Any respiratory disease that persistently obstructs bronchial airflow fall under the broad classification of COPD, also known as chronic airflow limitations (CAL). Chronic Obstructive Pulmonary Disease (COPD) is a condition of chronic dyspnea with expiratory airflow limitation that does not significantly fluctuate. Within that broad category, the primary cause of the obstruction may vary; examples include airway inflammation, mucous plugging, narrowed airway lumina, or airway destruction.
The term COPD mainly involves two related diseases — chronic bronchitis and emphysema. Although asthma also involves airway inflammation and periodic narrowing of the airway lumina (hyperreactivity), the condition is the result of individual response to a wide variety of stimuli/triggers and is therefore episodic in nature with fluctuations/exacerbations of symptoms.
COPD is also called chronic obstructive lung disease or COLD.
Asthma: Also known as chronic reactive airway disease, asthma is characterized by reversible inflammation and constriction of bronchial smooth muscle, hypersecretion of mucus, and edema. Precipitating factors include allergens, emotional upheaval, cold weather, exercise, chemicals, medications, and viral infections.
Chronic bronchitis: Widespread inflammation of airways with narrowing or blocking of airways, increased production of mucoid sputum, and marked cyanosis.
Emphysema: Most severe form of COPD, characterized by recurrent inflammation that damages and eventually destroys alveolar walls to create large blebs or bullae (air spaces) and collapsed bronchioles on expiration (air-trapping).
Nursing Care Plans
Here are 5 Chronic Obstructive Pulmonary Disease (COPD) Nursing Care Plans (NCP).
- Chest x-ray: May reveal hyperinflation of lungs, flattened diaphragm, increased retrosternal air space, decreased vascular markings/bullae (emphysema), increased bronchovascular markings (bronchitis), normal findings during periods of remission (asthma).
- Pulmonary function tests: Done to determine cause of dyspnea, whether functional abnormality is obstructive or restrictive, to estimate degree of dysfunction and to evaluate effects of therapy, e.g., bronchodilators. Exercise pulmonary function studies may also be done to evaluate activity tolerance in those with known pulmonary impairment/progression of disease.
- The forced expiratory volume over 1 second (FEV1): Reduced FEV1 not only is the standard way of assessing the clinical course and degree of reversibility in response to therapy, but also is an important predictor of prognosis.
- Total lung capacity (TLC), functional residual capacity (FRC), and residual volume (RV): May be increased, indicating air-trapping. In obstructive lung disease, the RV will make up the greater portion of the TLC.
- Arterial blood gases (ABGs): Determines degree and severity of disease process, e.g., most often Pao2is decreased, and Paco2 is normal or increased in chronic bronchitis and emphysema, but is often decreased in asthma; pH normal or acidotic, mild respiratory alkalosis secondary to hyperventilation (moderate emphysema or asthma).
- DL CO test: Assesses diffusion in lungs. Carbon monoxide is used to measure gas diffusion across the alveocapillary membrane. Because carbon monoxide combines with hemoglobin 200 times more easily than oxygen, it easily affects the alveoli and small airways where gas exchange occurs. Emphysema is the only obstructive disease that causes diffusion dysfunction.
- Bronchogram: Can show cylindrical dilation of bronchi on inspiration; bronchial collapse on forced expiration (emphysema); enlarged mucous ducts (bronchitis).
- Lung scan: Perfusion/ventilation studies may be done to differentiate between the various pulmonary diseases. COPD is characterized by a mismatch of perfusion and ventilation (i.e., areas of abnormal ventilation in area of perfusion defect).
- Complete blood count (CBC) and differential: Increased hemoglobin (advanced emphysema), increased eosinophils (asthma).
- Blood chemistry: alpha1-antitrypsin is measured to verify deficiency and diagnosis of primary emphysema.
- Sputum culture: Determines presence of infection, identifies pathogen.
- Cytologic examination: Rules out underlying malignancy or allergic disorder.
- Electrocardiogram (ECG): Right axis deviation, peaked P waves (severe asthma); atrial dysrhythmias (bronchitis), tall, peaked P waves in leads II, III, AVF (bronchitis, emphysema); vertical QRS axis (emphysema).
- Exercise ECG, stress test: Helps in assessing degree of pulmonary dysfunction, evaluating effectiveness of bronchodilator therapy, planning/evaluating exercise program.
- Maintain airway patency.
- Assist with measures to facilitate gas exchange.
- Enhance nutritional intake.
- Prevent complications, slow progression of condition.
- Provide information about disease process/prognosis and treatment regimen.
- Ventilation/oxygenation adequate to meet self-care needs.
- Nutritional intake meeting caloric needs.
- Infection treated/prevented.
- Disease process/prognosis and therapeutic regimen understood.
- Plan in place to meet needs after discharge.
May be related to
- Increased production of secretions; retained secretions; thick, viscous secretions
- Allergic airways
- Hyperplasia of bronchial walls
- Decreased energy/fatigue
Possibly evidenced by
- Statement of difficulty breathing
- Changes in depth/rate of respirations, use of accessory muscles
- Abnormal breath sounds, e.g., wheezes, rhonchi, crackles
- Cough (persistent), with/without sputum production
- Maintain airway patency with breath sounds clear/clearing.
