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Crit Care Nurs Q Vol. 27, No. 4, pp. 336352 c 2004 Lippincott Williams & Wilkins, Inc.

Acute Exacerbation of COPD

Nursing Application of Evidence-based Guidelines
Cynthia Gronkiewicz, MS, RN, APRN; Marilyn Borkgren-Okonek, MS, RN, APRN
Nurses in acute care settings play a vital role in caring for individuals during an acute exacerbation of chronic obstructive pulmonary disease (COPD), the fourth leading cause of death in the United States. In addressing this health concern, the Global Initiative for Chronic Obstructive Lung Disease Report summarized the goals for COPD management and recommended treatment supported by current data and research. It is imperative that our clinical nursing practice is based upon research-supported interventions: use of appropriate medications, monitoring acid-base status, administering controlled oxygen therapy, assessing the need for mechanical ventilation, and close monitoring of comorbid illnesses. Health promotion includes patient and family education on early recognition of symptoms, smoking cessation strategies, and participation in pulmonary rehabilitation that can reduce long-term morbidity from this chronic disease. Key words: acute exacerbation, COPD, oxygen therapy, pharmacotherapy, pulmonary rehabilitation

HRONIC Obstructive pulmonary disease (COPD) is the fourth leading cause of morbidity and mortality in the United States. Despite this fact, COPD often goes unrecognized and undiagnosed until the individual presents during an acute exacerbation. The US National Heart, Lung, and Blood Institute and the World Health Organization formed the Global Initiative for Chronic Obstructive Lung Disease (GOLD). The objectives of the GOLD Expert Panel were to not only increase awareness of disease prevalence but also summarize and recommend treatment strategies to achieve the goals of effective COPD management: (1) prevent disease progression, (2) relieve symptoms, (3) improve exercise tolerance, (4) improve health status, (5) prevent and treat complications, (6) prevent and treat exacerbations, and (7) reduce mortality.1

In the same year the GOLD guidelines were published, the American College of Chest Physicians and the American College of Physicians-American Society of Internal Medicine released their 2001 position papers on management of an acute exacerbation of COPD.2,3 Because nurses in the acute care setting play a vital role in assisting individuals to achieve these goals during hospitalization, this article provides clinical application of these evidence-based recommendations. This article will describe a broad range of therapeutic interventions applicable across the spectrum of disease severity.

PATHOPHYSIOLOGY COPD is characterized by chronic inflammation throughout the central and peripheral airways, lung parenchyma, and pulmonary vasculature. This inflammation is caused by exposure to inhaled noxious particles and gases. When the normal protective mechanisms of the lungs and airways fail and no repair occurs, COPD evolves. Smoking causes 85% to 90% of all cases, although genetic

From the Suburban Lung Associates, Elk Grove Village, Ill (Ms Borkgren-Okonek); and the College of Nursing, University of Illinois at Chicago (Ms Borkgren-Okonek). Corresponding author: Cynthia Gronkiewicz, MS, RN, APRN, 847 Ashland Ave, River Forest, IL 60305 (e-mail: cindygronk@aol.com).

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Acute Exacerbation of COPD factors, passive smoking, occupational exposure, air pollution, and possibly hyperresponsive airways can also play a role.3,4 In addition to the inflammation, 2 other processes are thought to contribute to airway obstruction: an imbalance of proteinases and antiproteinases and oxidative stress. Neutrophil elastase is an enzyme that breaks down elastin (a protein), which is a main component of alveolar wall structure. A small percentage of patients have a hereditary form of COPD known as alpha1-antitrypsin (AAT) deficiency. Because they lack AAT, an antiproteinase protecting the lung from destruction by neutrophil elastase, symptoms of COPD can present as early as the third or fourth decade of life. Oxidative stress is thought to contribute to COPD because of an oxidant/ antioxidant imbalance. There is a decrease in antiproteinase (protective) activity that directly damages lung tissue by activating the destructive proteinases and promoting inflammation.5 This inflammation affects the lung in a variety of ways. In the central airways, inflammatory cells infiltrate the surface epithelium where the increase in goblet cells causes hypersecretion of mucus. The peripheral airways undergo repeated cycles of injury and repair to their walls, resulting in structural remodeling and scar formation. This eventually narrows the lumen, causing fixed airway obstruction. Both oxidative stress and the imbalance of the proteinases and antiproteinases are involved in destruction of the lung parenchyma where respiratory bronchioles become dilated and destroyed. In the most severe cases, the pulmonary capillary bed can also be affected. The increase in inflammatory-cell infiltration of the smooth muscle causes further thickening of the vessel walls. As the disease progresses, peripheral airway obstruction, parenchymal destruction, and pulmonary vascular abnormalities reduce the ability for gas exchange.5 The ventilation abnormality results from airway inflammation, edema, bronchospasm, and increased mucus production. The perfusion abnormality stems from hypoxia-induced

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constriction of the arterioles, an abnormal respiratory pattern, and respiratory muscle fatigue. These pathologic changes lead to the characteristics of the disease: mucus hypersecretion, ciliary dysfunction, airflow limitation, and gas exchange abnormalities. Expiratory airflow limitation is the hallmark of physiologic change seen in COPD. Approximately 85% of patients have chronic bronchitis in which the intermittent airway inflammation leads to frequent episodes of a productive cough. In emphysema, there is destruction of the infrastructure of alveoli and distal airspaces, which provide the elastic recoil. Progression of the disease causes hypoxemia and/or hypercapnia. Pulmonary hypertension, the major cardiovascular complication of COPD, develops along with cor pulmonale.4

CLINICAL ASSESSMENT Evaluation of the patient is based on the history, physical examination, spirometry results, and selected diagnostic tools. Tracheobronchial infections and environmental exposures are the most common causes of an acute exacerbation. Despite advanced technology, one third of admitted patients have no known cause for their exacerbation. Conditions that may mimic an exacerbation include pneumonia, pneumothorax, pleural effusion, pulmonary embolism, congestive heart failure, and arrhythmias. Dyspnea is usually the reason a patient seeks medical care. The initial history should include the length of worsening symptoms or the presence of new symptoms. Signs of worsening COPD include progressive dyspnea, an increase in frequency or severity of cough, orthopnea, paroxysmal nocturnal dyspnea, an increase in sputum volume, purulent sputum, an increased need for bronchodilators, use of a glucocorticosteroid burst, limitations in daily activities, or an increase in oxygen requirements. Wheezing and chest tightness may accompany dyspnea. Frequency, severity,

