I. Pathophysiology
a. Chronic obstructive pulmonary disease (COPD): Chronic obstructive bronchitis and emphysema
i. Chronic airfl ow limitations (CAL): Caused by a mixture of small airway disease (obstructive bronchi- olitis) and parenchymal destruction (emphysema) ii. Airway infl ammation: Causes structural changes,
narrowing of lumina, and loss of elastic recoil in parenchyma
b. Asthma (also called chronic reactive airway disease) i. Chronic infl ammatory disorder— episodic exacerba-
tions of reversible infl ammation and hyperreactivity and variable constriction of bronchial smooth muscle, hypersecretion of mucus, and edema
II. Spirometric Classification of Severity of COPD (airflow limitation based on postbronchodilator FEV1— Global Initiative for Chronic Obstructive Lung Disease (GOLD), 2017 report
a. GOLD 1 (mild COPD)— mild airfl ow limitation (FVC < 0.70; FEV1≥ to 80% predicted)
b. GOLD 2 (moderate COPD)— worsening airfl ow limitation (FVC < 0.70; 50% ≤ FEV1< 80% predicted); shortness of breath on exertion, and chronic cough and sputum production may be pres ent
c. GOLD 3 (severe COPD)— continued worsening of airfl ow limitation (FVC < 0.70; 30% ≤ FEV1< 50% predicted);
increasing shortness of breath, reduced exercise capacity, fatigue, and repeated exacerbations
d. GOLD 4 (very severe COPD)— severe airfl ow limitation (FVC < 0.70; FEV1< 30% predicted)
e. Symptom evaluation: Although spirometry is necessary for making the diagnosis of COPD, assessment goals should focus on symptoms, risk for exacerbations, and determining effect of disease on client’s overall health. Updated COPD guidelines include groups A, B, C, and D that guide therapy (Haelle, 2017).
III. Etiology a. COPD
i. Risk factors: Smoking (primary irritant), indoor/
outdoor air pollution, second hand smoke (e.g., smoke
from cooking or heating fuels); history of childhood respiratory infections, heredity— a1- antitrypsin defi ciency; occupational dusts, vapors, fumes, gases, and other chemicals.
ii. Acute exacerbations usually due to pulmonary infections.
b. Asthma
i. Tends to be acute and intermittent or episodic.
ii. The severity is classifi ed as (1) intermittent, (2) mild per sis tent, (3) moderate per sis tent, or (4) severe per sis tent. This classifi cation is based on the impair- ment and risk related to disease, which is mea sured by (a) frequency and severity of symptoms, including nocturnal symptoms; (b) characteristics of acute episodes; (c) pulmonary function; and (d) exacerba- tions (Sharma & Gupta, 2016).
iii. Environmental and other factors (not a complete listing): House hold substances (such as dust mites, pets, cockroaches, mold), pollen, foods, latex, emotional upheaval, air pollution, cold weather, exercise, chemicals, medi cations, and viral infections are known to contribute to development of asthma.
iv. Ge ne tics: Although allergies and environmental exposure factors are known risk factors in the development of asthma, both twin and family studies point to a strong ge ne tic component. To date, linkage studies have identifi ed more than a dozen genomic regions linked to asthma (Barnes, 2016). According to a Centers for Disease Control and Prevention (CDC) report, if a person has a parent with asthma, he or she is three to six times more likely to develop asthma than someone who does not have a parent with asthma (Benaroch, 2016).
v. In most children, asthma develops before age 5 years, and in more than half, asthma develops before age 3 years. Multiple triggers or precipitants as above plus upper respiratory infections (most commonly viral), including respiratory syncytial virus (RSV) bronchi- olitis in infancy, irritants such as tobacco smoke,
CHAPTER 3Respiratory: COPD & Asthma IV. Statistics
a. COPD
i. Morbidity: Over 9 million Americans (3.8%) reported that they had been diagnosed with COPD in that year (2015) (CDC: National Center for Health Statistics, 2017a)
ii. Mortality: In 2014, death due to chronic lower respiratory diseases was the fi fth leading cause of death (23,894) in age group 45 to 64 and the third leading cause of death (124,693) in age group 65 and older (CDC, 2015a).
iii. Cost: In 2010, total national costs attributable to COPD and its sequelae were estimated at $32.1 billion (Ford et al, 2015).
b. Asthma
i. Morbidity: In 2015, over 18 million Americans were reported to have asthma, including 6.2 million children under 18 (CDC, National Center for Health Statistics, 2017b).
ii. Mortality: In 2015, there were 3651 deaths attributed to asthma.
iii. Cost: Annual direct healthcare cost is approximately
$50.1 billion; indirect costs (e.g., lost productivity) are
$5.9 billion, totaling $56.0 billion (Asthma & Allergy Foundation of Amer i ca [AAFA], 2015).
sports and games requiring continuous activity or that are played in cold weather, and changes in atmo- spheric or barometric pressure (Sharma & Gupta, 2016).
vi. The Severe Asthma Research Program of the National Heart, Lung, and Blood Institute identifi ed fi ve phenotypes of asthma (Moore et al, 2010):
1. Group 1 clients have early onset asthma with normal lung function treated with two or fewer controller medi cations and minimal healthcare utilization.
