Chronic Obstructive Pulmonary Disease (COPD) Nursing Care Management

You will meet COPD everywhere: outpatient, home care, the ED, the ICU, and hospice. It is chronic dyspnea with fixed expiratory airflow limitation that does not swing much day to day. GOLD (the Global Initiative for Chronic Obstructive Lung Disease) calls it a preventable and treatable disease with extrapulmonary effects that drive severity in individual patients. Your job is to keep the airway open, protect gas exchange, and catch the exacerbation that tips a stable patient into respiratory failure.

Classification

Two disease processes sit under COPD, and plenty of patients show features of both.

Chronic bronchitis is an airway disease, defined by cough and sputum production for at least 3 months in each of 2 consecutive years. These are the "blue bloaters." Pollutants and allergens irritate the airways, the mucus-secreting glands and goblet cells crank out sputum, and viral, bacterial, and mycoplasmal infections trigger acute episodes.

Emphysema is abnormal distention of airspaces beyond the terminal bronchioles with destruction of the alveolar walls. These are the "pink puffers." Destroyed, overdistended alveoli wreck CO2 and O2 exchange. Two patterns: panlobular destroys the respiratory bronchiole, alveolar duct, and alveolus so the whole lobule enlarges; centrilobular hits mainly the center of the secondary lobule.

Pathophysiology

Airflow limitation in COPD is progressive and driven by an abnormal inflammatory response to noxious gases and particles. The inflammation runs through the proximal and peripheral airways, the lung parenchyma, and the pulmonary vasculature. The airways narrow, goblet cells multiply, submucosal glands enlarge, and mucus floods the airway. Over time you get scar formation narrowing the lumen, alveolar wall destruction with loss of attachments and elastic recoil, and a thickened, hypertrophied pulmonary vasculature.

Epidemiology

COPD mortality keeps climbing while other diseases trend down. It is the fourth leading cause of death in the United States and kills 125,000 Americans a year. In 2005, more women than men died of COPD. About 12 million Americans carry the diagnosis and another 2 million likely have it undiagnosed. Annual cost runs about $42.6 billion, with overall healthcare expenditures of $26.7 billion.

Causes

COPD comes from environmental and host factors. Smoking depresses scavenger-cell activity and cripples the ciliary cleansing mechanism of the respiratory tract. Prolonged, intense occupational exposure to dust and chemicals, plus indoor and outdoor air pollution, all contribute. The well-documented genetic risk factor is alpha1-antitrypsin deficiency, loss of the enzyme inhibitor that protects lung parenchyma from injury.

Clinical Manifestations

The course is variable but generally progressive. Chronic cough is a primary symptom. Sputum production climbs as goblet cells and mucus glands are overstimulated. Dyspnea on exertion is progressive and persistent and worsens with activity; as disease advances, dyspnea appears at rest. Weight loss follows because dyspnea interferes with eating and the work of breathing burns energy. In emphysema, the barrel-chest thorax comes from ribs fixed in the inspiratory position and lost elasticity.

Prevention

Smoking cessation is the single most cost-effective intervention to cut the risk of developing COPD and to halt its progression. Spell out the risks of smoking and personalize the at-risk message to the patient.

Complications

The two life-threatening complications are respiratory insufficiency and respiratory failure. Onset and acuity of respiratory failure depend on baseline pulmonary function, pulse oximetry or arterial blood gas values, comorbidities, and the severity of other complications. Respiratory insufficiency can be acute or chronic and may need ventilator support until other acute problems are treated.

Assessment and Diagnostic Findings

The three main symptoms overlap with every other chronic lung disease, so diagnose carefully. Take a thorough health history. Pulmonary function studies confirm the diagnosis, grade severity, and track progression. Spirometry evaluates obstruction by the ratio of FEV1 to forced vital capacity. ABG assesses baseline oxygenation and gas exchange and matters most in advanced disease. Chest x-ray rules out alternative diagnoses, and CT chest helps with the differential. Screen for alpha1-antitrypsin deficiency in patients younger than 45 years and in those with a strong family history.

Chest x-ray may show hyperinflated lungs, a flattened diaphragm, increased retrosternal air space, decreased vascular markings or bullae (emphysema), increased bronchovascular markings (bronchitis), and normal findings during remission (asthma). Pulmonary function tests pin down the cause of dyspnea, sort obstructive from restrictive abnormality, estimate the degree of dysfunction, and gauge response to therapy such as bronchodilators; exercise studies evaluate activity tolerance and disease progression. Forced expiratory volume over 1 second (FEV1) is the standard measure of clinical course and reversibility and an important prognostic predictor. Total lung capacity (TLC), functional residual capacity (FRC), and residual volume (RV) may be increased, indicating air-trapping; in obstructive disease the RV makes up the greater portion of the TLC.

