Acute Exacerbation of COPD Nursing Application of Evidence-Based Guidelines

LWW/CCNQ AS332-04 October 6, 2004 23:5 Char Count=

Crit Care Nurs QVol. 27, No. 4, pp. 336–352c© 2004 Lippincott Williams & Wilkins, Inc.

Acute Exacerbation of COPDNursing Application ofEvidence-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 exacerba-tion of chronic obstructive pulmonary disease (COPD), the fourth leading cause of death in theUnited States. In addressing this health concern, the Global Initiative for Chronic Obstructive LungDisease Report summarized the goals for COPD management and recommended treatment sup-ported by current data and research. It is imperative that our clinical nursing practice is basedupon research-supported interventions: use of appropriate medications, monitoring acid-base sta-tus, administering controlled oxygen therapy, assessing the need for mechanical ventilation, andclose monitoring of comorbid illnesses. Health promotion includes patient and family educationon early recognition of symptoms, smoking cessation strategies, and participation in pulmonaryrehabilitation that can reduce long-term morbidity from this chronic disease. Key words: acuteexacerbation, COPD, oxygen therapy, pharmacotherapy, pulmonary rehabilitation

CHRONIC Obstructive pulmonary disease(COPD) is the fourth leading cause of

morbidity and mortality in the United States.Despite this fact, COPD often goes unrecog-nized and undiagnosed until the individualpresents during an acute exacerbation. TheUS National Heart, Lung, and Blood Instituteand the World Health Organization formedthe Global Initiative for Chronic ObstructiveLung Disease (GOLD). The objectives of theGOLD Expert Panel were to not only increaseawareness of disease prevalence but also sum-marize and recommend treatment strategiesto achieve the goals of effective COPD man-agement: (1) prevent disease progression, (2)relieve symptoms, (3) improve exercise toler-ance, (4) improve health status, (5) preventand treat complications, (6) prevent and treatexacerbations, and (7) reduce mortality.1

From the Suburban Lung Associates, Elk GroveVillage, Ill (Ms Borkgren-Okonek); and the College ofNursing, University of Illinois at Chicago (MsBorkgren-Okonek).

Corresponding author: Cynthia Gronkiewicz, MS, RN,APRN, 847 Ashland Ave, River Forest, IL 60305 (e-mail:[email protected]).

In the same year the GOLD guidelineswere published, the American College ofChest Physicians and the American Collegeof Physicians-American Society of InternalMedicine released their 2001 position paperson management of an acute exacerbation ofCOPD.2,3 Because nurses in the acute caresetting play a vital role in assisting individu-als to achieve these goals during hospitaliza-tion, this article provides clinical applicationof these evidence-based recommendations.This article will describe a broad range of ther-apeutic interventions applicable across thespectrum of disease severity.

PATHOPHYSIOLOGY

COPD is characterized by chronic inflam-mation throughout the central and peripheralairways, lung parenchyma, and pulmonaryvasculature. This inflammation is caused byexposure to inhaled noxious particles andgases. When the normal protective mecha-nisms of the lungs and airways fail and no re-pair occurs, COPD evolves. Smoking causes85% to 90% of all cases, although genetic

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Acute Exacerbation of COPD 337

factors, passive smoking, occupational expo-sure, air pollution, and possibly hyperrespon-sive airways can also play a role.3,4

In addition to the inflammation, 2 otherprocesses are thought to contribute to air-way obstruction: an imbalance of proteinasesand antiproteinases and oxidative stress. Neu-trophil elastase is an enzyme that breaks downelastin (a protein), which is a main compo-nent of alveolar wall structure. A small per-centage of patients have a hereditary form ofCOPD known as alpha1-antitrypsin (AAT) de-ficiency. Because they lack AAT, an antipro-teinase protecting the lung from destructionby neutrophil elastase, symptoms of COPDcan present as early as the third or fourthdecade of life. Oxidative stress is thought tocontribute to COPD because of an oxidant/antioxidant imbalance. There is a decreasein antiproteinase (protective) activity thatdirectly damages lung tissue by activatingthe destructive proteinases and promotinginflammation.5

This inflammation affects the lung in a va-riety of ways. In the central airways, inflam-matory cells infiltrate the surface epitheliumwhere the increase in goblet cells causes hy-persecretion of mucus. The peripheral air-ways undergo repeated cycles of injury andrepair to their walls, resulting in structuralremodeling and scar formation. This even-tually narrows the lumen, causing fixed air-way obstruction. Both oxidative stress andthe imbalance of the proteinases and antipro-teinases are involved in destruction of thelung parenchyma where respiratory bronchi-oles become dilated and destroyed. In themost severe cases, the pulmonary capillarybed can also be affected. The increase ininflammatory-cell infiltration of the smoothmuscle causes further thickening of the ves-sel walls. As the disease progresses, peripheralairway obstruction, parenchymal destruction,and pulmonary vascular abnormalities reducethe ability for gas exchange.5

The ventilation abnormality results fromairway inflammation, edema, bronchospasm,and increased mucus production. The perfu-sion abnormality stems from hypoxia-induced

constriction of the arterioles, an abnormalrespiratory pattern, and respiratory musclefatigue.

These pathologic changes lead to the char-acteristics of the disease: mucus hypersecre-tion, ciliary dysfunction, airflow limitation,and gas exchange abnormalities. Expiratoryairflow limitation is the hallmark of physio-logic change seen in COPD. Approximately85% of patients have chronic bronchitis inwhich the intermittent airway inflammationleads to frequent episodes of a productivecough. In emphysema, there is destructionof the infrastructure of alveoli and distalairspaces, which provide the elastic recoil.Progression of the disease causes hypox-emia and/or hypercapnia. Pulmonary hyper-tension, the major cardiovascular compli-cation of COPD, develops along with corpulmonale.4

CLINICAL ASSESSMENT

Evaluation of the patient is based onthe history, physical examination, spirom-etry results, and selected diagnostic tools.Tracheobronchial infections and environ-mental exposures are the most commoncauses of an acute exacerbation. Despiteadvanced technology, one third of admittedpatients have no known cause for theirexacerbation. Conditions that may mimic anexacerbation include pneumonia, pneumoth-orax, pleural effusion, pulmonary embolism,congestive heart failure, and arrhythmias.