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CRITICAL CARE NURSING QUARTERLY/OCTOBERDECEMBER 2004 a pH level of more than 7.55. In the presence of right heart failure, ankle edema and jugular vein distention can be present. Clubbing of the fingers indicates longstanding disease. DIAGNOSTIC TESTS Spirometry is an objective measurement of airflow limitation and the gold standard for the diagnosis and assessment of COPD. However, in the acutely ill patient, even the simplest maneuver of lung function can be difficult. Previous spirometric results should be retrieved to provide baseline information of disease severity. A forced expiratory volume in 1 second/forced vital capacity (FEV1 /FVC) less than 70% and a postbronchodilator FEV1 less than 80% confirm the disease.1 Arterial blood gases are recommended in all patients with an FEV1 of less than 40% of predicted, with clinical signs of right heart failure or with significant respiratory distress. Respiratory failure is present when PaO2 is less than 60 mm Hg, with or without a PaCO2 of more than 45 mm Hg on room air. An arterial measurement should be obtained as oxygen saturations via finger or ear oximetry are less reliable and the carbon dioxide level is a critical entity. A PaO2 of less than 50 mm Hg, a PaCO2 of more than 70, and a pH level of less than 7.30 indicate a life-threatening episode requiring intensive care management.1 The baseline chest x-ray (CXR) of a patient with moderate to severe emphysema may reveal the presence of bullae formation, hyperinflation, and/or flattening of the diaphragm.6 In the acute setting, the CXR is necessary to exclude alternative diagnosis that can mimic symptoms of an exacerbation and to identify the presence of comorbid disease such as pneumonia, congestive heart failure, or pneumothorax. A repeat x-ray is suggested when the patients condition worsens or he/she fails to respond to initial treatment.1 Shortness of breath or chest tightness may also indicate cardiac disease. An electrocardiogram (ECG) assists in the diagnosis of rightventricular hypertrophy, arrhythmias, and ischemic episodes. Pulmonary embolism can

and likely causes of past exacerbations should be reviewed. In addition, past hospitalizations, length of stay, and need for intubation suggest a more severe baseline disease. A thorough history taking may be limited because of their significant work of breathing with speaking, and the clinician then proceeds with the physical examination. The general appearance of the patient should be observed for altered mental status, anxiety, confusion, drowsiness or somnolence, reflecting neurologic impairment due to hypoxia and/or hypercarbia. The patient may assume a tripod position and use pursedlip breathing to ease the air hunger. A respiratory rate greater than 25 breaths per minute, tachypnea, is of as much concern as a decreased rate and impending apnea. The attempt to exhale against narrowed airways produces a prolonged expiratory phase of the respiratory cycle. Accessory muscle use and retracted intercostal spaces indicate respiratory distress. One common sign of respiratory muscle fatigue is paradoxical respirations observed by asynchronous chest and abdominal excursions. Another clue to fatigue is respiratory alternans observed when a patient alternates between chest wall motion and abdominal movement. Both abnormal patterns reflect a transfer of the work of breathing from the diaphragm and fatigued respiratory muscles to the abdominal muscles during respiratory distress. Auscultation of the chest reveals a wide range of abnormal lung sounds. The breath sounds may be diminished or distant because of the severe hyperinflation of the lungs. Coarse rhonchi indicate secretions in the large airways. Airway narrowing from bronchoconstriction or edema produces wheezing. The sudden opening of collapsed airways or fluid in the smaller airways is reflected in the crackles detected during inhalation. The most ominous finding is never absence of breath sounds associated with minimal air exchange. The cardiovascular responses to hypoxemia and dyspnea include tachycardia and hypertension. Cardiac arrhythmias can occur with

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Acute Exacerbation of COPD be difficult to determine from an acute exacerbation in severe COPD, as right-ventricular hypertrophy and large pulmonary arteries can alter the ECG. The presence of any of these entities can affect therapeutic interventions in the acute phase. An increase in sputum volume and purulence often indicate a bacterial cause and a need for starting antibiotic treatment. The most common pathogens in this population are Streptococcus pneumoniae, Hemophilus influenza, and Moraxella catarrhalis. Between 10% to 20% of individuals with an acute exacerbation have 2 or more pathogens identified.7 A subgroup of patients are more likely to be colonized with resistant organisms such as Pseudomonas. This subgroup includes nursing home patients, patients recently treated with antibiotics, and those admitted to intensive care units (ICUs).4 Cultures are recommended only when a patient has no initial response to therapy. A complete blood count is useful in identifying bleeding or the presence of polycythemia (hematocrit > 55) in a patient with chronic hypoxia. The white blood cell (WBC) count is not as helpful as a nonspecific leukocytosis can be seen with use of corticosteroids. Electrolytes should be followed to exclude a chemistry imbalance as an etiology or contributing factor. Of primary concern is any metabolic acid-base disturbance that places a demand on an already-compromised respiratory system. Those patients taking methylxanthines require a theophylline level with the initial labs. Toxicity can occur with a variety of concomitant drugs or disease states.

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respond to initial medical management, the presence of significant comorbidities, new onset of arrhythmias, older age, insufficient home support, or diagnostic uncertainty.1 On arrival to the emergency department, the first intervention is to provide controlled oxygen therapy and to determine if the condition is life threatening and warrants immediate ICU admission. Indications for ICU admission are severe dyspnea not responding to emergency treatment, a change in mental status, persistent or worsening hypoxemia (PaO2 < 50 mm Hg) or severe hypercapnia (PaCO2 > 70 mm Hg), or severe respiratory acidosis (pH < 7.30) despite supplemental oxygen.1 THERAPEUTIC INTERVENTIONS Management of a severe exacerbation of COPD requires close monitoring for any change in clinical symptoms, precise delivery of controlled oxygen therapy, and judicious use of bronchodilator therapy. Close scrutiny of fluid balance and treatment of associated conditions require these patients to be in an ICU setting. The risk of dying from an acute exacerbation of COPD is closely related to the development of respiratory acidosis, the presence of significant comorbidities, and the need for ventilatory support.1,8 Being familiar with the most current recommendations for an acute exacerbation of COPD provides the nurse with both an understanding of chosen treatment protocols and an increased awareness of possible intervention strategies. MEDICATIONS

CRITERIA FOR INTENSIVE CARE UNIT ADMISSION The GOLD Report recommends hospital admission for an acute exacerbation of COPD in all patients with a history of severe COPD, a marked increase in symptom intensity such as resting dyspnea, the onset of new physical signs as cyanosis or edema, the failure to

Pharmacotherapy for COPD is used to decrease the symptoms and potential complications associated with an acute exacerbation. Although none of the current medications have been shown to prevent or slow the progressive decrease in lung function, they are critical in decreasing airway resistance during the acute phase. Bronchodilators and glucocorticosteroids are the foundation of

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Table 1. Pharmacotherapy summary for COPD

Medication Bronchodilators Beta2-agonists (short-acting) Albuterol, Terbutaline, Pirbuterol Beta2-agonists (intermediate-acting) Levalbuterol Beta2-agonists (long-acting) Formoterol, Salmeterol Anticholinergics Ipratropium bromide (short-acting) Tiotropium bromide (long-acting) Combination agent Albuterol/Ipratroprium Methylxanthines Aminophylline, Theophylline Corticosteroids Systemic Prednisone Methylprednisolone Inhaled Flunisolide Budesonide Fluticasone Triamcinalone Beclomethasone Bronchodilator/steroid combination Salmeterol/Fluticasone

Acute management

Stable management

Nebulizer or MDI with spacer Nebulizer or MDI with spacer every 4 h every 4 h as needed Nebulizer every 68 h Nebulizer every 68 h Not recommended DPI every 12 h

