not necessary) and hold inhalation for up to 10 seconds to allow for drug deposition (Box 75-1). Reevaluation and reinforcement of proper technique should occur regularly. The administration of nebulized medications by compressor-driven devices was once believed to be the optimal method of β-agonist delivery. Compared with the MDI, however, nebulization is no more effective, requires a larger dose of the drug, takes longer to administer, and is more costly. Some patients continue to report greater relief of dyspnea from a nebulized treatment than MDI delivery, possibly because nebulization provides more drug compared with an MDI. The use of a nebulizer should be reserved for patients with severe disease who are unable to hold their breath when using an MDI or who are unable, even with a spacer device, to coordinate MDI use.

Box 75-1 - Proper Use of a Metered-dose Inhaler (MDI)

Shake the inhaler. Tilt the head back slightly and exhale normally. Forced exhalation to residual volume is not necessary. Hold the mouthpiece 1 to 1½ inches away from open mouth. If using a spacer, however, seal lips around the mouthpiece. Activate the MDI while simultaneously taking a slow, deep inhalation. Hold breath at the end of inspiration for 5 to 10 seconds. Slowly exhale through mouth. Wait 1 minute between puffs. If using a steroid inhaler, rinse mouth after use to avoid thrush or dysphonia.

[edit] Anticholinergics (Parasympatholytics).

Anticholinergic drugs antagonize the effect of the parasympathetic system on the airways, which mediates bronchoconstriction. Ipratropium, a quaternary anticholinergic bronchodilator available by MDI, is more efficacious than inhaled β-agonist therapy and should supplant β-agonists as first-line therapy in COPD. In clinical studies, ipratropium achieves greater bronchodilatory effect in COPD than β-agonists or theophylline when comparing FEV₁. In addition, ipratropium has a longer duration of action and wider margin of safety than β-agonists, making it a cornerstone of pharmacologic therapy for COPD. The traditional dosage of ipratropium (2 puffs, four times a day) may be suboptimal and can be safely increased to 3 to 6 puffs four times a day. Ipratropium is appropriate for maintenance treatment of COPD and is not indicated in the initial treatment of acute exacerbations because of its slow onset of action (about 20 minutes) compared with β-agonists. Ipratropium is poorly absorbed from the airways and thus has few systemic adverse effects, unlike with β-agonists. Potential side effects include dry mouth and cough. Ipratropium (available as MDI or for nebulization) is the only anticholinergic bronchodilator available in the United States.

[edit] Beta-adrenergic Agonists.

Short-acting β-agonists have been the traditional cornerstone in the management of COPD. The role of β-agonists in COPD pharmacotherapy continues to evolve, however, particularly with the established efficacy and safety of the anticholinergic ipratropium. Most authorities recommend that short-acting β-agonists be used as second-line therapy, either to supplement or to replace ipratropium in patients who do not obtain satisfactory clinical benefit from ipratropium alone. Combivent combines a fixed dose of ipratropium and albuterol in a single MDI and may have an additive effect compared with using each agent alone for stable COPD.

The use of β-agonist bronchodilators can increase airflow, improve mucociliary clearance, and reduce dyspnea in patients with COPD. Administering higher doses of β-agonists (2 to 6 puffs four to six times a day) may result in greater achievement of airway bronchodilation without additional side effects than with the traditional dosage of 2 puffs four times a day. With concern over reported deaths associated with the overuse of β-agonists in patients with asthma, however, there is reluctance to recommend higher doses. In addition, tachyphylaxis, rebound bronchoconstriction, and bronchial hyperreactivity may occur with β-agonists.

The many short-acting β-agonist MDIs in clinical use are relatively selective for β₂-receptor sites that mediate bronchial smooth muscle relaxation. Although the inhaled route helps to minimize systemic side effects, β-agonists can result in tachycardia, palpitations, tremor, and metabolic derangements such as hypokalemia. Patients should administer β-agonists prophylactically before engaging in physical activity known to provoke bronchospasm. A long-acting inhaled β-agonist, salmeterol, may improve lung function and symptoms in COPD, although it is formally approved only for asthma.^[6] The use of oral β-agonists is strongly discouraged because they are no more effective than MDIs, absorption is unpredictable, and the incidence of systemic adverse effects is higher than from MDIs. However, patients with COPD who cannot use a MDI or who have nocturnal symptoms without relief from short-acting inhaled β-agonists may benefit from use of a sustained-release oral β-agonist. The latter group of patients may also benefit from salmeterol.