Dyspnea is usually the reason a patientseeks medical care. The initial history shouldinclude the length of worsening symptoms orthe presence of new symptoms. Signs of wors-ening COPD include progressive dyspnea, anincrease in frequency or severity of cough, or-thopnea, paroxysmal nocturnal dyspnea, anincrease in sputum volume, purulent spu-tum, an increased need for bronchodilators,use of a glucocorticosteroid burst, limitationsin daily activities, or an increase in oxygenrequirements. Wheezing and chest tightnessmay accompany dyspnea. Frequency, severity,


338 CRITICAL CARE NURSING QUARTERLY/OCTOBER–DECEMBER 2004

and likely causes of past exacerbations shouldbe reviewed. In addition, past hospitaliza-tions, length of stay, and need for intubationsuggest a more severe baseline disease. A thor-ough history taking may be limited because oftheir significant work of breathing with speak-ing, and the clinician then proceeds with thephysical examination.

The general appearance of the patientshould be observed for altered mental sta-tus, anxiety, confusion, drowsiness or somno-lence, reflecting neurologic impairment dueto hypoxia and/or hypercarbia. The patientmay assume a tripod position and use pursed-lip breathing to ease the air hunger.

A respiratory rate greater than 25 breathsper minute, tachypnea, is of as much concernas a decreased rate and impending apnea. Theattempt to exhale against narrowed airwaysproduces a prolonged expiratory phase of therespiratory cycle. Accessory muscle use andretracted intercostal spaces indicate respira-tory distress. One common sign of respira-tory muscle fatigue is paradoxical respirationsobserved by asynchronous chest and abdomi-nal excursions. Another clue to fatigue is res-piratory alternans observed when a patientalternates between chest wall motion and ab-dominal movement. Both abnormal patternsreflect a transfer of the work of breathingfrom the diaphragm and fatigued respiratorymuscles to the abdominal muscles during res-piratory distress.

Auscultation of the chest reveals a widerange of abnormal lung sounds. The breathsounds may be diminished or distant becauseof the severe hyperinflation of the lungs.Coarse rhonchi indicate secretions in thelarge airways. Airway narrowing from bron-choconstriction or edema produces wheez-ing. The sudden opening of collapsed airwaysor fluid in the smaller airways is reflectedin the crackles detected during inhalation.The most ominous finding is never absenceof breath sounds associated with minimal airexchange.

The cardiovascular responses to hypoxemiaand dyspnea include tachycardia and hyper-tension. Cardiac arrhythmias can occur with

a pH level of more than 7.55. In the presenceof right heart failure, ankle edema and jugu-lar vein distention can be present. Clubbingof the fingers indicates longstanding disease.

DIAGNOSTIC TESTS

Spirometry is an objective measurement ofairflow limitation and the gold standard forthe diagnosis and assessment of COPD. How-ever, in the acutely ill patient, even the sim-plest maneuver of lung function can be dif-ficult. Previous spirometric results should beretrieved to provide baseline information ofdisease severity. A forced expiratory volumein 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 allpatients with an FEV1 of less than 40% of pre-dicted, with clinical signs of right heart failureor with significant respiratory distress. Respi-ratory failure is present when PaO2 is less than60 mm Hg, with or without a PaCO2 of morethan 45 mm Hg on room air. An arterial mea-surement should be obtained as oxygen satu-rations via finger or ear oximetry are less reli-able and the carbon dioxide level is a criticalentity. A PaO2 of less than 50 mm Hg, a PaCO2

of more than 70, and a pH level of less than7.30 indicate a life-threatening episode requir-ing intensive care management.1

The baseline chest x-ray (CXR) of a patientwith moderate to severe emphysema may re-veal the presence of bullae formation, hyper-inflation, and/or flattening of the diaphragm.6

In the acute setting, the CXR is necessary toexclude alternative diagnosis that can mimicsymptoms of an exacerbation and to iden-tify the presence of comorbid disease such aspneumonia, congestive heart failure, or pneu-mothorax. A repeat x-ray is suggested whenthe patient’s condition worsens or he/she failsto respond to initial treatment.1

Shortness of breath or chest tightness mayalso indicate cardiac disease. An electrocar-diogram (ECG) assists in the diagnosis of right-ventricular hypertrophy, arrhythmias, and is-chemic episodes. Pulmonary embolism can



be difficult to determine from an acute exac-erbation in severe COPD, as right-ventricularhypertrophy and large pulmonary arteries canalter the ECG. The presence of any of theseentities can affect therapeutic interventions inthe acute phase.

An increase in sputum volume and puru-lence often indicate a bacterial cause and aneed for starting antibiotic treatment. Themost common pathogens in this populationare Streptococcus pneumoniae, Hemophilusinfluenza, and Moraxella catarrhalis. Be-tween 10% to 20% of individuals with anacute exacerbation have 2 or more pathogensidentified.7 A subgroup of patients are morelikely to be colonized with resistant organ-isms such as Pseudomonas. This subgroupincludes nursing home patients, patients re-cently treated with antibiotics, and those ad-mitted to intensive care units (ICUs).4 Cul-tures are recommended only when a patienthas no initial response to therapy.

A complete blood count is useful in identify-ing bleeding or the presence of polycythemia(hematocrit > 55) in a patient with chronichypoxia. The white blood cell (WBC) countis not as helpful as a nonspecific leukocytosiscan be seen with use of corticosteroids.

Electrolytes should be followed to excludea chemistry imbalance as an etiology or con-tributing factor. Of primary concern is anymetabolic acid-base disturbance that places ademand on an already-compromised respira-tory system.

Those patients taking methylxanthines re-quire a theophylline level with the initial labs.Toxicity can occur with a variety of concomi-tant drugs or disease states.