Nebulizer or MDI every 46 h Nebulizer or MDI every 46 h Not recommended Once daily Nebulizer or MDI with spacer Nebulizer or MDI with spacer every 46 h every 46 h Continue oral dose to achieve Continue oral dose to achieve level 815 mg/L level 815 mg/L 3040 mg po for 1014 days Equivalent intravenous dose Not recommended

Not recommended Most administered twice daily

Not recommended

DPI every 12 h

Budesonide only ICS also delivered via nebulizer; other ICS are in MDI or DPI forms.

pharmacotherapy in both acute and chronic COPD (Table 1). Bronchodilators Bronchodilators are critical to the symptomatic management of COPD to prevent or reduce symptoms. The key bronchodilators are beta2-agonists (albuterol), anticholinergics (ipratropium bromide), methyl xanthines (theophylline), or a combination of these agents. Short-acting inhaled beta2-agonists are the preferred treatment. The addition of an anticholinergic is recommended even though evidence of combination effectiveness is controversial. Several reports suggest that com-

bination therapy produces an added benefit without the side effects of a higher dose of 1 agent.1,3,9 Beta2-agonists produce bronchodilation, improve hyperinflation, decrease dyspnea, reduce airway hyperresponsiveness, increase ciliary activity, and inhibit inflammatory mediator release from mast cells and basophils. Beta2-receptors on airway smooth muscle are activated by circulating catecholamines to antagonize muscle contraction and produce bronchodilation. These circulating catecholamines also stimulate beta-receptors to modulate acetylcholine release and decrease bronchomotor tone.9

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Acute Exacerbation of COPD In the acute setting, short-acting beta2agonists are preferred because of their rapid onset of action. It is recommended these drugs be delivered through the inhaled route to minimize systemic toxicity: albuterol 2 to 4 puffs every 4 hours by MDI with a spacer, or the use of albuterol 2.5 mg in an aerosolized formulation by a handheld nebulizer or in-line with the ventilator circuit. Higher doses may increase side effects without improving bronchodilation. The most common side effects are attributed to the beta-receptor stimulation: tachycardia, palpitations, tremors, headaches, and excitability. Hypokalemia can occur with higher doses of beta2-agonists and may be potentiated by concomitant use of corticosteroids. Hence, cardiac monitoring should be used in patients with new-onset cardiac disease and the elderly. Inhaled anticholergic agents are a key component of COPD management. Some clinicians recommend starting these agents before beta2-agonists because of fewer and milder side effects.2 There are multiple cholinergic receptors present in the lung that stimulate smooth muscle contraction and mucous gland secretion. These medications can produce equal or greater bronchodilation than do betaagonists, reduce mucous hypersecretion, and decrease dyspnea. Anticholinergics produce a slower onset of action, but a longer duration of action than beta2-agonists. Recommended dosing is ipratropium bromide 2 to 4 puffs by metered dose inhaler with a spacer device 4 times per day. This can also be delivered as a 0.25- to 0.5-mg solution with or without albuterol in the nebulizer or in-line with the ventilator. Because these agents do not readily cross biologic barriers, there are minimal side effects. Most complaints are of a dry mouth, a metallic taste, nausea, or blurred vision.9 The role of methylxanthines remains controversial, with the most recent guidelines showing no additional role for parental use in the acute phase. The direct bronchodilator effects result from selective inhibition of phosphodiesterase receptors. Inhibition of some of these receptors have anti-inflammatory ef-

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fects. These medications have been shown to produce bronchodilation, improve diaphragm function, increase mucociliary clearance, and improve pulmonary vasodilation so as to improve right-ventricular function.2 Numerous side effects are associated with theophylline because of its narrow therapeutic range. Recommended serum levels are 8 to 15 mg/L when continuing an oral agent. Close monitoring of these levels is required because of side effects and potential drug interactions. Initial complaints include gastrointestinal distress or tremors, but arrhythmias and seizures are also risks of therapy. Serum levels can be affected by hepatic disease, phenytoin, macrolides, quinolones, or cimetidine.9 Anti-inflammatory agents The use of systemic corticosteroids suppresses the inflammatory process in the airways and lungs to improve airflow and gas exchange. Steroid use in the acute phase has been shown to improve symptoms, help restore lung function more quickly, shorten recovery time in reducing hospital days, decrease treatment failure rates, and reduce relapse rates.2 Patients receiving steroids on arrival to the emergency department showed significant improvement over the first 6 hours of treatment.10 Although the exact dose has not been determined, an oral or intravenous (IV) equivalent of prednisone 30 to 40 mg/d for 10 to 14 days is recommended for all hospitalized patients during an acute exacerbation. This dose is a balance between efficacy and safety, with prolonged treatment after 2 weeks increasing the risk of side effects without additional benefits, especially in the elderly population.1,11 The adverse effects seen on a short-term basis that warrant close nursing monitoring are transient hyperglycemia, hypertension, gastric irritation, risk of infection, psychological effects, and cutaneous effects. Antibiotics Bacteria can contribute to airway damage and accelerate airway obstruction. More than

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CRITICAL CARE NURSING QUARTERLY/OCTOBERDECEMBER 2004 and coughing following inhaled bronchodilators can facilitate airway clearance. Although some patients report subjective relief from mucolytic agents, no study supports their use.1,2,4 Similarly, neither inhaled hypertonic saline nor expectorants have any mucolytic action. Because cough plays a valuable and protective role in airway clearance, antitussives are contraindicated. Decongestants should also be used with caution as they have the potential to increase sputum viscosity and impair secretion clearance.9 Controlled oxygen therapy Correcting hypoxemia is the cornerstone of acute medical treatment. Oxygen relieves pulmonary vasoconstriction and right heart strain and lessens myocardial ischemia to improve cardiac output. A saturation goal of 90% ensures adequate oxygen delivery and preservation of organ function.4 Judicious use of oxygen is critical as a gradual rise in carbon dioxide can occur with minimal change in a patients symptoms. Supplemental oxygen can be delivered via nasal cannula or venturi mask. Low flow rates by cannula increase the inspired oxygen concentration by 3% to 4% for each increase of liter flow per minute. However, the oxygen flow rate via cannula varies with the patients own respiratory rate. Venturi masks provide more precise oxygen delivery than does nasal cannula but not all patients can tolerate a device covering the face. These devices are initially set to deliver 24% to 28%. Once oxygen therapy is initiated, a follow-up ABG in 30 minutes is recommended to ensure adequate oxygenation without excessive CO2 retention. A mild elevation in PaCO2 is acceptable when striving for an adequate level of oxygenation. If adequate oxygenation is not achieved or respiratory acidosis worsens, assisted ventilation may be required.1,13 Ventilatory support The primary objectives for using mechanical support during an acute exacerbation are to relieve symptoms and to decrease mortality and morbidity. Ventilatory support includes