[edit] Theophylline.

A methylxanthine derivative, theophylline, has been shown to act as a bronchodilator, improve gas exchange, decrease dyspnea, improve mucociliary clearance, enhance respiratory muscle performance, have a positive inotropic effect, and increase neuroinspiratory drive. The belief that theophylline relaxes bronchial smooth muscle by inhibiting phosphodiesterase has been supplanted by other proposed mechanisms, including antagonism of prostaglandins and adenosine, alteration of cellular calcium metabolism, and inhibition of phosphodiesterase isozymes. The precise role of theophylline in the management of COPD has been controversial, particularly with the availability of inhaled anticholinergics. Over the past few years, theophylline once again seems to have fallen out of favor.

The toxicity of theophylline and its interactions with other drugs make it a relatively complex drug to dose. Common side effects of theophylline include nausea, diarrhea, tremor, anxiety, and insomnia and even include life-threatening side effects such as seizures and cardiac dysrhythmias. A number of factors reduce the clearance of theophylline, which contributes to an increased risk for toxicity. These factors include antibiotics (e.g., erythromycin, quinolones), histamine blockers (e.g., cimetidine, calcium channel blockers), liver disease, cor pulmonale, and pregnancy. Although the therapeutic range for theophylline levels has been debated, the usual therapeutic serum level ranges from 10 to 20 μg/ml. However, most potential bronchodilation is believed to occur once levels of 10 to 15 μg/ml have been reached. Therefore a serum level of 8 to 12 μg/ml has been suggested as the therapeutic goal.

The decision to institute theophylline therapy must be individualized and should not be universally made in all patients with COPD. Theophylline may be added to the treatment plan in patients who have not achieved an optimal clinical response to β-agonist and ipratropium MDIs. Theophylline should be continued only if there is a clinical benefit to the patient, such as an objective improvement in spirometry or a decrease in dyspnea. The usual dose of theophylline is 400 to 900 mg/day of a long-acting preparation, but the precise dose depends on concurrent drug administration, the patient's medical problems, and the drug's metabolism. Serum theophylline levels must be checked in 1 to 2 weeks and dosages adjusted to achieve and maintain an adequate clinical response without side effects. Subsequent serum levels should be monitored twice annually and doses adjusted if levels are subtherapeutic or supratherapeutic, if drugs are prescribed that may alter the metabolism of theophylline, or if a change occurs in the patient's medical condition that might alter theophylline metabolism.

[edit] Systemic Corticosteroids.

Unlike ipratropium, β agonists, and oral theophylline, which are bronchodilators, corticosteroids are antiinflammatory agents. They objectively benefit about 10% of clinically stable outpatients with COPD and are thought to increase the clinical response to β-agonists, possibly by increasing β-adrenergic responsiveness of the airways. In addition, the antiinflammatory property of corticosteroids may decrease the airway inflammation seen in COPD. The onset of action of the antiinflammatory effect of corticosteroids is several hours.

The role of oral corticosteroids in COPD is not well defined, partly because of their serious adverse effects and lack of evidence in their favor. Oral corticosteroids should be considered in outpatients with stable COPD whose symptoms are not optimally controlled by a regimen of β-agonists, ipratropium, and possibly theophylline. Although it can be difficult to predict which patients with COPD will respond to corticosteroids, factors such as a significant response to bronchodilators during spirometry or clinical features of asthmatic bronchitis suggest that a trial of steroids is warranted. A therapeutic trial of corticosteroids must be preceded by spirometry to verify objective improvement in pulmonary function (FEV₁) after initiation of therapy. Prednisone (approximately 0.5 to 1 mg/kg once daily) is begun and spirometry repeated 2 weeks after start of therapy. Although no formal criteria exist, most providers continue prednisone only if significant improvement in FEV₁ (defined as greater than 20%) results. Subjective improvement in dyspnea alone without objective improvement in spirometry is not an indication for continuation of corticosteroids. It is not known whether oral corticosteroids ultimately affect the natural progression of COPD.