- Demonstrate behaviors to improve airway clearance, e.g., cough effectively and expectorate secretions.
|Auscultate breath sounds. Note adventitious breath sounds (wheezes, crackles, rhonchi).||Some degree of bronchospasm is present with obstructions in airway and may or may not be manifested in adventitious breath sounds such as scattered, moist crackles (bronchitis); faint sounds, with expiratory wheezes (emphysema); or absent breath sounds (severe asthma).|
|Assess and monitor respirations and breath sounds, noting rate and sounds (tachypnea, stridor, crackles, wheezes). Note inspiratory and expiratory ratio.||Tachypnea is usually present to some degree and may be pronounced on admission or during stress or concurrent acute infectious process. Respirations may be shallow and rapid, with prolonged expiration in comparison to inspiration.|
|Note presence and degree of dyspnea as for reports of “air hunger,” restlessness, anxiety, respiratory distress, use of accessory muscles. Use 0–10 scale or American Thoracic Society’s “Grade of Breathlessness Scale” to rate breathing difficulty. Ascertain precipitating factors when possible. Differentiate acute episode from exacerbation of chronic dyspnea.||Respiratory dysfunction is variable depending on the underlying process such as infection, allergic reaction, and the stage of chronicity in a patient with established COPD. Note: Using a 0–10 scale to rate dyspnea aids in quantifying and tracking changes in respiratory distress. Rapid onset of acute dyspnea may reflect pulmonary embolus.|
|Assist patient to assume position of comfort (elevate head of bed, have patient lean on overbed table or sit on edge of bed).||Elevation of the head of the bed facilitates respiratory function by use of gravity; however, patient in severe distress will seek the position that most eases breathing. Supporting arms and legs with table, pillows, and so on helps reduce muscle fatigue and can aid chest expansion.|
|Keep environmental pollution to a minimum such as dust, smoke, and feather pillows, according to individual situation.||Precipitators of allergic type of respiratory reactions that can trigger or exacerbate onset of acute episode.|
|Encourage abdominal or pursed-lip breathing exercises.||Provides patient with some means to cope with or control dyspnea and reduce air-trapping.|
|Observe characteristics of cough (persistent, hacking, moist). Assist with measures to improve effectiveness of cough effort.||Cough can be persistent but ineffective, especially if patient is elderly, acutely ill, or debilitated. Coughing is most effective in an upright or in a head-down position after chest percussion.|
|Increase fluid intake to 3000 mL per day within cardiac tolerance. Provide warm or tepid liquids. Recommend intake of fluids between, instead of during, meals.||Hydration helps decrease the viscosity of secretions, facilitating expectoration. Using warm liquids may decrease bronchospasm. Fluids during meals can increase gastric distension and pressure on the diaphragm.|
|Monitor and graph serial ABGs, pulse oximetry, chest x-ray.||Establishes baseline for monitoring progression or regression of disease process an complications. Note: Pulse oximetry readings detect changes in saturation as they are happening, helping to identify trends before patient is symptomatic. However, studies have shown that the accuracy of pulse oximetry may be questioned if patient has severe peripheral vasoconstriction.|
May be related to
- Altered oxygen supply (obstruction of airways by secretions, bronchospasm; air-trapping)
- Alveoli destruction
- Alveolar-capillary membrane changes
Possibly evidenced by
- Abnormal breathing
- Confusion, restlessness
- Inability to move secretions
- Abnormal ABG values (hypoxia and hypercapnia)
- Changes in vital signs
- Reduced tolerance for activity
- Demonstrate improved ventilation and adequate oxygenation of tissues by ABGs within patient’s normal range and be free of symptoms of respiratory distress.
- Participate in treatment regimen within level of ability/situation.
|Assess and record respiratory rate, depth. Note use of accessory muscles, pursed-lip breathing, inability to speak or converse.||Useful in evaluating the degree of respiratory distress or chronicity of the disease process.|
|Elevate head of bed, assist patient to assume position to ease work of breathing. Include periods of time in prone position as tolerated. Encourage deep-slow or pursed-lip breathing as individually needed or tolerated.||Oxygen delivery may be improved by upright position and breathing exercises to decrease airway collapse, dyspnea, and work of breathing. Note: Recent research supports use of prone position to increase Pao2.|
|Assess and routinely monitor skin and mucous membrane color.||Cyanosis may be peripheral (noted in nailbeds) or central (noted around lips/or earlobes). Duskiness and central cyanosis indicate advanced hypoxemia.|
|Encourage expectoration of sputum; suction when indicated.||Thick, tenacious, copious secretions are a major source of impaired gas exchange in small airways. Deep suctioning may be required when cough is ineffective for expectoration of secretions.|
|Auscultate breath sounds, noting areas of decreased airflow and adventitious sounds.||Breath sounds may be faint because of decreased airflow or areas of consolidation. Presence of wheezes may indicate bronchospasm or retained secretions. Scattered moist crackles may indicate interstitial fluid or cardiac decompensation.|
|Palpate for fremitus.||Decrease of vibratory tremors suggests fluid collection or air-trapping.|
|Monitor level of consciousness and mental status. Investigate changes.||Restlessness and anxiety are common manifestations of hypoxia. Worsening ABGs accompanied by confusion/ somnolence are indicative of cerebral dysfunction due to hypoxemia.|
|Evaluate level of activity tolerance. Provide calm, quiet environment. Limit patient’s activity or encourage bed or chair rest during acute phase. Have patient resume activity gradually and increase as individually tolerated.||During severe, acute or refractory respiratory distress, patient may be totally unable to perform basic self-care activities because of hypoxemia and dyspnea. Rest interspersed with care activities remains an important part of treatment regimen. An exercise program is aimed at increasing endurance and strength without causing severe dyspnea and can enhance sense of well-being.|
|Evaluate sleep patterns, note reports of difficulties and whether patient feels well rested. Provide quiet environment, group care or monitoring activities to allow periods of uninterrupted sleep; limit stimulants such as caffeine; encourage position of comfort.||Multiple external stimuli and presence of dyspnea may prevent relaxation and inhibit sleep.|
|Monitor vital signs and cardiac rhythm.||Tachycardia, dysrhythmias, and changes in BP can reflect effect of systemic hypoxemia on cardiac function.|