half of COPD patients have a lower respiratory tract colonized with bacteria. This is most likely from impaired host defenses and the inflammatory process. The early use of antibiotics is recommended for patients with worsening dyspnea and cough who have an increase in sputum volume and purulence. The particular antibiotic selected should be one with sensitivity to the most common pathogens: S. pneumoniae, H. influenza, and M. catarrhalis.1 Broad-spectrum antibiotics are recommended for hospitalized patients: macrolides, cephalosporins, amoxicillin/ clavulanate, or doxycycline. Critically ill patients risk factors of FEV1 less than 50% of predicted, comorbid illness, or recent exacerbations require gram-negative coverage with fluoroquinolones. Ciprofloxacin is preferred if Pseudomonas aeruginosa is suspected.12 In those with a suboptimal or no initial response to therapy, those with recent or recurrent hospitalizations, or patients with recent antibiotic use, cultures should be sent to identify the organism or a potentially resistant strain. Respiratory stimulants Respiratory stimulants are not recommended for the treatment of hypoxemia or hypercapnia in COPD patients. The stimulating effects of these agents are short acting, there are numerous side effects, and the stimulation of already-overworked respiratory muscles may worsen respiratory failure.9 Respiratory therapy The GOLD Report recommends manual or mechanical chest percussion and postural drainage in those patients producing more than 25 cc of sputum each day as well as in those with lobar atelectasis. Patients should be evaluated on an individual basis as some cannot tolerate the various position changes required for effective drainage. The effort expended to clear copious amounts of sputum can exhaust the already dyspneic patient. For some, instruction on effective deep breathing

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Acute Exacerbation of COPD both noninvasive positive-pressure ventilation (NIPPV) via a tight-fitting mask and invasive positive pressure ventilation by tracheal intubation. NIPPV is considered the first choice of ventilation mode for an acute exacerbation of COPD.14 As worsening hypoxemia, hypercapnia, and acidosis increase the ventilatory demands of the respiratory muscles, the use of NIPPV allows these muscles to rest until the underlying airway problems reverse.2,7 This intervention decreases breathlessness, improves oxygenation, reduces PaCO2 , increases pH, reduces hospital mortality, decreases the need for invasive mechanical ventilation and intubation, decreases the incidence of nosocomial pneumonia, and decreases the number of both ICU and hospital days.7 However, NIPPV is not appropriate for all patients. At least two of the following criteria should be present prior to initiation: moderate to severe SOB with accessory muscle use and evidence of respiratory muscle fatigue, acidosis (pH 7.307.35), hypercapnia (PaCO2 45 to 60 mm Hg), or a respiratory rate of greater than 25 breaths per minute.1,7 Individuals to be excluded from use of NIPPV are those with copious secretions, respiratory arrest, cardiovascular instability (hypotension, arrhythmias, new myocardial infarction), decreased mental status, somnolence, poor cooperation, or a high risk of aspiration. These individuals underlying condition compromises the effective use of a secure fitting mask to maintain positive pressure through the airways.1 In those patients who fail a trial of NIPPV and there is impending respiratory failure, conventional mechanical ventilation must be initiated. It is also indicated for any COPD patient with severe SOB and evidence of respiratory muscle fatigue, a respiratory rate greater than 35 breaths per minute, hypoxemia (PaO2 < 40 mm Hg), severe acidosis (pH < 7.25), hypercapnia (PaCO2 > 60 mm Hg), somnolence or a decreased mental status, or cardiovascular conditions such as hypotension or shock. Complications such as sepsis, a se-

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vere metabolic abnormality, pneumonia, pulmonary embolism, or barotrauma may necessitate the need for ventilatory assistance.1,14 The most common modes of mechanical ventilation used are assist- control ventilation, pressure-support ventilation alone or in combination with intermittent mandatory ventilation. Mechanical ventilation is appropriate when the current cause of the acute exacerbation is reversible and when it is in compliance with the individuals desire for its use. The major risks include ventilator-acquired pneumonia, barotrauma, and failure to wean. Patients requiring mechanical ventilation for more than 72 hours are at an increased risk for death and long-term ventilatory support.15 Mortality among COPD patients with respiratory failure is no greater than mortality among patients on mechanical support for non-COPD causes. Again, advance directives and a living will can facilitate the clinicians decision making prior to this point.1 TREATMENT OF COMORBID DISEASE In addition to the need for ventilatory support, the GOLD Report states that the risk of dying from an acute exacerbation of COPD is closely related to the presence of a comorbidity.1,8 Cor pulmonale, pulmonary hypertension, and heart failure commonly coexist with COPD, but adequate oxygen levels and COPD management can halt their progression. The use of diuretics can improve right- and left-ventricular functions in some patients. Close monitoring for hypotension or any fluid/electrolyte imbalance is crucial.9 Hyponatremia, hypokalemia, hypomagnesia, or an elevated BUN/creatinine can result from diuretic therapy. Meeting nutritional needs Serum chemistries may also reveal the existence of low proteins often associated with malnutrition. Weight loss is a component of the disease progression, and nutritional intervention is part of comprehensive management during the acute phase. Nutritional

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CRITICAL CARE NURSING QUARTERLY/OCTOBERDECEMBER 2004 cant cognitive and psychological impairment related to hypoxemia as well as the stress and disability of their disease. These emotions often get magnified during an acute exacerbation. Depression is frequently unrecognized and may manifest as anxiety or insomnia. Anxiety itself can be a cause or result of the dyspnea and potentially interfere with management of the underlying exacerbation. Treatment of the presenting physical condition needs to be maximized along with a calm and reassuring approach by the healthcare team. Providing adequate time for therapeutic interventions and deferring to patients preferences when feasible can reduce anxiety. When anxiety or depression is an obstacle to management of a life-threatening exacerbation, psychological and pharmacological interventions should be pursued. Buspirone is a mild anxiolytic without respiratory depression effects. The serotonin-selecting reuptake inhibitors are commonly prescribed to treat both depression and anxiety.9 Prevention of complications Critically ill patients are more susceptible to developing upper gastrointestinal bleeding from stress ulceration. Previously, routine treatment included prophylaxis against stress ulceration. Current findings cite the high cost and incidence of side effects (an increased risk of nosocomial or ventilator-assisted pneumonia) as reason to treat only those at high risk of developing clinically significant bleeding. High-risk patients include those on mechanical ventilation for more than 48 hours, those with hypotension or shock, victims of major trauma, or those with a history of ulcers or previous GI bleeding. Recommended first-choice agents are H2 blockers: ranitidine 50 mg every 8 hours or famotidine 20 mg every 12 hours.18 Low-molecular-weight heparin or low-dose unfractionated heparin should be instituted in patients who are immobilized, dehydrated, or polycythemic with or without a history of thromboembolic disease. Prevention of deep vein thrombosis includes early