Oral corticosteroids are associated with significant toxicity when administered chronically. Potential adverse effects include adrenal suppression, osteoporosis, hypertension, cataracts, myopathy, diabetes mellitus, and rarely, opportunistic infections. Therefore, if a patient demonstrates a significant objective clinical response to oral corticosteroids, the dose should be promptly tapered to the lowest possible dose that continues to provide objective spirometric benefit. Subjective worsening, such as an increase in dyspnea during a corticosteroid taper, should not be equated with a worsening of the FEV₁. Spirometry should be repeated to determine whether a correlation exists between subjective worsening and a decrement in pulmonary function. Alternate-day oral therapy may minimize side effects, although this remains unproved. Patients taking corticosteroids should continue to receive maximal therapy with inhaled bronchodilators and theophylline in an effort to minimize the requirement of oral corticosteroids. Calcium, vitamin D, estrogen, or bisphosphonates should be considered, as applicable, to prevent glucocorticoid-induced osteoporosis.^[7]

[edit] Inhaled Corticosteroids and Other Antiinflammatory Agents.

Inhaled corticosteroids are an established part of asthma therapy. The role of inhaled steroids in the treatment of COPD is uncertain, however, leading some investigators to believe that the airway inflammation in COPD is fundamentally different from that of asthma. Despite the lack of evidence, many physicians prescribe inhaled corticosteroids to patients with COPD.^[8][9] Inhaled corticosteroids cause less serious side effects than oral corticosteroids because lower doses are administered and minimal systemic absorption occurs, although with the availability of potent inhaled corticosteroids, side effects from these agents are being recognized. The main side effects at low doses include oropharyngeal candidiasis and dysphonia. Inhaled corticosteroids most likely benefit patients who have shown clinical benefit from oral corticosteroids or who have asthmatic bronchitis. Until additional clinical studies identify the subset of COPD patients who will benefit most from these inhaled agents, no firm recommendation can be made regarding their use in COPD.

Other antiinflammatory agents, such as cromolyn, nedocromil, or the leukotriene antagonists, have not been studied in COPD and cannot be recommended at this time. These agents have a clear role in some patients with asthma.

[edit] Mucolytics and Expectorants.

The benefits of mucolytics and expectorants in the management of secretions are not well documented. Mucolytics, such as iodinated glycerol and acetylcysteine, are postulated to work by helping to liquefy tenacious mucus in the bronchial tree. The results from the National Mucolytic Study indicate that although patients with chronic bronchitis treated with iodinated glycerol reported subjective improvement in chest symptoms, pulmonary function was not affected. In contrast to mucolytics, oral expectorants such as guaifenesin may help to loosen bronchial secretions by stimulating the flow of respiratory tract fluid and facilitating the movement of secretions by ciliary motion and coughing. Patients with chronic bronchitis often subjectively report that these expectorants help them to raise their secretions more readily, but clinical efficacy of such products has not been demonstrated. No standard role exists for expectorants or mucolytics in symptomatic treatment of COPD.

[edit] Antibiotics.

Antibiotics are frequently prescribed for patients with COPD to treat or prevent an acute infectious exacerbation of COPD. Three organisms, Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella (Branhamella) catarrhalis have emerged as the major bacterial pathogens in infected patients with COPD. Acute infectious exacerbations, characterized by worsening dyspnea, increased cough, sputum production, and sputum purulence, may worsen pulmonary function during the infection, although controversy surrounds whether pulmonary function is permanently altered. Antibiotic prophylaxis with alternating agents administered 1 week a month may reduce the frequency of exacerbations in the subset of patients with COPD who have four or more exacerbations a year.