CRITERIA FOR INTENSIVE CAREUNIT ADMISSION

The GOLD Report recommends hospital ad-mission for an acute exacerbation of COPD inall patients with a history of severe COPD, amarked increase in symptom intensity suchas resting dyspnea, the onset of new physi-cal signs as cyanosis or edema, the failure to

respond to initial medical management, thepresence of significant comorbidities, newonset of arrhythmias, older age, insufficienthome support, or diagnostic uncertainty.1

On arrival to the emergency department,the first intervention is to provide controlledoxygen therapy and to determine if the con-dition is life threatening and warrants imme-diate ICU admission. Indications for ICU ad-mission are severe dyspnea not respondingto emergency treatment, a change in men-tal status, persistent or worsening hypoxemia(PaO2 < 50 mm Hg) or severe hypercapnia(PaCO2 > 70 mm Hg), or severe respiratoryacidosis (pH < 7.30) despite supplementaloxygen.1

THERAPEUTIC INTERVENTIONS

Management of a severe exacerbation ofCOPD requires close monitoring for anychange in clinical symptoms, precise deliveryof controlled oxygen therapy, and judicioususe of bronchodilator therapy. Close scrutinyof fluid balance and treatment of associatedconditions require these patients to be in anICU setting. The risk of dying from an acuteexacerbation of COPD is closely related tothe development of respiratory acidosis, thepresence of significant comorbidities, and theneed for ventilatory support.1,8 Being familiarwith the most current recommendations foran acute exacerbation of COPD provides thenurse with both an understanding of chosentreatment protocols and an increased aware-ness of possible intervention strategies.

MEDICATIONS

Pharmacotherapy for COPD is used to de-crease the symptoms and potential complica-tions associated with an acute exacerbation.Although none of the current medicationshave been shown to prevent or slow theprogressive decrease in lung function, theyare critical in decreasing airway resistanceduring the acute phase. Bronchodilators andglucocorticosteroids are the foundation of



Table 1. Pharmacotherapy summary for COPD

Medication Acute management Stable management

BronchodilatorsBeta2-agonists (short-acting) Nebulizer or MDI with spacer Nebulizer or MDI with spacer

Albuterol, Terbutaline, Pirbuterol every 4 h every 4 h as neededBeta2-agonists (intermediate-acting) Nebulizer every 6–8 h Nebulizer every 6–8 h

LevalbuterolBeta2-agonists (long-acting) Not recommended DPI every 12 h

Formoterol, SalmeterolAnticholinergicsIpratropium bromide (short-acting) Nebulizer or MDI every 4–6 h Nebulizer or MDI every 4–6 hTiotropium bromide (long-acting) Not recommended Once dailyCombination agent Nebulizer or MDI with spacer Nebulizer or MDI with spacerAlbuterol/Ipratroprium every 4–6 h every 4–6 hMethylxanthinesAminophylline, Theophylline Continue oral dose to achieve Continue oral dose to achieve

level 8–15 mg/L level 8–15 mg/LCorticosteroidsSystemic 30–40 mg po for 10–14 days Not recommended

PrednisoneMethylprednisolone Equivalent intravenous dose

InhaledFlunisolideBudesonide∗ Not recommendedFluticasone Most administered twice dailyTriamcinaloneBeclomethasone

Bronchodilator/steroidcombination

Salmeterol/Fluticasone 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 chronicCOPD (Table 1).

Bronchodilators

Bronchodilators are critical to the symp-tomatic management of COPD to prevent orreduce symptoms. The key bronchodilatorsare beta2-agonists (albuterol), anticholiner-gics (ipratropium bromide), methyl xanthines(theophylline), or a combination of theseagents. Short-acting inhaled beta2-agonists arethe preferred treatment. The addition of ananticholinergic is recommended even thoughevidence of combination effectiveness is con-troversial. Several reports suggest that com-

bination therapy produces an added benefitwithout the side effects of a higher dose of 1agent.1,3,9

Beta2-agonists produce bronchodilation,improve hyperinflation, decrease dyspnea,reduce airway hyperresponsiveness, increaseciliary activity, and inhibit inflammatory me-diator release from mast cells and basophils.Beta2-receptors on airway smooth muscle areactivated by circulating catecholamines toantagonize muscle contraction and producebronchodilation. These circulating cate-cholamines also stimulate beta-receptors tomodulate acetylcholine release and decreasebronchomotor tone.9



In the acute setting, short-acting beta2-agonists are preferred because of their rapidonset of action. It is recommended thesedrugs be delivered through the inhaled routeto minimize systemic toxicity: albuterol 2 to 4puffs every 4 hours by MDI with a spacer, orthe use of albuterol 2.5 mg in an aerosolizedformulation by a handheld nebulizer or in-linewith the ventilator circuit. Higher doses mayincrease side effects without improving bron-chodilation.

The most common side effects are at-tributed to the beta-receptor stimulation:tachycardia, palpitations, tremors, headaches,and excitability. Hypokalemia can occur withhigher doses of beta2-agonists and may bepotentiated by concomitant use of corticos-teroids. Hence, cardiac monitoring should beused in patients with new-onset cardiac dis-ease and the elderly.

Inhaled anticholergic agents are a key com-ponent of COPD management. Some clini-cians recommend starting these agents beforebeta2-agonists because of fewer and milderside effects.2 There are multiple cholinergicreceptors present in the lung that stimulatesmooth muscle contraction and mucous glandsecretion. These medications can produceequal or greater bronchodilation than do beta-agonists, reduce mucous hypersecretion, anddecrease dyspnea. Anticholinergics produce aslower onset of action, but a longer durationof action than beta2-agonists. Recommendeddosing is ipratropium bromide 2 to 4 puffs bymetered dose inhaler with a spacer device 4times per day. This can also be delivered asa 0.25- to 0.5-mg solution with or without al-buterol in the nebulizer or in-line with theventilator. Because these agents do not readilycross biologic barriers, there are minimal sideeffects. Most complaints are of a dry mouth, ametallic taste, nausea, or blurred vision.9

The role of methylxanthines remains con-troversial, with the most recent guidelinesshowing no additional role for parental use inthe acute phase. The direct bronchodilator ef-fects result from selective inhibition of phos-phodiesterase receptors. Inhibition of someof these receptors have anti-inflammatory ef-

fects. These medications have been shownto produce bronchodilation, improve di-aphragm function, increase mucociliary clear-ance, and improve pulmonary vasodilation soas to improve right-ventricular function.2

Numerous side effects are associated withtheophylline because of its narrow therapeu-tic range. Recommended serum levels are 8 to15 mg/L when continuing an oral agent. Closemonitoring of these levels is required becauseof side effects and potential drug interactions.Initial complaints include gastrointestinal dis-tress or tremors, but arrhythmias and seizuresare also risks of therapy. Serum levels canbe affected by hepatic disease, phenytoin,macrolides, quinolones, or cimetidine.9

Anti-inflammatory agents

The use of systemic corticosteroids sup-presses the inflammatory process in the air-ways and lungs to improve airflow and gasexchange. Steroid use in the acute phase hasbeen shown to improve symptoms, help re-store lung function more quickly, shortenrecovery time in reducing hospital days, de-crease treatment failure rates, and reduce re-lapse rates.2 Patients receiving steroids on ar-rival to the emergency department showedsignificant improvement over the first 6 hoursof treatment.10 Although the exact dose hasnot been determined, an oral or intravenous(IV) equivalent of prednisone 30 to 40 mg/dfor 10 to 14 days is recommended for all hos-pitalized patients during an acute exacerba-tion. This dose is a balance between efficacyand safety, with prolonged treatment after 2weeks increasing the risk of side effects with-out additional benefits, especially in the el-derly population.1,11

The adverse effects seen on a short-term ba-sis that warrant close nursing monitoring aretransient hyperglycemia, hypertension, gas-tric irritation, risk of infection, psychologicaleffects, and cutaneous effects.