depletion contributes to peripheral skeletal muscle wasting, a decrease in diaphragm muscle mass, impairment of ventilatory drive, and immune dysfunction.13 Weight loss is a factor in poor outcomes of acute exacerbations and has been associated with increased morbidity and mortality.8,13,16 Patients with COPD have a higher resting energy expenditure from the work of breathing, an increased activity-related energy, and a low-dietary intake all contributing to weight loss and muscle wasting. Weight loss, particularly fat mass, occurs when energy expenditure exceeds the dietary intake. The low intake is attributed to the dyspnea and oxygen desaturation associated with chewing, swallowing, and alteration in respiratory pattern. Gastric filling may limit diaphragm excursion, reduce functional residual capacity, and increase dyspnea. The negative energy balance during an acute exacerbation stems from an increase in resting energy expenditure and the temporary decrease in dietary intake. The 2 factors contributing to weight loss and muscle wasting during acute exacerbations are the increased dyspnea and fatigue and the use of high doses of glucocorticosteroids.17 Optimal nutritional support strategies are critical at this time and in improving survival time after discharge.8 Goals include both maintaining body weight and preventing protein breakdown. Daily protein intake should include at least 1.5 mg/kg of body weight for optimal protein synthesis. Reduced dietary intake is also characterized by a restricted fat intake.17 Providing nasal cannula with meals and monitoring oximetry ensure adequate oxygenation. Offering nutritional supplements between small meals reduces the sensation of gastric fullness to further reduce dyspnea. Encouraging initial activity such as getting out of bed can further stimulate the patients appetite. Treatment of anxiety and depression Anxiety and depression are additional comorbid conditions frequently contributing to dyspnea in COPD. Patients may have signifi-

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Acute Exacerbation of COPD mobility, adequate hydration, and avoiding prolonged bedrest.19 Nurses play the key role in early mobilizing and positioning of the patient. There are physiological benefits to elevating the head of the bed, getting the patient out of bed, sitting upright in a chair, and early ambulation. Repositioning improves drainage from the upper lobes, increases diaphragm excursion, improves volume changes in the lower lobes, and mobilizes secretion clearance. An elevated head of the bed improves cough efficacy due to a greater ability to increase intraabdominal pressure. The overall net effect is reducing ventilation/perfusion mismatch and improving oxygenation.20 In addition, the elevated head can decrease the risk of pneumonia in ventilated patients.21 As many patients presenting during an acute exacerbation are severely deconditioned or debilitated because of their significant dyspnea and muscle wasting, every effort should be made to prevent further decompensation associated with inactivity. These individuals are at increased risk for morbidity and mortality. Connors et al reported data on a group of over 1000 patients with severe COPD (PaCO2 50 mm Hg) admitted to 1 of 5 tertiary hospitals. There was an 11% to 24% mortality rate in patients needing ICU admission. Although 89% survived the hospital stay, there was a 33% risk of death over the next 6 months, a 42% risk at 1 year, and a 49% risk at 2 years. Fifty percent were readmitted in the 6 months after discharge and reported a fair to poor quality of life, dependence on others for some daily care, and limitations from dyspnea and cough. Only 26% reported a good to excellent quality of life.8

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sequelae. Preparation of the COPD patient for discharge from the hospital requires coordination among several disciplines. The attending provider or pulmonary consultant identifies the expected discharge date based on the patients clinical improvement, while supporting team members contribute information regarding the patients functional status, oxygenation, and home care needs. All team members including the staff level or advanced practice pulmonary nurse, respiratory therapist, physical and occupational therapists, and social worker or discharge planner must communicate with the provider, patient, and family to ensure a smooth transition from hospital to home. Patients with COPD are at risk for recurrent exacerbations and admissions.22 Optimal coordination, patient education, and referrals for follow-up help to minimize the potential for repeated hospitalizations. The GOLD guidelines identify the following criteria to determine a patients readiness for discharge.1 Arterial blood gases and clinical status must be stable for 12 to 24 hours. In addition, the need for inhaled bronchodilator therapy (beta2-agonist and/or anticholinergic agent) should be no more than every 4 hours. The patient or home caregiver must understand the medication regime. If ambulatory prior to admission, the patient should be able to walk across the room at near his baseline level of dyspnea. The patient must also be able to sleep and eat without dyspnea. Finally, arrangements for home nursing care, home physical therapy, respiratory equipment, and meals are to be completed before discharge. Home oxygen therapy If oxygen is ordered, Medicare requires that the qualifying data be obtained no more than 2 days prior to discharge on the basis of the expectation that poor oxygenation on admission improves during and after the hospital stay. The need for oxygen therapy is assessed both at rest and with ambulation and requires an oxygen saturation below 89% or a PaO2 less than or equal to 55 mm Hg on room air. With concomitant conditions such

PREPARATION FOR DISCHARGE While Connors et als study focused on those with severe COPD, the data lend support to the need for early intervention during an acute exacerbation in all COPD patients to prevent long hospital stays and the associated

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CRITICAL CARE NURSING QUARTERLY/OCTOBERDECEMBER 2004 proves lung mechanics, exercise capacity, hemodynamics, mental acuity, and hematologic characteristics.25,26 Dyspnea may be ameliorated (but not always eliminated) by use of supplemental oxygen. Patients must understand that oxygen is a medication to be used as prescribed rather than as needed to relieve shortness of breath. Hypoxemia may occur with or without dyspnea. Medications for stable COPD Patient education regarding the home medication regime is of paramount importance. At the time of discharge, most patients are prescribed both oral and inhaled medications. Whether or not a patient is new to the diagnosis of COPD, correct use of inhaled medications warrants frequent and repeated instruction. The patient or home caregiver must be able to demonstrate correct use of the inhaled medication, either by nebulizer, metered-dose inhaler with spacer device, or by one of the new dry powder, propellant-free devices. As new inhaled delivery devices become available, hospital and home care nursing staff must learn correct techniques for their administration. Bronchodilator therapy is the foundation of symptom management in stable COPD, and the inhaled route of administration is preferred.1 On the basis of the GOLD recommendations, bronchodilator medications are prescribed on an as-needed or routine basis to prevent or reduce cough, dyspnea, and wheezing. While short-acting agents are favored during inpatient treatment of an acute exacerbation, long-acting medications offer the convenience of once- or twicedaily administration in the home or extended care setting. The available long-acting beta2agonists are salmeterol (discus device) and formoterol (an encapsulated dry powder delivery system). Both agents have acceptable adverse event profiles including mild tachycardia and tremor. In addition, these medications have shown benefits over theophylline and the short-acting anticholinergic ipratropium in improving symptoms, FEV1 , and

as cor pulmonale, pulmonary hypertension, polycythemia, or heart failure, a PaO2 between 55 and 60 mm Hg qualifies a Medicare patient for home oxygen. Other insurance payors may or may not require that a patient meet these standardized criteria for coverage of home oxygen. For COPD patients not previously requiring home oxygen, a reassessment of rest and ambulatory oxygenation is indicated within 1 to 3 months following the exacerbation. Up to 30% of these patients will improve substantially and no longer require supplemental oxygen.23 The inpatient respiratory and/or physical therapist perform resting and exercise oximetry or blood gases. If hypoxemia is present, an individualized titration evaluation is undertaken to determine the supplemental oxygen flow rates required to maintain a PaO2 greater than or equal to 60 mm Hg or SpO2 greater than or equal to 90% at rest and during the patients usual activity level. Continuous overnight oximetry assessment may help determine oxygen needs during sleep. However, sleep-disordered breathing is present in 10% to 15% of patients with COPD alone and cannot effectively be evaluated without a full polysomnographic study. The incidence of apnea (eg, obstructive or central sleep apnea) may be greater in high-risk patients with comorbidities including obesity and cardiovascular disease. Ideally, the home oxygen prescription includes the source of oxygen (gas or liquid), method of delivery, and specific flow rates at rest, during sleep, and with exercise. Following discharge, the pulmonary team will identify the optimal oxygen delivery system to meet an individual patients lifestyle needs. Oxygen systems that offer ease of use and portability such as lightweight gas tanks, liquid oxygen systems, and other conserving devices (eg, pulse delivery, reservoir cannula, or transtracheal oxygen delivery) enhance compliance with prescribed oxygen therapy. Long-term administration of oxygen (15 18 h/d) is the only medical therapy shown to increase survival in COPD patients with chronic hypoxemia.23,24 Oxygen also im-

