Chronic obstructive pulmonary disease

9 Chronic obstructive pulmonary disease




Overview/pathophysiology


Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death in the United States. It is a disease state characterized by airflow limitation that is not fully reversible. Airflow limitation usually is progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases and characterized by chronic inflammation throughout the airways, parenchyma, and pulmonary vasculature.


The chronic airflow limitation characteristic of COPD is caused by a mixture of small airway disease (obstructive bronchiolitis) and parenchymal destruction (emphysema), the relative contributions of each varying from person to person.



Health care setting


Any health care setting: primary care, home care, acute care, intensive care, and/or long-term care



Assessment




Signs and symptoms:


Chronic cough with sputum production is usually the first symptom to develop. Dyspnea that interferes with daily activities is the main reason patients seek medical attention. As lung function deteriorates, dyspnea worsens and additional complications such as respiratory failure, right heart failure, weight loss, and arterial hypoxemia may develop.



Physical assessment:


Use of accessory muscles of respiration, prolonged expiratory phase, digital clubbing, decreased thoracic expansion, barrel chest appearance, dullness over areas of consolidation, adventitious breath sounds (especially coarse rhonchi and wheezing), ankle edema, distended neck veins, bloated appearance.



Risk factors:


Include both genetic factors and exposures to particles. Genetic factors (e.g., hereditary deficiency of alpha-1 antitrypsin) increase risk for disease development and progression. Inhalation exposures include cigarette smoking, the most commonly encountered risk factor, and other outdoor/indoor air pollutants. Passive exposure to cigarettes also may contribute to COPD. Indoor air pollutants, especially from burning biomass fuels in confined spaces, is associated with increased risk for COPD in developing countries, especially among women.



Diagnostic tests




Chest x-ray:


Rarely diagnostic unless bullous disease is present. Radiologic changes in COPD include signs of hyperinflation (i.e., flattened diaphragm on lateral chest film and increase in volume of the retrosternal airspace).



Arterial blood gas (ABG) values:


Important in advanced COPD and should be obtained when forced expiratory volume in one second (FEV1) is less than 50% predicted normal value or there are signs of right-sided (diastolic) heart failure (e.g., jugular vein distention, peripheral edema) or respiratory failure (PaO2 less than 60 mm Hg with or without PaCO2 greater than 50 mm Hg).



Oximetry:


Will reveal decreased O2 saturation (90% or less).



Alpha-1 antitrypsin deficiency screen:


Performed in patients who develop COPD at a young age (younger than 45 yr) or who have a strong family history of the disease.



Spirometry:


Confirms diagnosis of COPD. Clinical indicators and an FEV1 diagnose and classify severity of COPD.



Differential diagnosis:


COPD may mimic many other diseases.





Nursing diagnosis:


Ineffective breathing pattern

related to decreased lung expansion occurring with chronic airflow limitations


Desired Outcome: Following treatment/intervention, patient’s breathing pattern improves as evidenced by reduction in or absence of dyspnea and related symptoms with O2 saturation greater than 90% with or without oxygen therapy, pH higher than 7.35, and PaCO2 less than 50 mm Hg.



























ASSESSMENT/INTERVENTIONS RATIONALES
Assess respiratory status q2-4h and as needed. Restlessness, anxiety, mental status changes, shortness of breath, tachypnea, and use of accessory muscles of respiration are signs of respiratory distress, which should be reported promptly for immediate intervention.
Auscultate breath sounds q2-4h and as needed. A decrease in breath sounds or an increase in adventitious breath sounds (crackles, wheezes, rhonchi) may indicate respiratory status change and necessitate prompt intervention.
Administer bronchodilator therapy as prescribed. Bronchodilators increase FEV1 by altering airway smooth muscle tone.
Monitor for tachycardia and dysrhythmias. These are side effects of bronchodilator therapy.
Administer inhaled glucocorticoid steroids as prescribed. For patients with FEV1 at less than 60%, regular treatment can decrease the rate of decline of lung function.
Administer combination inhaled glucocorticoid steroid and bronchodilator therapy as prescribed. Glucocorticoids combined with a long-acting beta-2 agonist are more effective than any one individual treatment in reducing exacerbations and overall improvement of lung function.

Monitor patient’s response to prescribed O2 therapy.
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Jul 18, 2016 | Posted by in NURSING | Comments Off on Chronic obstructive pulmonary disease

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