2. Group 2 clients have early onset asthma and preserved lung function but increased medi cation requirements (three or more medi cations) and healthcare utilization.
3. Group 3 comprises mostly older obese women with late- onset asthma, moderate reductions in pulmo- nary function, and frequent oral corticosteroid use to manage exacerbations.
4. Group 4 and 5 clients have severe airfl ow obstruc- tion with bronchodilator responsiveness but differ in their ability to attain normal lung function, age of asthma onset, atopic status, and use of oral corticosteroids.
Asthma: Chronic, reversible infl ammation of the airways caused by a reaction of the airways to vari ous stimuli.
Bronchiectasis: Condition in which damage to the airways causes them to widen and become fl abby and scarred.
Bronchiectasis is usually the result of infection or other condition that injures airway walls and causes loss of ability to clear mucus.
CAT (COPD Assessment Test) Score: Range from 0 to 40.
Represents disease impact; score less than 10 equals low impact; greater than 10 equals high impact. A change of score of two or more points is considered clinically signifi cant.
Chronic bronchitis: Infl ammation and scarring of the lining of the bronchi.
Chronic obstructive pulmonary disease (COPD): Disease state characterized by an airfl ow limitation that is not fully reversible. It is usually progressive and associated with an abnormal infl ammatory response to noxious particles or gases.
Dyspnea: Shortness of breath that may be per sis tent, worse with activity, and progressive over time.
Emphysema: Destruction of the alveoli, which leads to overdistention of the air spaces. Damage is irreversible.
FEV1: Forced expired volume in 1 second.
FVC: Forced vital capacity.
Hypercapnia: Condition in which there is increased level of carbon dioxide in blood. This condition is closely associ- ated with hypoxemia (low level of oxygen), which causes breathing diffi culty and breathing/respiratory failure.
G L O S S A R Y
CARE SETTING
Primarily community level; however, severe exacerbations may necessitate emergency or inpatient hospital stay.
RELATED CONCERNS
Heart failure: chronic, page 38 Pediatric considerations, page 993 Pneumonia, page 147
Psychosocial aspects of care, page 835 Surgical intervention, page 873
Respiratory failure: ventilatory assistance, page 187
D I A G N O S T I C D I V I S I O N
M A Y R E P O R T M A Y E X H I B I T
Activity/Rest
• Fatigue, exhaustion, malaise • Fatigue
• Restlessness, insomnia
• General debilitation or loss of muscle mass
• Inability to perform basic activities of daily living (ADLs) because of breathlessness
• Inability to sleep, need to sleep sitting up
• Dyspnea at rest or in response to activity or exercise
Circulation
• Swelling of lower extremities • Elevated blood pressure (BP)
• Elevated heart rate or severe tachycardia, dysrhythmias
• Distended neck veins, with advanced disease
• Dependent edema, which may not be related to heart disease
• Faint heart sounds due to increased anteroposterior (AP) chest dia meter
• Skin color and mucous membranes may be pale or bluish and cyanotic, clubbing of nails and peripheral cyanosis, pallor (can indicate anemia)
Ego Integrity
• Increased stress factors • Anxious, fearful, irritable be hav ior, emotional distress
• Changes in lifestyle • Apathy, change in alertness, dull affect, withdrawal
• Feelings of hopelessness, loss of interest in life
Food/Fluid
• Nausea— side effect of medi cation or mucus production • Poor skin turgor
• Poor appetite, anorexia (emphysema) • Dependent edema
• Altered taste due to medi cations • Diaphoresis
• Inability to eat because of respiratory distress • Abdominal palpation may reveal hepatomegaly
• Per sis tent weight loss, decreased muscle mass or subcutaneous fat (emphysema)
• Weight gain refl ecting edema (bronchitis, prednisone use)
Hygiene
• Decreased ability and increased need for assistance with ADLs • Poor hygiene
Pain/Discomfort
• Chest tightness (asthma)
Respiration
• Variable levels of dyspnea, with insidious and progressive onset (predominant symptom in emphysema), especially on exertion
• Respirations:
• Usually rapid and may be shallow
• Prolonged expiratory phase with grunting, pursed- lip breathing (emphysema)
• Assumption of three- point (“tripod”) position for breathing—
especially with acute exacerbation of chronic bronchitis
• Use of accessory muscles for respiration, such as elevated shoulder girdle, retraction of supraclavicular fossae, fl aring of nares
• Chest may appear hyperinfl ated with increased AP dia meter (barrel- shaped), minimal diaphragmatic movement
• Breath sounds:
• May be faint with expiratory wheezes (emphysema)
• Scattered, fi ne, or coarse moist crackles (bronchitis)
• Seasonal or episodic occurrence of breathlessness (asthma);
inability to breathe (asthma); chronic “air hunger” (COPD)
• Use of oxygen at night or continuously
C L I E N T A S S E S S M E N T D A T A B A S E
M A Y R E P O R T (continued) M A Y E X H I B I T (continued)
• Rhonchi, wheezing throughout lung fi elds on expiration and possibly during inspiration, progressing to diminished or absent breath sounds. Wheezing of COPD can vary from day to day or time of day. Widespread wheezing may be heard on inspiration or expiration. Laryngeal- level wheezing can be pres ent without other abnormal breath sounds (asthma).