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Acute Exacerbation of COPD quality of life, while reducing exacerbation rates.2729 The new, once-daily anticholinergic agent tiotropium significantly reduces exacerbations and improves pulmonary function, symptoms, health status, and exercise capacity.28,30,31 For some patients, maintenance treatment will consist of 1 or more long-acting bronchodilator medications taken regularly and then supplemented by a short-acting agent as needed.28 Others prefer routine (eg, up to QID) dosing of short-acting beta-adrenergic plus anticholinergic combination therapy, a regimen shown to produce greater improvements in FEV1 than single-drug therapy with albuterol or ipratropium alone.32 This standard regime may be administered by nebulizer or metered-dose inhaler. A recent meta-analysis on the effectiveness of oral theophylline in stable COPD revealed the drug has a modest effect on FEV1 and FVC and slightly improves arterial blood gases in patients with moderate to severe COPD.33 However, because of potential adverse effects, multiple drug interactions, and the need for serum drug level monitoring, theophylline is seldom first-line therapy for stable COPD in recent years. The choice between various bronchodilator regimes, single or combination agents, and delivery systems depends on disease severity, medication availability, affordability, and the individual patients subjective perception of symptom control and side effects.1,28 All bronchodilators have been shown to produce temporary improvement in FEV1 and increase exercise capacity, despite their inability to prevent long-term decline in pulmonary function.1 Glucocorticosteroids are the second category of pharmacologic agents prescribed for patients with acute or stable COPD. Evidence is lacking regarding benefit from longterm systemic corticosteroid therapy. The usual duration of short-term therapy is 10 to 14 days beginning in the hospital parenterally or by mouth, and continued in tapering oral doses following discharge. Significant adverse effects may develop in patients receiving months or years of sustained

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treatment with oral corticosteroids including hyperglycemia, cataracts, and cushingoid appearance with truncal weight gain. Furthermore, osteoporosis and steroid myopathy are important contributors to muscle weakness, deconditioning, and progressive disability in patients taking systemic corticosteroids. Therefore, chronic use of these drugs is not recommended for maintenance treatment of COPD.1 In contrast, long-term treatment with inhaled corticosteroids should be considered for select patients; ie, patients with moderate to severe COPD (FEV1 < 50% of predicted) experiencing frequent exacerbations or those demonstrating spirometric improvement related to inhaled steroid therapy (FEV1 increased by 15% and 200 mL).1 A trial of 6 weeks to 3 months is recommended.1 Reduced rates of exacerbation and hospitalization have been shown in studies of longterm inhaled corticosteroid therapy when used alone or in combination with long-acting bronchodilators.29,34 Safety outcome analyses confirm that minimal systemic absorption or effects occur when inhaled corticosteroids are taken at recommended dosages. Most recent studies of inhaled corticosteroid efficacy in COPD evaluated the medications budesonide (available in both turbuhaler and nebulizer solution) and fluticasone (metered-dose inhaler or combined with salmeterol in the discus device). Older agents still available as metered-dose inhalers include triamcinolone, beclomethasone, and flunisolide. Hoarseness, dry mouth, and oral candidiasis are the chief adverse effects of inhaled steroid therapy. Their incidence is minimized by use of a spacer device (with metered-dose inhalers) and by thoroughly rinsing the mouth after administration of these agents. Smoking cessation Comprehensive discharge education also includes discussion of pharmacotherapy initiated to aid in smoking cessation for current or recent smokers. Smoking cessation is the single most effective (and cost-effective) approach to halt progression of COPD.1

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CRITICAL CARE NURSING QUARTERLY/OCTOBERDECEMBER 2004 treatment regimen, and oxygenation.1 Strategies to prevent future exacerbations should also be reviewed. A majority of exacerbations are caused by viral or bacterial infection. Patients with COPD are at high risk for pneumonia and severe illness related to influenza infection. Thus, vaccination against influenza and pneumococcal infections is recommended for all patients with mild to severe COPD.1,38,39 The influenza vaccine is reformulated annually and should be administered intramuscularly beginning in October. At present the intranasal influenza vaccination is not recommended for patients with airway disease. The current 23-valent pneumococcal vaccine has greater than 60% efficacy in producing antibodies in immunocompetent patients following a single administration.9 Vaccination may fully prevent or minimize the severity of pneumococcal illnesses including pneumonia, bacteremia, or meningitis caused by S. pneumoniae bacterial infection. Revaccination is recommended after 5 years when a patients initial vaccination occurred before age 65.39 This vaccine can be administered during any time of the year. Recognizing the onset of an exacerbation can be difficult, as the severity of COPD symptoms may vary from day to day. Sudden or progressive dyspnea, decline in ability to perform routine activities, or infectious signs or symptoms should prompt the patient or caregiver to seek medical evaluation. Avoidance of extended outdoor exposure or strenuous outdoor activity during high-pollution conditions is also advised as a preventive measure. Patients at highest risk for hospitalization with exacerbations are those with low body mass index (20 kg/m2 ), limited baseline ambulatory capacity, abnormal gas exchange (baseline hypoxemia or hypercarbia), and pulmonary hypertension.40 Discussion of advance directives should be initiated with the patient and family at the posthospital visit, especially in those patients suffering from severe lung disease, multiple comorbidities, repeated hospitalizations, or a history of respiratory failure. Although

A 5-step intervention approach is outlined for healthcare providers in the US Public Health Service document Treating Tobacco Use and Dependence: A Clinical Practice Guideline.35 Practical counseling, formal group support treatment, and social support outside a formal smoking cessation program are the most effective nonpharmacologic strategies. If needed, nicotine replacement medications may be started during or after treatment of an acute exacerbation of COPD in the absence of medical contraindications. All forms of nicotine replacement therapy (gum, transdermal patch, inhaler, nasal spray, and lozenge) increase long-term smoking abstinence rates.1 Usual protocols for nicotine replacement products range from 6 to 12 weeks.9 Other medications have been utilized to minimize symptoms of nicotine withdrawal including anxiolytics (buspirone or benzodiazepines), antidepressants (buproprion), and the alpha2-agonist clonidine.9 Combining nicotine replacement therapy with behavioral counseling or with other medications (eg, buproprion) results in abstinence rates in the 30% to 40% range, as compared with 6- to 12month abstinence rates of 20% to 25% using single therapy.36,37 In COPD, successful long-term pharmacologic intervention and compliance depend upon thorough patient education regarding medication purpose, expected benefits, proper dosing and administration, and potential side effects.9 Collaborative management helps the provider and the patient evaluate treatment efficacy and tailor an individualized medication regime to achieve optimal control of symptoms. DISCHARGE FOLLOW-UP Follow-up assessment is recommended 4 to 6 weeks after hospital discharge for patients recovering from acute exacerbations of COPD. At this office visit, the provider evaluates the patients functional capacity (ability to manage activities of daily living in the home environment), FEV1 , medication efficacy, inhaler device technique, understanding of the