Although the role of antibiotics in managing exacerbations of COPD is controversial, it has become standard practice to prescribe a course of antimicrobial therapy when a patient presents with an acute exacerbation of COPD, particularly if the exacerbation appears infectious, as characterized by an increase in sputum volume and purulence. The most common antimicrobial agents used in the treatment of patients with acute infectious exacerbations of COPD include amoxicillin, amoxicillin/clavulanate, tetracycline, macrolides (e.g., erythromycin, clarithromycin, azithromycin), or trimethoprim-sulfamethoxazole. Gram's stain and culture of the sputum are important because M. catarrhalis and 15% to 25% of H. influenzae strains are typically resistant to amoxicillin.

[edit] α₁-Protease Inhibitor Replacement.

Patients with COPD and a documented homozygous α₁-PI deficiency with serum levels less than 11 μM may potentially benefit from weekly intravenous α₁-PI replacement derived from human plasma. Although replacement therapy is safe and feasible and can increase levels of α₁-PI, the efficacy of replacement therapy in terms of preservation of pulmonary function is unknown. Patients with α₁-PI deficiency and COPD should be referred to specialty centers for evaluation for replacement therapy.

[edit] Relief of Dyspnea.

The best way to relieve dyspnea in patients with COPD is through maximal use of bronchodilators, oral and inhaled corticosteroids, and theophylline. Benzodiazepines are generally of no clinical benefit, although opiates such as morphine may help relieve dyspnea. Opiates are associated with respiratory depression, however, and extreme caution is warranted when considering their use in disabling dyspnea.

[edit] Prevention of Influenza and Pneumococcal Pneumonia.

Since pulmonary infection is a common complication in COPD that can lead to worsening pulmonary function and respiratory failure, an annual prophylactic vaccine against influenza is recommended in those individuals who are not sensitive to egg protein. This vaccine is associated with a 60% to 80% protection rate. Amantadine can be considered in patients with COPD who have not received the vaccination and who are at risk for influenza A or in patients with early influenza A. The polyvalent pneumococcal vaccination, administered one time, is also recommended for people with COPD over 50 years of age. Revaccination is currently advised only if the patient received the vaccine 5 or more years earlier and was under age 65 at the time of primary vaccination.^[10] In immunocompromised persons an initial vaccine is recommended, and a single revaccination should be administered 5 years after the initial dose.

[edit] Supplemental Oxygen Therapy.

Oxygen (O₂) is a component of the pharmacotherapy of COPD because it is a potent pulmonary arterial vasodilator.^[11] Since hypoxemia can cause pulmonary arterial hypertension and right ventricular failure (cor pulmonale), supplemental O₂ would be expected to blunt pulmonary arterial hypertension and prevent cor pulmonale. The importance of supplemental O₂, termed long-term oxygen therapy (LTOT), in a subset of patients with COPD has been derived from two clinical trials conducted in the early 1980s. The trials demonstrated that supplemental O₂ therapy significantly decreased morbidity and mortality in COPD patients with chronic hypoxemia. Additional benefits included an improvement in neuropsychiatric functioning and an increase in exercise tolerance. %Box 75-2 lists the three criteria for the initiation of LTOT. ABGs should be obtained from an approved laboratory for the initial evaluation of the need for LTOT. Pulse oximetry is easily obtained, noninvasive, and less expensive but is less accurate and gives no information regarding arterial carbon dioxide pressure (PaCO₂). The identification of patients with hypercapnia is extremely important, since hypercapnia may worsen with the institution of LTOT. A subset of patients with

Box 75-2 - Indications for Long-term Supplemental Oxygen Therapy✢

Resting state, room air Pao2 ≤55 mm Hg or Sao2 ≤88%. Resting state, room air Pao2 of 56-59 mm Hg or Sao2 ≤89%, if patient has polycythemia (hematocrit ≤52%) or clinical or electrocardiographic evidence of cor pulmonale Pao2 ≤55 mm Hg or Sao2 ≤88% during exercise (documented by 6-or 23-minute walk test) or sleep (documented by sleep study) regardless of Pao2 at resting state and room air. Pao2, Arterial oxygen partial pressure (tension); Sao2, arterial oxygen saturation. ✢All assessments must be done during a stable clinical state and not during an acute illness. When long-term O2 therapy is initiated, arterial blood gases (room air, resting state) should be repeated within 3 months to confirm a continued need for oxygen.