• Percussion: May reveal hyperresonance over lung fi elds (air- trapping with emphysema) or dullness over lung fi elds (consolidation, fl uid, mucus)
• Coughing: • Cough may be productive or nonproductive.
• Intermittent cough episodes (note chronic cough is often fi rst symptom of COPD)
• Per sis tent cough with sputum production (gray, white, or yellow), which may be copious (chronic bronchitis).
• Paroxysms of cough (asthma) • Sputum production may be small, large, or intermittent.
• Large volumes of sputum can accompany under lying bronchiectasis or bacterial exacerbations.
• Skin color • May be normal despite abnormal gas exchange and rapid
respiratory rate (moderate emphysema, known as “pink puffers”)
• Pallor, with cyanosis of lips, nailbeds; overall duskiness; ruddy color (chronic bronchitis, sometimes called “blue bloater”)
• Voice • Diffi culty speaking sentences of more than four or fi ve words
at one time, loss of voice
• History of recurrent respiratory infections (asthma) (particu- larly during childhood)
• Long- term exposure to indoor or outdoor air pollution or respiratory irritants (asthma)
• Occupational or environmental exposures to smoke, dust, particulates, and fumes (e.g., chemical agents, coal burning and coal dust; biomass fuels [from organic materials such as wood and sawdust, animal dung, crop residues]) (asthma)
• Smoking (cigarette, pipe, cigar, water pipe) (cigarette smoking is the most commonly occurring risk factor for COPD)
• Concomitant chronic diseases frequently include cardiovascu- lar disease, skeletal muscle dysfunction, metabolic syndrome, osteoporosis, depression, anxiety, and lung cancer
• Familial and hereditary factors, that is, defi ciency of a1- antitrypsin (emphysema)
Safety
• History of allergic reactions or sensitivity to substances or environmental factors
• Flushing, perspiration (asthma)
• Recent or recurrent infections
Sexuality
• Decreased libido
Social Interaction
• Dependent relationship(s)
• Insuffi cient support from or to partner or signifi cant other (SO), lack of support systems
• Prolonged disease or disability progression
• Inability to converse or maintain voice because of respiratory distress
• Limited physical mobility
• Neglectful relationships with other family members
• Inability to perform or inattention to employment responsibili- ties, absenteeism, confi rmed disability
Teaching/Learning
• Use or misuse of respiratory drugs
• Use of herbal supplements, such as astragalus, coleus, echinacea
(continues on page 136)
CHAPTER 3Respiratory: COPD & Asthma
T E S T
W H Y I T I S D O N E W H A T I T T E L L S M E Pulmonary function tests (PFTs)
• Numerous specifi c tests are included as part of the comprehen- sive PFT and fall within three categories: airway fl ow rates, lung volumes and capacities, and gas exchange.
Used to establish baseline lung function, evaluate dyspnea, detect pulmonary disease, and monitor effects of therapies used to treat respiratory disease. Note: The spirometer is also used as an exercise tool for improving lung function, for example, after surgery.
• Total lung capacity (TLC): Maximum amount of air that lungs can hold, mea sured at the top of an inhalation.
Increased in obstructive lung disease. Decreased in restrictive lung disease.
• Residual volume (RV): Air remaining in the lungs after maximum exhalation.