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Acute Exacerbation of COPD previous reports indicate that pulmonary function predicts mortality, recent work reveals that the severity of dyspnea is a better predictor of 5-year survival.41 The following characteristics are associated with increased risk of death from COPD within 1 year: FEV1 less than 30% of predicted, declining independence in simple activities of daily living, walking distance limited to a few steps, more then 1 hospitalization within the past year, chronic comorbid illness, depression, living alone, and older age.42 Hospice referral is indicated when life expectancy is less than or equal to 6 months and quality of life is poor related to distressing dyspnea and severely limited activity tolerance. Pulmonary rehabilitation For the majority of patients with COPD, referral to a pulmonary rehabilitation program is indicated. Pulmonary rehabilitation is defined as a multidisciplinary, individually tailored program of education and exercise designed to maximize functional capacity and self-management skills in patients with COPD.43 Key elements of a comprehensive pulmonary rehabilitation program are medical evaluation, goal setting, application of therapeutic modalities (skeletal and respiratory muscle training, psychological counseling, breathing retraining, nutritional counseling, education, smoking cessation), and outcome assessment. Extensive research has confirmed the benefits of rehabilitation in patients with mild to severe COPD.44 Increased exercise tolerance, reduced dyspnea and fatigue, and improved quality of life have been demonstrated in numerous controlled trials.43,45 Reduced hospitalization has also been reported.43 Although pulmonary rehabilitation does not significantly improve spirometric measurements of lung function, it is widely recognized as critical therapy to optimize the physical and psychological status of individuals with chronic respiratory impairment. Activity limitation in COPD is attributed to a cycle of factors including impaired lung and respiratory muscle me-

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chanics, skeletal muscle weakness, dyspnea, anxiety, and deconditioning. Physiologic abnormalities cause dyspnea on exertion. As a result, patients develop fear of exercise and often cope by reducing their overall level of activity causing progressive deconditioning and disability.43 Successful pulmonary rehabilitation programs can be conducted in hospital, outpatient, or home settings.46 Several components of pulmonary rehabilitation can be implemented during hospitalization or in a temporary, postdischarge extended care facility. For example, physical and occupational therapies provide instruction on breathing retraining and energy-conservation strategies for activities of daily living. Pursed-lip breathing and diaphragmatic breathing are commonly taught and may reduce dyspnea for some, but not all, patients. Diaphragmatic breathing can be detrimental to those individuals with severe COPD and marked hyperinflation by causing thoracoabdominal paradox and increased fatigue.47 Pursed-lip breathing involves slow inhalation through the nose and prolonged exhalation over 4 to 6 seconds through lightly pursed lips to prevent airway collapse in patients with reduced elastic recoil.43 Airway clearance strategies including postural drainage, chest physiotherapy, and effective cough techniques are advised for patients with chronic sputum production. Finally, the dietitian conducts a nutritional assessment and develops an individualized plan for optimal nutritional repletion or weight reduction as indicated. Education, psychosocial support, and exercise comprise the principal components of outpatient pulmonary rehabilitation. Among these interventions, exercise training is the foundation.46 Patients undergo exercise or chemical-induced stress testing prior to entry to establish baseline exercise capacity, provide data for the exercise prescription, and exclude unstable cardiovascular disease. The optimal strategies for exercise training modality and intensity in COPD are not fully clear.45 Studies demonstrate efficacy when cycle ergometry, treadmill or free walking,

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CRITICAL CARE NURSING QUARTERLY/OCTOBERDECEMBER 2004 Most outpatient pulmonary rehabilitation programs in the United States are 4 to 12 weeks in duration. Patients must continue exercising for a long term on their own or in a maintenance phase of the formal program to sustain initial benefits. Research reveals that patients with severe COPD require programs lasting at least 6 months to achieve significant improvements in exercise tolerance and health status.44 The socialization offered to patients and families through participation in rehabilitation or support groups helps to reinforce positive health practices while reducing feelings of isolation and anxiety. Psychosocial support, professional counseling, and antidepressant therapy, if indicated, should be available to all patients having difficulty coping with chronic respiratory disease. In conclusion, application of evidencebased guidelines enables healthcare professionals to minimize morbidity and complications from this prevalent chronic disease. Nurses provide the vital link in improving the quality of life for COPD patients from acute hospital care through home management.

stair-climbing, weight training, and upper extremity exercise regimens are used alone or in combination. Exercise sessions should be conducted at least 3 times each week for 30 to 45 minutes to achieve desired goals.43 Inspiratory muscle training (IMT), using small handheld devices, reduces dyspnea and improves the strength and endurance of respiratory muscles in patients with COPD.48 Results are most favorable when IMT is incorporated into a program of aerobic exercise such as walking or cycling.49 Not all patients have access to formally structured programs. Inadequate insurance coverage, lack of transportation, geographic distance, or other medical conditions (eg, severe orthopedic limitations, unstable cardiac disease) will preclude participation in rehabilitation for some patients. Nevertheless, all patients should be provided basic components of rehabilitation over an extended time continuum to improve clinical outcomes and functioning.43 A simple walking program should be prescribed to patients at the time of discharge or at the postdischarge office evaluation if formal rehabilitation is not feasible. REFERENCES
1. Pauwels RA, Buist AS, Calverley PMA, Jenkins CR, Hurd SS. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2001;163:12561276. 2. Snow V, Lascher S, Mottur-Pilson C. Evidence base for management of acute exacerbations of chronic obstructive pulmonary disease. Ann Intern Med. 2001;134:595599. 3. Bach PB, Brown C, Gelfand BA, McCrory DC. Management of acute exacerbation of chronic obstructive pulmonary disease: a summary and appraisal of published evidence. Ann Intern Med. 2001;134:600620. 4. McCrory DC, Brown C, Gelfand SE, Bach PB. Management of acute exacerbations of COPD: a summary and appraisal of published evidence. Chest. 2001;119:11901209. 5. Barnes PJ. Chronic obstructive pulmonary disease. N Engl J Med. 2000;343(4):269278. 6. Cleverley JR, Muller NL. Advances in radiologic assessment of chronic obstructive pulmonary disease. Clin Chest Med. 2000;21(4):653663.