Antibiotics

Bacteria can contribute to airway damageand accelerate airway obstruction. More than



half of COPD patients have a lower respira-tory tract colonized with bacteria. This is mostlikely from impaired host defenses and theinflammatory process. The early use of antibi-otics is recommended for patients with wors-ening dyspnea and cough who have an in-crease in sputum volume and purulence.

The particular antibiotic selected shouldbe one with sensitivity to the most commonpathogens: S. pneumoniae, H. influenza, andM. catarrhalis.1 Broad-spectrum antibioticsare recommended for hospitalized patients:macrolides, cephalosporins, amoxicillin/clavulanate, or doxycycline. Critically illpatients risk factors of FEV1 less than 50%of predicted, comorbid illness, or recentexacerbations require gram-negative cover-age with fluoroquinolones. Ciprofloxacinis preferred if Pseudomonas aeruginosa issuspected.12

In those with a suboptimal or no initial re-sponse to therapy, those with recent or re-current hospitalizations, or patients with re-cent antibiotic use, cultures should be sent toidentify the organism or a potentially resistantstrain.

Respiratory stimulants

Respiratory stimulants are not recom-mended for the treatment of hypoxemia orhypercapnia in COPD patients. The stimulat-ing effects of these agents are short acting,there are numerous side effects, and the stim-ulation of already-overworked respiratorymuscles may worsen respiratory failure.9

Respiratory therapy

The GOLD Report recommends manualor mechanical chest percussion and postu-ral drainage in those patients producing morethan 25 cc of sputum each day as well as inthose with lobar atelectasis. Patients shouldbe evaluated on an individual basis as somecannot tolerate the various position changesrequired for effective drainage. The effort ex-pended to clear copious amounts of sputumcan exhaust the already dyspneic patient. Forsome, instruction on effective deep breathing

and coughing following inhaled bronchodila-tors can facilitate airway clearance.

Although some patients report subjectiverelief from mucolytic agents, no study sup-ports their use.1,2,4 Similarly, neither inhaledhypertonic saline nor expectorants have anymucolytic action. Because cough plays a valu-able and protective role in airway clearance,antitussives are contraindicated. Deconges-tants should also be used with caution as theyhave the potential to increase sputum viscos-ity and impair secretion clearance.9

Controlled oxygen therapy

Correcting hypoxemia is the cornerstoneof acute medical treatment. Oxygen relievespulmonary vasoconstriction and right heartstrain and lessens myocardial ischemia to im-prove cardiac output. A saturation goal of 90%ensures adequate oxygen delivery and preser-vation of organ function.4 Judicious use ofoxygen is critical as a gradual rise in carbondioxide can occur with minimal change in apatient’s symptoms.

Supplemental oxygen can be delivered vianasal cannula or venturi mask. Low flow ratesby cannula increase the inspired oxygen con-centration by 3% to 4% for each increase ofliter flow per minute. However, the oxygenflow rate via cannula varies with the patient’sown respiratory rate. Venturi masks providemore precise oxygen delivery than does nasalcannula but not all patients can tolerate a de-vice covering the face. These devices are ini-tially set to deliver 24% to 28%. Once oxygentherapy is initiated, a follow-up ABG in 30 min-utes is recommended to ensure adequate oxy-genation without excessive CO2 retention. Amild elevation in PaCO2 is acceptable whenstriving for an adequate level of oxygenation.If adequate oxygenation is not achieved or res-piratory acidosis worsens, assisted ventilationmay be required.1,13

Ventilatory support

The primary objectives for using mechani-cal support during an acute exacerbation areto relieve symptoms and to decrease mortalityand morbidity. Ventilatory support includes



both noninvasive positive-pressure ventilation(NIPPV) via a tight-fitting mask and inva-sive positive pressure ventilation by trachealintubation.

NIPPV is considered the first choice of ven-tilation mode for an acute exacerbation ofCOPD.14 As worsening hypoxemia, hypercap-nia, and acidosis increase the ventilatory de-mands of the respiratory muscles, the useof NIPPV allows these muscles to rest un-til the underlying airway problems reverse.2,7

This intervention decreases breathlessness,improves oxygenation, reduces PaCO2, in-creases pH, reduces hospital mortality, de-creases the need for invasive mechanical ven-tilation and intubation, decreases the inci-dence of nosocomial pneumonia, and de-creases the number of both ICU and hospitaldays.7

However, NIPPV is not appropriate for allpatients. At least two of the following criteriashould be present prior to initiation: moder-ate to severe SOB with accessory muscle useand evidence of respiratory muscle fatigue,acidosis (pH 7.30–7.35), hypercapnia (PaCO2

45 to 60 mm Hg), or a respiratory rate ofgreater than 25 breaths per minute.1,7

Individuals to be excluded from use ofNIPPV are those with copious secretions,respiratory arrest, cardiovascular instability(hypotension, arrhythmias, new myocardialinfarction), decreased mental status, somno-lence, poor cooperation, or a high risk ofaspiration. These individuals’ underlying con-dition compromises the effective use of a se-cure fitting mask to maintain positive pressurethrough the airways.1

In those patients who fail a trial of NIPPVand there is impending respiratory failure,conventional mechanical ventilation must beinitiated. It is also indicated for any COPD pa-tient with severe SOB and evidence of respira-tory muscle fatigue, a respiratory rate greaterthan 35 breaths per minute, hypoxemia (PaO2

< 40 mm Hg), severe acidosis (pH < 7.25),hypercapnia (PaCO2 > 60 mm Hg), somno-lence or a decreased mental status, or car-diovascular conditions such as hypotensionor shock. Complications such as sepsis, a se-

vere metabolic abnormality, pneumonia, pul-monary embolism, or barotrauma may neces-sitate the need for ventilatory assistance.1,14

The most common modes of mechanicalventilation used are assist- control ventilation,pressure-support ventilation alone or in com-bination with intermittent mandatory venti-lation. Mechanical ventilation is appropriatewhen the current cause of the acute exacerba-tion is reversible and when it is in compliancewith the individual’s desire for its use.