Increased in obstructive lung disease. Decreased in restrictive lung disease.
• Vital capacity (VC): Maximum amount of air that can be exhaled during a normal or slow exhalation after fullest pos si ble inhalation. Impor tant mea sure ment in assessing the client’s ability to cough and protect airway.
Normal or decreased in obstructive lung disease.
Decreased in restrictive lung disease.
• Spirometry testing, including FVC and FEV1: Mea sures the amount of air taken in (volume) and exhaled as a function of time (e.g., after deepest pos si ble inhalation), which is also known as forced vital capacity (FVC).
Increased in obstructive lung disease. Note: Spirometry is required to make the diagnosis of COPD; presence of a postbronchodilator FEV1/FVC <0.70 confi rms presence of per sis tent airfl ow limitation. Note: Spirometry may be done at the same time as body plethysmography using the same equipment.
• Peak expiratory fl ow: Mea sures the speed of exhaling and lung constriction.
People with asthma often use this test routinely to monitor their asthma control.
• Plethysmography: Test that takes lung volume mea sure- ments (inhaling and exhaling). The test involves sitting in an airtight booth and blowing into a mouthpiece while a computer rec ords mea sure ments.
Helps diagnose respiratory diseases with similar symptoms, including asthma, pulmonary fi brosis, and chronic obstructive pulmonary disease (COPD).
Bronchial provocation tests
• Exercise challenge: Baseline spirometry followed by exercise on a treadmill or bicycle to heart rate greater than 60% of predicted maximum, with monitoring of the ECG and oxyhemoglobin saturation.
The diagnosis of asthma can be confi rmed with the exercise challenge in a patient with history of exercise- induced symptoms (e.g., cough, wheeze, chest tightness or pain) (Sharma & Gupta, 2016).
• Inhalation challenge test: Mea sures how much and how quickly client can breathe air in and out before and after taking medicine.
Determines whether bronchial tubes overreact to environmental factors (e.g., breathing cold air, highly humid air) or to inhaling certain substances (e.g., methacholine, histamine, or respira- tory inhalers). This may support a diagnosis of asthma.
M A Y R E P O R T (continued) M A Y E X H I B I T (continued)
• Smoking or diffi culty stopping smoking, chronic exposure to second hand smoke, smoking substances other than tobacco
• Regular use of alcohol
• Failure to improve over long period of time
Discharge Plan Considerations
• Episodic or long- term assistance with shopping, transportation, self- care needs, homemaker or home maintenance tasks
• Changes in medi cation and therapeutic treatments, use of supplemental oxygen, ventilator support; end- of- life issues
➧ Refer to section at end of plan for postdischarge considerations.
D I A G N O S T I C S T U D I E S
C L I E N T A S S E S S M E N T D A T A B A S E (contd.)
DISCHARGE GOALS
1. Ventilation/oxygenation adequate to meet self- care needs.
2. Nutritional intake meeting caloric needs.
3. Infection treated or prevented.
4. Disease pro cess, prognosis, and therapeutic regimen understood.
5. Plan in place to meet needs after discharge.
NURSING PRIORITIES
1. Maintain airway patency.
2. Assist with mea sures to facilitate gas exchange.
3. Enhance nutritional intake.
4. Prevent complications and slow progression of condition.
5. Provide information about disease pro cess, prognosis, and treatment regimen.
W H Y I T I S D O N E (continued) W H A T I T T E L L S M E (continued)
Other diagnostic studies
• Chest x- ray: Evaluates organs or structures within the chest. May reveal hyperinfl ation of lungs with increased AP dia meter, fl attened diaphragm, increased retrosternal air space, de- creased vascular markings/bullae (emphysema), increased bronchovascular markings (bronchitis), and normal fi ndings during periods of remission (asthma).
• Pulse oximetry: Refl ects oxygen saturation through mea sure ment of the portion of light transmitted by oxygen- ated hemoglobin using a sensor attached to fi ngers/earlobes.
Noninvasive mea sure of arterial blood oxygen and diffusion.
Abnormally low levels (<88%) indicate impaired gas exchange.
ABG analy sis is recommended when SaO2< 80% (Kee et al, 2010).
Blood Tests
• Arterial blood gases (ABGs): Mea sures oxygen and carbon dioxide levels to assess and monitor gas exchange.
Gas exchange abnormalities result in hypoxemia and hypercap- nia. Gas transfer for oxygen and carbon dioxide worsens as disease progresses. Reduced ventilation may also be due to reduced ventilatory drive or increased dead space (Elbehairy et al, 2015). Most often PaO2 is 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) (Kee et al, 2010).