7. Heffner JE, Highland KB. Chronic obstructive pulmonary disease in geriatric critical care. Crit Care Clin. 2003;19:713727. 8. Connors AF, Dawson NV, Thomas C, et al. Outcomes following acute exacerbation of severe chronic obstructive lung disease. Am J Resp Crit Care Med. 1996;154:959967. 9. Ferguson GT. Update on pharmacologic therapy for chronic obstructive pulmonary disease. Clin Chest Med. 2000;21(4):723738. 10. Bullard MJ, Liaw S, Tsai Y, Min HP. Early corticosteroid use in acute exacerbations of chronic airflow obstruction. Am J Emerg Med. 1996;14(2):139 143. 11. McEvoy CE, Niewoehner DE. Corticosteroids in chronic obstructive pulmonary disease: clinical benefits and risks. Clin Chest Med. 2000;21(4):739 752. 12. Miravitlles M, Espinosa C, Fernandez-Laso E, et al, and the study group of bacterial infections in COPD. Relationship between flora in sputum and functional impairment in patients with acute exacerbations of COPD. Chest. 1999;116:4046.

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13. Sherk PA, Grossman RF. The chronic obstructive disease exacerbation. Clin Chest Med. 2000;21(4):705 721. 14. Hill NS. Noninvasive ventilation in chronic obstructive pulmonary disease. Clin Chest Med. 2000;21(4): 783797. 15. Nevins ML, Epstein SK. Predictors of outcomes for patients with COPD requiring invasive mechanical ventilation. Chest. 2001;119:18401849. 16. Pouw EM, Ten Velde GPM, Croonen BHPM, Kester ADM, Schols AMWJ, Wouters EFM. Early non-elective readmission for chronic obstructive pulmonary disease is associated with weight loss. Clin Nutr. 2000;19:9599. 17. Schols AMWJ, Wouters EFM. Nutritional abnormalities and supplementation in chronic obstructive pulmonary disease. Clin Chest Med. 2000;21(4):753 762. 18. Sheth SG, LaMont JT. Gastrointestinal problems in the chronically critically ill patient. Clin Chest Med. 2001;22(1):135147. 19. Geerts W, Heit J, Clagett G. Prevention of venous thromboembolism. Chest. 2001;119(S):S132S135. 20. Wunderlink RG. Tis a gift to be simple . . .. Chest. 2003;124(3):777778. 21. Drakulovic MB, Torres A, Bauer TT, Nicolas JM, Nogue S, Ferrer M. Supine body position as a risk factor for nosocomial pneumonia in mechanically ventilated patients: a randomised trial. Lancet. 1999;354:18511858. 22. Seemungal T, Donaldson G, Bhowmik A, Jeffries D, Wedzicha J. Time course and recovery of exacerbations in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2000;161:1608 1613. 23. Cote CG, Celli BR. Answers to nine key questions on COPD. Contemp Intern Med. 1998;10(3):915. 24. Nocturnal Oxygen Therapy Trial Group. Continuous or nocturnal oxygen therapy in chronic obstructive lung disease. Ann Intern Med. 1980;93:391 398. 25. American Thoracic Society Statement: standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1995;152S:77121. 26. Tarpy SP, Celli BR. Long-term oxygen therapy. N Engl J Med. 1995;333:710714. 27. Dougherty JA, Didur BL, Aboussouan LS. Long-acting inhaled beta2 agonists for stable COPD. Ann Pharmacother. 2003;37(9):12471255 28. Tashkin D, Cooper C. The role of long-acting bronchodilators in the management of stable COPD. Chest. 2004;125:249259. 29. Sin D, McAlister F, Man SF, Anthonisen N. Contemporary management of chronic obstructive pulmonary disease: a scientific review. JAMA. 2003;290:2301 2312. 30. Brusasco V, Hodder R, Miravitlles M, Korducki L,

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44. Salman G, Mosier M, Beasley M, Calkins D. Rehabilitation for patients with chronic obstructive pulmonary disease: meta-analysis of randomized controlled trials. J Gen Intern Med. 2003;18:213221. 45. Bourjeily G, Rochester C. Exercise training in chronic obstructive pulmonary disease. Clin Chest Med. 2000;21:763781. 46. Pulmonary rehabilitation1999. The official statement of the American Thoracic Society. Am J Respir Crit Care Med. 1999;159:16661682. 47. Cahalin L, Braga M, Matsuo Y, Hernandez E. Efficacy

STATEMENT OF OWNERSHIP, MANAGEMENT, AND CIRCULATION (Act of August 12, 1970; Section 3685; Title 39 United States Code) Date of FilingOctober 1, 2004. Title of PublicationCritical Care Nursing Quarterly; Frequency of IssueQuarterly; Annual Subscription Price$79.00; Location of Known Ofce of PublicationLippincott Williams & Wilkins, Inc., 16522 Hunters Green Parkway, Hagerstown, MD 21740-2116; Location of the Headquarters or General Business Ofces of the PublisherLippincott Williams & Wilkins, Inc., 530 Walnut Street, Philadelphia, PA 19106; Publisher Lippincott Williams & Wilkins, Inc., 530 Walnut Street, Philadelphia, PA 19106; EditorJanet M. Barber, RN, MS, CEN, 9383 E. County Road 500 S., Greensburd, IN 47240-8138. Managing EditorKaryn Crislip, Lippincott Williams & Wilkins, 530 Walnut Street, Philadelphia, PA 19106; OwnerLippincott Williams & Wilkins, Inc., 530 Walnut Street, Philadelphia, PA 19106, 351 West Camden Street, Baltimore, MD 21201; Wolters Kluwer, US, 333 Seventh Avenue, New York, NY 10001; Wolters Kluwer nv (owns 100% of stock), Stadouderskade 1, 1054 FS Amsterdam, The Netherlands; Known Bond Holders, Mortgagees, and other security holders owning or holding 1 percent or more of the total amount of bonds, mortgages, or other securitiesNone. A. Total no. of copies printed (net press run), average 2,500, actual 2,400. B. Paid and/or requested circulation 1. Paid/requested outside-county mail subscriptions stated on form 3541, average 1,528, actual 1,403; 2. Paid in-county subscriptions, none; 3. Sales through dealers and carriers, street vendors, counter sales, and other non-USPS paid distribution, average 173, actual 158; 4. Other classes mailed through the USPS, none. C. Total paid and/or requested circulation [sum of B (1), (2), (3), and (4)], average 1,701, actual 1,561. D. Free distribution by mail (samples, complimentary, and other free). 1. Outside-county as stated on form 3541, average 101, actual 97; 2. In-county as stated on form 3541, none; 3. Other classes mailed through the USPS, none. E. Free distribution outside the mail (carriers or other means), average 4, actual 4. F. Total free distribution (sum of D and E), average 105, actual 101. G. Total distribution (sum of C and F), average 1,806, actual 1,662. H. Copies not distributed, average 694, actual 738. I. Total (sum of G and H), average 2,500, actual 2,400. Percent paid and/or requested circulation, average 94.19%, actual 93.92%. I certify that the statements made by me above are correct and complete. Jeffrey Brown, Manager, Periodicals Operations.