The major risks include ventilator-acquiredpneumonia, barotrauma, and failure to wean.Patients requiring mechanical ventilation formore than 72 hours are at an increased riskfor death and long-term ventilatory support.15

Mortality among COPD patients with respi-ratory failure is no greater than mortalityamong patients on mechanical support fornon-COPD causes. Again, advance directivesand a “living will” can facilitate the clinician’sdecision making prior to this point.1

TREATMENT OF COMORBID DISEASE

In addition to the need for ventilatorysupport, the GOLD Report states that therisk of dying from an acute exacerbation ofCOPD is closely related to the presence ofa comorbidity.1,8 Cor pulmonale, pulmonaryhypertension, and heart failure commonly co-exist with COPD, but adequate oxygen lev-els and COPD management can halt their pro-gression. The use of diuretics can improveright- and left-ventricular functions in somepatients. Close monitoring for hypotension orany fluid/electrolyte imbalance is crucial.9 Hy-ponatremia, hypokalemia, hypomagnesia, oran elevated BUN/creatinine can result fromdiuretic therapy.

Meeting nutritional needs

Serum chemistries may also reveal the ex-istence of low proteins often associated withmalnutrition. Weight loss is a component ofthe disease progression, and nutritional in-tervention is part of comprehensive man-agement during the acute phase. Nutritional



depletion contributes to peripheral skeletalmuscle wasting, a decrease in diaphragm mus-cle mass, impairment of ventilatory drive, andimmune dysfunction.13 Weight loss is a factorin poor outcomes of acute exacerbations andhas been associated with increased morbidityand mortality.8,13,16

Patients with COPD have a higher restingenergy expenditure from the work of breath-ing, an increased activity-related energy, anda low-dietary intake all contributing to weightloss and muscle wasting. Weight loss, partic-ularly fat mass, occurs when energy expendi-ture exceeds the dietary intake. The low in-take is attributed to the dyspnea and oxygendesaturation associated with chewing, swal-lowing, and alteration in respiratory pattern.Gastric filling may limit diaphragm excursion,reduce functional residual capacity, and in-crease dyspnea. The negative energy balanceduring an acute exacerbation stems from anincrease in resting energy expenditure andthe temporary decrease in dietary intake. The2 factors contributing to weight loss and mus-cle wasting during acute exacerbations arethe increased dyspnea and fatigue and the useof high doses of glucocorticosteroids.17

Optimal nutritional support strategies arecritical at this time and in improving sur-vival time after discharge.8 Goals include bothmaintaining body weight and preventing pro-tein breakdown. Daily protein intake shouldinclude at least 1.5 mg/kg of body weightfor optimal protein synthesis. Reduced dietaryintake is also characterized by a restrictedfat intake.17 Providing nasal cannula withmeals and monitoring oximetry ensure ade-quate oxygenation. Offering nutritional sup-plements between small meals reduces thesensation of gastric fullness to further reducedyspnea. Encouraging initial activity such asgetting out of bed can further stimulate thepatient’s appetite.

Treatment of anxiety and depression

Anxiety and depression are additional co-morbid conditions frequently contributing todyspnea in COPD. Patients may have signifi-

cant cognitive and psychological impairmentrelated to hypoxemia as well as the stressand disability of their disease. These emo-tions often get magnified during an acuteexacerbation. Depression is frequently unrec-ognized and may manifest as anxiety or in-somnia. Anxiety itself can be a cause or re-sult of the dyspnea and potentially interferewith management of the underlying exacer-bation. Treatment of the presenting physicalcondition needs to be maximized along witha calm and reassuring approach by the health-care team. Providing adequate time for thera-peutic interventions and deferring to patient’spreferences when feasible can reduce anxi-ety. When anxiety or depression is an obsta-cle to management of a life-threatening exac-erbation, psychological and pharmacologicalinterventions should be pursued. Buspirone isa mild anxiolytic without respiratory depres-sion effects. The serotonin-selecting reuptakeinhibitors are commonly prescribed to treatboth depression and anxiety.9

Prevention of complications

Critically ill patients are more susceptibleto developing upper gastrointestinal bleed-ing from stress ulceration. Previously, routinetreatment included prophylaxis against stressulceration. Current findings cite the high costand incidence of side effects (an increasedrisk of nosocomial or ventilator-assisted pneu-monia) as reason to treat only those at highrisk of developing clinically significant bleed-ing. High-risk patients include those on me-chanical ventilation for more than 48 hours,those with hypotension or shock, victims ofmajor trauma, or those with a history of ul-cers or previous GI bleeding. Recommendedfirst-choice agents are H2 blockers: ranitidine50 mg every 8 hours or famotidine 20 mg ev-ery 12 hours.18

Low-molecular-weight heparin or low-doseunfractionated heparin should be institutedin patients who are immobilized, dehy-drated, or polycythemic with or without ahistory of thromboembolic disease. Preven-tion of deep vein thrombosis includes early



mobility, adequate hydration, and avoidingprolonged bedrest.19

Nurses play the key role in early mobiliz-ing and positioning of the patient. There arephysiological benefits to elevating the headof the bed, getting the patient out of bed,sitting upright in a chair, and early ambula-tion. Repositioning improves drainage fromthe upper lobes, increases diaphragm excur-sion, improves volume changes in the lowerlobes, and mobilizes secretion clearance. Anelevated head of the bed improves cough effi-cacy due to a greater ability to increase intra-abdominal pressure. The overall net effect isreducing ventilation/perfusion mismatch andimproving oxygenation.20 In addition, the el-evated head can decrease the risk of pneumo-nia in ventilated patients.21