COPD may be at risk for desaturation during exercise or sleep even if the patient does not meet the criteria for LTOT based on resting ABGs (criteria 1 and 2). Room air, resting arterial oxygen pressure (Pao₂) levels between 60 and 65 mm Hg, a reduced DLco, and complaints of dyspnea on exertion warrant consideration of a 6-minute standardized walk test with pulse oximetry to evaluate the need for supplemental O₂ during exercise (criterion 3). Some investigators also recommend a sleep study in this same group to evaluate for nocturnal desaturation that would warrant supplemental O₂ therapy during sleep, particularly in patients who are obese or hypercapnic or have erythrocytosis (hematocrit 52% or greater) or cor pulmonale. Most studies use resting oxyhemoglobin saturation criteria as the basis to prescribe LTOT. LTOT prescribed to patients who do not meet criteria at rest, however, but only with exercise or sleep, has been shown to improve exercise tolerance and quality of life and may improve survival.

The majority of patients who meet the indications for LTOT warrant the use of O₂ therapy on a continuous basis unless O₂ was prescribed based solely on exercise-or sleep-induced criteria. In these two instances, O₂ should be prescribed only during the times of desaturation. Dyspnea without evidence of significant hypoxemia at rest or exercise is not an indication for LTOT.

[edit] Components of Oxygen Prescription

[edit] Oxygen flow.

The majority of patients with COPD can attain a Pao₂ of 60 mm Hg or greater (corresponding to an oxyhemoglobin saturation of about 90%) on a flow of 1 to 2 L/min of supplemental O₂ while at rest. A small subset of patients with hypoxemic COPD develop hypercapnia with oxygen supplementation, and careful titration in these patients is essential. In addition to the flow prescribed at rest, some physicians prescribe a separate O₂ flow for exercise and sleep. This is usually accomplished by empirically increasing the resting O₂ flow by 1 L/min during exercise and sleep. A more precise method to evaluate the degree of desaturation with exercise and thus prescribe a more precise flow of O₂ is by conducting a 6-or 12-minute walk test. If sleep studies have been conducted, desaturation during the study will determine flow rates during sleep, although sleep studies should not be done unless clinically indicated.

[edit] Routine delivery devices.

The most often used O₂ delivery device for LTOT is the nasal cannula. It is easy for patients to use and has few side effects (dryness of the nasal membranes, facial irritation). A disadvantage of the nasal cannula is that the amount of O₂ inspired is variable because of variations in the breathing pattern, including breathing through the mouth. In addition, since O₂ flow is continuous, even during expiration, O₂ is wasted. LTOT can also be delivered through a tracheostomy mask in patients with a tracheostomy. Unlike delivery through a nasal cannula, humidification should be provided with a tracheostomy mask.

[edit] Oxygen-conserving delivery devices.

Oxygen for LTOT is expensive. O₂-conserving devices decrease the waste of oxygen to cut costs and maximize the duration of use of portable systems. A conserving device should be considered for patients who require flow rates greater than 2 L/min, who use liquid O₂, or who are active and spend more than 6 hours a day away from the stationary O₂ delivery system. Examples of conserving devices include reservoir nasal cannulas, pulsed O₂ devices, and transtracheal (TT) O₂ therapy. The reservoir nasal cannula allows for O₂ conservation by storing O₂ delivered from the equipment system in a reservoir during exhalation, which can result in an O₂ savings of 50% or more during rest. The pulsed O₂ delivery device, which allows for O₂ flow only during inhalation, can be attached to an ambulatory O₂ unit (Fig. 75-2). The TT catheter delivers O₂ directly into the trachea through an 18-gauge catheter. This delivery method is very efficient, decreasing the amount of O₂ use by 33% to 50%. Oxygen delivered by TT catheter may increase exercise tolerance more than other methods of O₂ delivery by decreasing inspired minute ventilation. Since the TT catheter can be concealed under a scarf or necktie, the patient has no reason to remove the O₂ source, which can improve compliance. Insertion of a TT catheter is an invasive procedure, however, and catheters may become obstructed, and local infection may occur. Patients must take an active role in catheter care and must be able to problem solve to achieve success. Interested patients should be referred to an established TT program for insertion and follow-up care.