• Complete blood count (CBC) and differential: Provides baseline data about the hematologic system and yields information related to oxygen- carrying capacity and infection.
Findings are variable and can include increased hemoglobin (advanced emphysema) and increased eosinophils (asthma);
elevated white blood cells (WBCs) in severe respiratory infection.
• Alpha-1 antitrypsin (AAT): A defi ciency in AAT is a ge ne tic trait considered to be a risk factor for the development of COPD. Performed when COPD develops in patients < 45 years old, of Caucasian descent, with strong family history of COPD (Kee et al, 2010).
Decreased levels are seen in early onset emphysema in adults;
increased levels are pres ent in acute and chronic infl ammatory disorders.
• Allergy testing Can identify allergic factors that may signifi cantly contribute to
asthma.
• Histologic evaluation of airways Typically reveal infi ltration with infl ammatory cells, narrowing of airway lumina, bronchial and bronchiolar epithelial denudation, and mucus plugs (Sharma & Gupta, 2016).
N U R S I N G D I A G N O S I S :
in effec tive Airway Clearance
May Be Related To
Obstructed airway: Chronic obstructive pulmonary disease; airway spasm; excessive mucus; retained secretions, exudate in the alveoli
Physiological factors: Asthma; infection
Environmental factors: Smoking, exposure to smoke; second hand smoke Possibly Evidenced By
Dyspnea, difficulty verbalizing Alteration in respiratory rate or pattern
(continues on page 138)
CHAPTER 3Respiratory: COPD & Asthma
ACTIONS/INTERVENTIONS RATIONALE
Airway Management NIC In de pen dent
Auscultate breath sounds. Note adventitious breath sounds such as wheezes, crackles, or rhonchi.
Some degree of bronchospasm is pres ent with obstructions in airway and may or may not be manifested in adventi- tious breath sounds, such as scattered, moist crackles (bronchitis); faint sounds, with expiratory wheezes (emphysema); or absent breath sounds (severe asthma).
Assess and monitor respiratory rate. Note inspiratory- to- expiratory ratio.
Tachypnea is usually pres ent to some degree and may be pronounced on admission, during stress, or during concurrent acute infectious pro cess. Respirations may be shallow and rapid, with prolonged expiration in compari- son to inspiration.
Note presence and degree of dyspnea, for example, reports of “air hunger,” restlessness, anxiety, respiratory distress, and use of accessory muscles. Use a 0 to 10 scale or American Thoracic Society’s Grade of Breathlessness Scale to rate breathing difficulty. Ascertain precipitating factors when pos si ble. Differentiate acute episode from exacerbation of chronic dyspnea.
Respiratory dysfunction is variable depending on the under lying pro cess, for example, infection, allergic reaction, and the stage of chronicity in a client with established COPD. Note: Using a scale to rate dyspnea aids in quantifying and tracking changes in respiratory distress.
Check peak expiratory flow rate (PEFR) before and after treatments using peak flow meter (PFM).
Monitors effectiveness of drug therapy; identifies need for change in regimen in children age 5 and older. Note:
Although peak flow monitoring in the emergency room (ER) may prove helpful for assessment of lung function and response to treatment, it’s usually pos si ble only if client is familiar with the technique because he or she already uses it at home (Volpe et al, 2011).
Assist client to maintain a comfortable position to facilitate breathing by elevating the head of bed, leaning on over- bed table, or sitting on edge of bed.
Elevation of the head of the bed facilitates respiratory function using gravity; however, client in severe distress will seek the position that most eases breathing. Support- ing arms and legs with table, pillows, and so on helps reduce muscle fatigue and can aid chest expansion.
Encourage and assist client with COPD to practice abdomi- nal or pursed- lip breathing exercises.
Provides client with some means to cope with and control dyspnea and reduce air- trapping.
Observe for per sis tent, hacking, or moist cough. Assist with mea sures to improve effectiveness of cough effort.
Cough can be per sis tent but in effec tive, especially if client is el derly, 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/d 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 distention and pressure on the diaphragm.
Avoid iced liquids, especially in children. May trigger bronchospasm.
Limit exposure to environmental pollutants 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.
N U R S I N G D I A G N O S I S :
in effec tive Airway Clearance
(continued)Diminished/adventitious breath [rales, crackles; wheezes, rhonchi]
In effec tive cough Restlessness, cyanosis
Desired Outcomes/Evaluation Criteria— Client Will Respiratory Status: Airway Patency NOC
Maintain patent airway with breath sounds clear or clearing.
Demonstrate be hav iors to improve airway clearance.