As many patients presenting during anacute exacerbation are severely decondi-tioned or debilitated because of their sig-nificant dyspnea and muscle wasting, everyeffort should be made to prevent furtherdecompensation associated with inactivity.These individuals are at increased risk for mor-bidity and mortality. Connors et al reporteddata on a group of over 1000 patients withsevere COPD (PaCO2 ≥ 50 mm Hg) admit-ted to 1 of 5 tertiary hospitals. There was an11% to 24% mortality rate in patients need-ing ICU admission. Although 89% survived thehospital stay, there was a 33% risk of deathover the next 6 months, a 42% risk at 1 year,and a 49% risk at 2 years. Fifty percent werereadmitted in the 6 months after dischargeand reported a fair to poor quality of life,dependence on others for some daily care,and limitations from dyspnea and cough. Only26% reported a good to excellent quality oflife.8

PREPARATION FOR DISCHARGE

While Connors et al’s study focused onthose with severe COPD, the data lend sup-port to the need for early intervention duringan acute exacerbation in all COPD patients toprevent long hospital stays and the associated

sequelae. Preparation of the COPD patient fordischarge from the hospital requires coordi-nation among several disciplines. The attend-ing provider or pulmonary consultant iden-tifies the expected discharge date based onthe patient’s clinical improvement, while sup-porting team members contribute informa-tion regarding the patient’s functional status,oxygenation, and home care needs. All teammembers including the staff level or advancedpractice pulmonary nurse, respiratory thera-pist, physical and occupational therapists, andsocial worker or discharge planner must com-municate with the provider, patient, and fam-ily to ensure a smooth transition from hospi-tal to home. Patients with COPD are at riskfor recurrent exacerbations and admissions.22

Optimal coordination, patient education, andreferrals for follow-up help to minimize thepotential for repeated hospitalizations.

The GOLD guidelines identify the follow-ing criteria to determine a patient’s readinessfor discharge.1 Arterial blood gases and clini-cal status must be stable for 12 to 24 hours.In addition, the need for inhaled bronchodila-tor therapy (beta2-agonist and/or anticholin-ergic agent) should be no more than every4 hours. The patient or home caregiver mustunderstand the medication regime. If ambula-tory prior to admission, the patient should beable to walk across the room at near his base-line level of dyspnea. The patient must also beable to sleep and eat without dyspnea. Finally,arrangements for home nursing care, homephysical therapy, respiratory equipment, andmeals are to be completed before discharge.

Home oxygen therapy

If oxygen is ordered, Medicare requires thatthe qualifying data be obtained no more than2 days prior to discharge on the basis of theexpectation that poor oxygenation on admis-sion improves during and after the hospi-tal stay. The need for oxygen therapy is as-sessed both at rest and with ambulation andrequires an oxygen saturation below 89% ora PaO2 less than or equal to 55 mm Hg onroom air. With concomitant conditions such



as cor pulmonale, pulmonary hypertension,polycythemia, or heart failure, a PaO2 be-tween 55 and 60 mm Hg qualifies a Medicarepatient for home oxygen. Other insurancepayors may or may not require that a patientmeet these standardized criteria for coverageof home oxygen. For COPD patients not previ-ously requiring home oxygen, a reassessmentof rest and ambulatory oxygenation is indi-cated within 1 to 3 months following the ex-acerbation. Up to 30% of these patients willimprove substantially and no longer requiresupplemental oxygen.23

The inpatient respiratory and/or physicaltherapist perform resting and exercise oxime-try or blood gases. If hypoxemia is present,an individualized titration evaluation is un-dertaken to determine the supplemental oxy-gen 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 dur-ing the patient’s usual activity level. Continu-ous overnight oximetry assessment may helpdetermine oxygen needs during sleep. How-ever, sleep-disordered breathing is present in10% to 15% of patients with COPD alone andcannot effectively be evaluated without a fullpolysomnographic study. The incidence of ap-nea (eg, obstructive or central sleep apnea)may be greater in high-risk patients with co-morbidities including obesity and cardiovas-cular disease. Ideally, the home oxygen pres-cription includes the source of oxygen (gas orliquid), method of delivery, and specific flowrates at rest, during sleep, and with exercise.

Following discharge, the pulmonary teamwill identify the optimal oxygen delivery sys-tem to meet an individual patient’s lifestyleneeds. Oxygen systems that offer ease of useand portability such as lightweight gas tanks,liquid oxygen systems, and other conserv-ing devices (eg, pulse delivery, reservoir can-nula, or transtracheal oxygen delivery) en-hance compliance with prescribed oxygentherapy.

Long-term administration of oxygen (≥15–18 h/d) is the only medical therapy shownto increase survival in COPD patients withchronic hypoxemia.23,24 Oxygen also im-

proves lung mechanics, exercise capacity,hemodynamics, mental acuity, and hemato-logic characteristics.25,26 Dyspnea may beameliorated (but not always eliminated) byuse of supplemental oxygen. Patients must un-derstand that oxygen is a medication to beused as prescribed rather than “as needed” torelieve shortness of breath. Hypoxemia mayoccur with or without dyspnea.

Medications for stable COPD

Patient education regarding the home med-ication regime is of paramount importance.At the time of discharge, most patients areprescribed both oral and inhaled medications.Whether or not a patient is new to the diag-nosis of COPD, correct use of inhaled medica-tions warrants frequent and repeated instruc-tion. The patient or home caregiver must beable to demonstrate correct use of the inhaledmedication, either by nebulizer, metered-doseinhaler with spacer device, or by one ofthe new dry powder, propellant-free devices.As new inhaled delivery devices becomeavailable, hospital and home care nursingstaff must learn correct techniques for theiradministration.

Bronchodilator therapy is the foundationof symptom management in stable COPD,and the inhaled route of administration ispreferred.1 On the basis of the GOLD rec-ommendations, bronchodilator medicationsare prescribed on an as-needed or routinebasis to prevent or reduce cough, dysp-nea, and wheezing. While short-acting agentsare favored during inpatient treatment of anacute exacerbation, long-acting medicationsoffer the convenience of once- or twice-daily administration in the home or extendedcare setting. The available long-acting beta2-agonists are salmeterol (discus device) andformoterol (an encapsulated dry powder de-livery system). Both agents have acceptableadverse event profiles including mild tachy-cardia and tremor. In addition, these medica-tions have shown benefits over theophyllineand the short-acting anticholinergic iprat-ropium in improving symptoms, FEV1, and



quality of life, while reducing exacerbationrates.27–29 The new, once-daily anticholiner-gic agent tiotropium significantly reduces ex-acerbations and improves pulmonary func-tion, symptoms, health status, and exercisecapacity.28,30,31