Arterial blood gases grade severity: most often PaO2 is decreased, PaCO2 is normal or increased in chronic bronchitis and emphysema but often decreased in asthma, with pH normal or acidotic, or a mild respiratory alkalosis from hyperventilation in moderate emphysema or asthma. The DLCO test assesses diffusion across the alveocapillary membrane using carbon monoxide, which binds hemoglobin 200 times more easily than oxygen; emphysema is the only obstructive disease that causes diffusion dysfunction. Bronchogram can show cylindrical dilation of bronchi on inspiration and bronchial collapse on forced expiration (emphysema) or enlarged mucous ducts (bronchitis). A lung scan with perfusion/ventilation studies differentiates lung diseases; COPD shows a mismatch of perfusion and ventilation. CBC with differential shows increased hemoglobin in advanced emphysema and increased eosinophils in asthma. Blood chemistry measures alpha1-antitrypsin to confirm deficiency and primary emphysema. Sputum culture identifies the pathogen, and cytologic exam rules out malignancy or allergic disorder. ECG may show right axis deviation and peaked P waves (severe asthma), atrial dysrhythmias (bronchitis), tall peaked P waves in leads II, III, and AVF (bronchitis, emphysema), and a vertical QRS axis (emphysema). Exercise ECG and stress testing gauge pulmonary dysfunction, bronchodilator effectiveness, and exercise planning.

Medical Management

Match the intervention to the manifestation in front of you.

Pharmacologic therapy. Bronchodilators relieve bronchospasm by altering smooth muscle tone, cutting airway obstruction, improving oxygen distribution, and improving alveolar ventilation. A short trial of oral corticosteroids tells you whether pulmonary function improves and symptoms drop. Other agents include alpha1-antitrypsin augmentation therapy, antibiotics, mucolytics, antitussives, vasodilators, and narcotics.

Managing exacerbations. Optimizing bronchodilators is first-line therapy: find the best drug or combination on a regular schedule for that patient. Hospitalize for severe dyspnea unresponsive to initial therapy, confusion or lethargy, respiratory muscle fatigue, paradoxical chest wall movement, or peripheral edema. On ED arrival, give supplemental oxygen and rapidly assess whether the exacerbation is life-threatening. Antibiotics help patients with increased dyspnea, increased sputum production, and increased sputum purulence.

Surgical Management

Bullectomy is an option for select patients with bullous emphysema and can reduce dyspnea and improve lung function. Lung volume reduction surgery is palliative for homogenous or focal disease that is not widespread. Lung transplantation is the definitive surgical option for end-stage emphysema.

Nursing Management

Care centers on teaching and improving respiratory status.

Assessment. Move fast but stay accurate. Check exposure to risk factors, past and present medical history, the signs and symptoms of COPD and their severity, the patient's knowledge of the disease, vital signs, and breath sounds and pattern.

Diagnosis. Common nursing diagnoses include impaired gas exchange from chronic inhalation of toxins; ineffective airway clearance related to bronchoconstriction, increased mucus, and ineffective cough; ineffective breathing pattern related to dyspnea, mucus, bronchoconstriction, and airway irritants; self-care deficit related to fatigue; and activity intolerance related to hypoxemia and ineffective breathing.

Planning and goals. Aim for improved gas exchange, airway clearance, a better breathing pattern, independence in self-care, improved activity tolerance, ventilation and oxygenation adequate for self-care, caloric intake met, infection treated or prevented, the disease process and regimen understood, and a discharge plan in place.

Nursing priorities: maintain airway patency, assist gas exchange, enhance nutrition, prevent complications and slow progression, and teach the disease process and treatment regimen.

Interventions. Patient and family teaching drives self-management. For airway clearance, give bronchodilators and corticosteroids correctly and watch for side effects, and teach direct or controlled coughing, which works better and tires the patient less than forceful undirected coughing. For breathing pattern, use inspiratory muscle training, diaphragmatic breathing (slows the rate, raises alveolar ventilation, helps expel air on expiration), and pursed-lip breathing (slows expiration, prevents small-airway collapse, controls rate and depth). For activity intolerance, pace daily activities and use support devices to cut energy expenditure, build upper and lower extremity strength with exercise training, and add walking aids to improve ambulation. To catch complications, monitor for cognitive changes (personality, behavior, memory), follow pulse oximetry to guide supplemental oxygen, and prevent infection by immunizing against influenza and S. pneumoniae, since these patients are prone to respiratory infection.

Evaluation. The patient identifies the hazards of cigarette smoking and resources for cessation, enrolls in a cessation program, minimizes or eliminates exposures, verbalizes the need for fluids, stays free of infection, practices breathing techniques, and does activities with less shortness of breath.

Discharge and Home Care Guidelines

Assess what the patient and family know about self-care and the regimen. Set goals to the severity: in mild COPD, increase exercise tolerance and prevent further loss of pulmonary function; in severe COPD, preserve current function and relieve symptoms. Teach temperature control: avoid heat and cold extremes, since heat raises temperature and oxygen requirements and high altitudes worsen hypoxemia. Push moderate activity and steer clear of emotional or stressful triggers that set off coughing. Provide breathing retraining to optimize functional status.

Documentation Guidelines

Document respiratory rate, breath sounds, and the frequency, amount, and appearance of secretions, plus lab findings and mentation. Document conditions that interfere with oxygen supply, the plan of care and specific interventions, liters of supplemental oxygen, the patient's responses to treatment and teaching, the teaching plan, any modifications to the plan, and progress toward goals.