[edit] Equipment systems.

The three major types of O₂ systems for use in the home are the O₂ concentrator, compressed O₂, and liquid O₂. The O₂ concentrator separates atmospheric O₂ from nitrogen (N₂) and delivers O₂. This system operates by electrical power and is not portable; thus it is the most acceptable system for the homebound or less active patient. The concentrator is economical, is low maintenance, and refills are not needed. Compressed O₂ is usually prescribed in conjunction with the O₂ concentrator as a portable source of O₂ therapy for the patient when away from home (Fig. 75-3). Compressed O₂ tanks of various sizes are provided on a stroller. These compressed sources need to be exchanged for full tanks when empty. Delivery schedules are usually arranged between the O₂ vendor and the patient. A more recent advancement is a portable concentrator that weighs approximately 35 pounds. This concentrator is A/C battery driven and is rechargeable from a cigarette lighter in an automobile. This state-of-the-art technology permits patients to travel without the need for refilling O₂ tanks. This O₂ delivery system costs approximately $3000 and is not covered by medical insurance. Liquid O₂ is 100% pure and provided to the patient in cylinders filled with cryogenic O₂ (Fig. 75-4) When the system is turned on, the O₂ is warmed to room temperature before delivery to the patient. For portability the patient can fill a shoulder-bag tank by attaching the portable tank to the main liquid O₂ reservoir. This portable liquid system weighs approximately 8 to 10 pounds and allows about 6 hours of O₂ at 2 L/min. The liquid O₂ system requires frequent refills by the O₂ vendor depending on the prescribed liter flow; therefore this is the most expensive O₂ delivery system and should be reserved for patients who are active and mobile.

[edit] Follow-up Evaluations.

LTOT is frequently initiated before discharge from an acute care facility before the patient's clinical pulmonary status has returned to baseline. Patients may no longer meet the criteria for LTOT after discharge. Therefore it is recommended that ABGs be repeated on room air, in a resting state, within 1 to 3 months after initiation of LTOT to reevaluate its need. If LTOT is continued, annual documentation of ABGs or oxyhemoglobin saturation by pulse oximetry is recommended to assess the patient's clinical and physiologic status. In contrast, if LTOT is discontinued, ABGs should be repeated 1 to 2 weeks after cessation to verify continued adequate oxygenation.

[edit] Air Travel

The pressure of inspired oxygen falls considerably with altitude because of a decrease in total barometric pressure. Commercial aircraft cruise between 22,000 and 44,000 feet above sea level. Hypoxemia can occur during air travel because the aircraft cabin is only pressurized to a median altitude of 6214 feet above sea level, which results in a significant decrease in inspired oxygen pressure. All travelers develop some degree of arterial oxygen desaturation during flight from the decrease in inspired oxygen, but patients with lung disease, including COPD, are particularly prone to develop significant hypoxemia. Patients at risk must be identified in advance. Those with ground-level, room air Pao₂ levels of less than 70 mm Hg should be referred to a pulmonary function laboratory for an evaluation that will determine the need for and amount of O₂ supplementation during flight. The most effective treatment of significant altitude hypoxemia is supplemental O₂ to attain a Pao₂ of at least 50 mm Hg during flight.Patients with COPD who are interested in air travel and need supplemental O₂ must contact the airline for specific policy details and instructions for authorization. A written medical statement from a physician is required at least 48 hours in advance of a scheduled flight for medical clearance. Commercial airlines provide their own supplemental O₂ equipment and will not accept the patient's equipment. The cost varies from approximately $40 to $150, depending on the number of cylinders used and the number of segments of the trip.

[edit] REFERENCES