For some patients, maintenance treatmentwill consist of 1 or more long-acting bron-chodilator medications taken regularly andthen supplemented by a short-acting agent asneeded.28 Others prefer routine (eg, up toQID) dosing of short-acting beta-adrenergicplus anticholinergic combination therapy, aregimen shown to produce greater improve-ments in FEV1 than single-drug therapy withalbuterol or ipratropium alone.32 This stan-dard regime may be administered by neb-ulizer or metered-dose inhaler. A recentmeta-analysis on the effectiveness of oral theo-phylline in stable COPD revealed the drughas a modest effect on FEV1 and FVC andslightly improves arterial blood gases in pa-tients with moderate to severe COPD.33 How-ever, because of potential adverse effects,multiple drug interactions, and the need forserum drug level monitoring, theophyllineis seldom first-line therapy for stable COPDin recent years. The choice between vari-ous bronchodilator regimes, single or combi-nation agents, and delivery systems dependson disease severity, medication availability, af-fordability, and the individual patient’s sub-jective perception of symptom control andside effects.1,28 All bronchodilators have beenshown to produce temporary improvement inFEV1 and increase exercise capacity, despitetheir inability to prevent long-term decline inpulmonary function.1

Glucocorticosteroids are the second cat-egory of pharmacologic agents prescribedfor patients with acute or stable COPD. Evi-dence is lacking regarding benefit from long-term systemic corticosteroid therapy. Theusual duration of short-term therapy is 10to 14 days beginning in the hospital par-enterally or by mouth, and continued intapering oral doses following discharge. Sig-nificant adverse effects may develop in pa-tients receiving months or years of sustained

treatment with oral corticosteroids includ-ing hyperglycemia, cataracts, and cushingoidappearance with truncal weight gain. Fur-thermore, osteoporosis and steroid myopathyare important contributors to muscle weak-ness, deconditioning, and progressive disabil-ity in patients taking systemic corticosteroids.Therefore, chronic use of these drugs is notrecommended for maintenance treatment ofCOPD.1

In contrast, long-term treatment with in-haled corticosteroids should be consideredfor select patients; ie, patients with moder-ate to severe COPD (FEV1 < 50% of pre-dicted) experiencing frequent exacerbationsor those demonstrating spirometric improve-ment related to inhaled steroid therapy (FEV1

increased by 15% and 200 mL).1 A trial of6 weeks to 3 months is recommended.1 Re-duced rates of exacerbation and hospitaliza-tion have been shown in studies of long-term inhaled corticosteroid therapy whenused alone or in combination with long-actingbronchodilators.29,34 Safety outcome analysesconfirm that minimal systemic absorption oreffects occur when inhaled corticosteroidsare taken at recommended dosages. Most re-cent studies of inhaled corticosteroid efficacyin COPD evaluated the medications budes-onide (available in both turbuhaler and nebu-lizer solution) and fluticasone (metered-doseinhaler or combined with salmeterol in thediscus device). Older agents still available asmetered-dose inhalers include triamcinolone,beclomethasone, and flunisolide. Hoarseness,dry mouth, and oral candidiasis are the chiefadverse effects of inhaled steroid therapy.Their incidence is minimized by use of aspacer device (with metered-dose inhalers)and by thoroughly rinsing the mouth after ad-ministration of these agents.

Smoking cessation

Comprehensive discharge education also in-cludes discussion of pharmacotherapy initi-ated to aid in smoking cessation for cur-rent or recent smokers. Smoking cessation isthe single most effective (and cost-effective)approach to halt progression of COPD.1



A 5-step intervention approach is outlinedfor healthcare providers in the US Pub-lic Health Service document Treating To-bacco Use and Dependence: A Clinical Prac-tice Guideline.35 Practical counseling, formalgroup support treatment, and social supportoutside a formal smoking cessation programare the most effective nonpharmacologicstrategies. If needed, nicotine replacementmedications may be started during or aftertreatment of an acute exacerbation of COPDin the absence of medical contraindications.All forms of nicotine replacement therapy(gum, transdermal patch, inhaler, nasal spray,and lozenge) increase long-term smoking ab-stinence rates.1 Usual protocols for nicotinereplacement products range from 6 to 12weeks.9 Other medications have been utilizedto minimize symptoms of nicotine withdrawalincluding anxiolytics (buspirone or benzodi-azepines), antidepressants (buproprion), andthe alpha2-agonist clonidine.9 Combiningnicotine replacement therapy with behavioralcounseling or with other medications (eg,buproprion) results in abstinence rates in the30% to 40% range, as compared with 6- to 12-month abstinence rates of 20% to 25% usingsingle therapy.36,37

In COPD, successful long-term pharmaco-logic intervention and compliance dependupon thorough patient education regard-ing medication purpose, expected benefits,proper dosing and administration, and poten-tial side effects.9 Collaborative managementhelps the provider and the patient evaluatetreatment efficacy and tailor an individualizedmedication regime to achieve optimal controlof symptoms.

DISCHARGE FOLLOW-UP

Follow-up assessment is recommended 4to 6 weeks after hospital discharge for pa-tients recovering from acute exacerbations ofCOPD. At this office visit, the provider eval-uates the patient’s functional capacity (abilityto manage activities of daily living in the homeenvironment), FEV1, medication efficacy, in-haler device technique, understanding of the

treatment regimen, and oxygenation.1 Strate-gies to prevent future exacerbations shouldalso be reviewed.

A majority of exacerbations are causedby viral or bacterial infection. Patients withCOPD are at high risk for pneumonia andsevere illness related to influenza infection.Thus, vaccination against influenza and pneu-mococcal infections is recommended for allpatients with mild to severe COPD.1,38,39 Theinfluenza vaccine is reformulated annuallyand should be administered intramuscu-larly beginning in October. At present theintranasal influenza vaccination is not recom-mended for patients with airway disease. Thecurrent 23-valent pneumococcal vaccine hasgreater than 60% efficacy in producing anti-bodies in immunocompetent patients follow-ing a single administration.9 Vaccination mayfully prevent or minimize the severity of pneu-mococcal illnesses including pneumonia,bacteremia, or meningitis caused by S. pneu-moniae bacterial infection. Revaccination isrecommended after 5 years when a patient’sinitial vaccination occurred before age 65.39

This vaccine can be administered during anytime of the year.

Recognizing the onset of an exacerbationcan be difficult, as the severity of COPD symp-toms may vary from day to day. Sudden orprogressive dyspnea, decline in ability to per-form routine activities, or infectious signs orsymptoms should prompt the patient or care-giver to seek medical evaluation. Avoidanceof extended outdoor exposure or strenuousoutdoor activity during high-pollution con-ditions is also advised as a preventive mea-sure. Patients at highest risk for hospitaliza-tion with exacerbations are those with lowbody mass index (≤20 kg/m2), limited base-line ambulatory capacity, abnormal gas ex-change (baseline hypoxemia or hypercarbia),and pulmonary hypertension.40

Discussion of advance directives shouldbe initiated with the patient and family atthe posthospital visit, especially in those pa-tients suffering from severe lung disease, mul-tiple comorbidities, repeated hospitalizations,or a history of respiratory failure. Although



previous reports indicate that pulmonaryfunction predicts mortality, recent work re-veals that the severity of dyspnea is a betterpredictor of 5-year survival.41 The followingcharacteristics are associated with increasedrisk of death from COPD within 1 year: FEV1

less than 30% of predicted, declining inde-pendence in simple activities of daily living,walking distance limited to a few steps, morethen 1 hospitalization within the past year,chronic comorbid illness, depression, livingalone, and older age.42 Hospice referral is in-dicated when life expectancy is less than orequal to 6 months and quality of life is poor re-lated to distressing dyspnea and severely lim-ited activity tolerance.

Pulmonary rehabilitation

For the majority of patients with COPD,referral to a pulmonary rehabilitation pro-gram is indicated. Pulmonary rehabilitationis defined as a multidisciplinary, individu-ally tailored program of education and ex-ercise designed to maximize functional ca-pacity and self-management skills in patientswith COPD.43 Key elements of a compre-hensive pulmonary rehabilitation program aremedical evaluation, goal setting, applicationof therapeutic modalities (skeletal and respi-ratory muscle training, psychological coun-seling, breathing retraining, nutritional coun-seling, education, smoking cessation), andoutcome assessment. Extensive research hasconfirmed the benefits of rehabilitation inpatients with mild to severe COPD.44 In-creased exercise tolerance, reduced dyspneaand fatigue, and improved quality of life havebeen demonstrated in numerous controlledtrials.43,45 Reduced hospitalization has alsobeen reported.43 Although pulmonary reha-bilitation does not significantly improve spiro-metric measurements of lung function, it iswidely recognized as critical therapy to op-timize the physical and psychological sta-tus of individuals with chronic respiratoryimpairment. Activity limitation in COPD isattributed to a cycle of factors includingimpaired lung and respiratory muscle me-

chanics, skeletal muscle weakness, dyspnea,anxiety, and deconditioning. Physiologic ab-normalities cause dyspnea on exertion. As aresult, patients develop fear of exercise and of-ten cope by reducing their overall level of ac-tivity causing progressive deconditioning anddisability.43

Successful pulmonary rehabilitation pro-grams can be conducted in hospital, outpa-tient, or home settings.46 Several componentsof pulmonary rehabilitation can be imple-mented during hospitalization or in a tem-porary, postdischarge extended care facility.For example, physical and occupational thera-pies provide instruction on breathing retrain-ing and energy-conservation strategies for ac-tivities of daily living.

Pursed-lip breathing and diaphragmaticbreathing are commonly taught and may re-duce dyspnea for some, but not all, patients.Diaphragmatic breathing can be detrimen-tal to those individuals with severe COPDand marked hyperinflation by causing thora-coabdominal paradox and increased fatigue.47

Pursed-lip breathing involves slow inhalationthrough the nose and prolonged exhalationover 4 to 6 seconds through lightly pursed lipsto prevent airway collapse in patients with re-duced elastic recoil.43 Airway clearance strate-gies including postural drainage, chest phys-iotherapy, and effective cough techniques areadvised for patients with chronic sputum pro-duction. Finally, the dietitian conducts a nutri-tional assessment and develops an individual-ized plan for optimal nutritional repletion orweight reduction as indicated.

Education, psychosocial support, and exer-cise comprise the principal components ofoutpatient pulmonary rehabilitation. Amongthese interventions, exercise training is thefoundation.46 Patients undergo exercise orchemical-induced stress testing prior to en-try to establish baseline exercise capacity, pro-vide data for the exercise prescription, andexclude unstable cardiovascular disease. Theoptimal strategies for exercise training modal-ity and intensity in COPD are not fullyclear.45 Studies demonstrate efficacy whencycle ergometry, treadmill or free walking,



stair-climbing, weight training, and upper ex-tremity exercise regimens are used alone orin combination. Exercise sessions should beconducted at least 3 times each week for30 to 45 minutes to achieve desired goals.43

Inspiratory muscle training (IMT), usingsmall handheld devices, reduces dyspnea andimproves the strength and endurance of res-piratory muscles in patients with COPD.48 Re-sults are most favorable when IMT is incorpo-rated into a program of aerobic exercise suchas walking or cycling.49

Not all patients have access to formallystructured programs. Inadequate insurancecoverage, lack of transportation, geographicdistance, or other medical conditions (eg,severe orthopedic limitations, unstable car-diac disease) will preclude participation in re-habilitation for some patients. Nevertheless,all patients should be provided basic com-ponents of rehabilitation over an extendedtime continuum to improve clinical outcomesand functioning.43 A simple walking programshould be prescribed to patients at the time ofdischarge or at the postdischarge office evalu-ation if formal rehabilitation is not feasible.

Most outpatient pulmonary rehabilitationprograms in the United States are 4 to 12weeks in duration. Patients must continue ex-ercising for a long term on their own or in amaintenance phase of the formal program tosustain initial benefits. Research reveals thatpatients with severe COPD require programslasting at least 6 months to achieve signifi-cant improvements in exercise tolerance andhealth status.44

The socialization offered to patients andfamilies through participation in rehabilita-tion or support groups helps to reinforce pos-itive health practices while reducing feelingsof isolation and anxiety. Psychosocial support,professional counseling, and antidepressanttherapy, if indicated, should be available to allpatients having difficulty coping with chronicrespiratory disease.

In conclusion, application of evidence-based guidelines enables healthcare profes-sionals to minimize morbidity and compli-cations from this prevalent chronic disease.Nurses provide the vital link in improving thequality of life for COPD patients from acutehospital care through home management.

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Acute Exacerbation of COPD Nursing Application of Evidence-Based Guidelines