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N24: Class #8
Obstructive and Inflammatory
Lung Disease
Emphysema
 Chronic Bronchitis
 Asthma

Christine Hooper, Ed.D., RN
Spring 2006
Class Objectives
Differentiate among the etiology,
pathophysiology, clinical manifestations,
collaborative care, and appropriate
nursing diagnoses of the client with
emphysema and chronic bronchitis.
 Describe the etiology, pathophysiology,
clinical manifestations, collaborative care,
and appropriate nursing diagnoses of the
client with asthma.
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Chronic Obstructive
Pulmonary Disease: COPD
Disease of airflow obstruction
that is not totally reversible
Chronic
Bronchitis
Emphysema
QuickTime™ and a
TIFF (LZW) decompressor
are needed to see this picture.
COPD: Etiology
Cigarette smoking #1
 Recurrent respiratory infection
 Alpha 1-antitrypsin deficiency
 Aging
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Chronic Bronchitis
Recurrent or chronic productive cough for
a minimum of 3 months for 2 consecutive
years.
 Risk factors
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Cigarette smoke
 Air pollution
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Chronic Bronchitis
Pathophysiology
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Chronic inflammation
Hypertrophy &
hyperplasia of
bronchial glands that
secrete mucus
Increase number of
goblet cells
Cilia are destroyed
Chronic Bronchitis
Pathophysiology
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Narrowing of airway
Starting w/ bronchi 
smaller airways
airflow resistance
work of breathing
Hypoventilation & CO2
retention  hypoxemia &
hypercapnea
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Chronic Bronchitis
Pathophysiology
Bronchospasm often occurs
 End result
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Hypoxemia
 Hypercapnea
 Polycythemia (increase RBCs)
 Cyanosis
 Cor pulmonale (enlargement of right side of heart)
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Chronic Bronchitis:
Clinical Manifestations
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In early stages
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Clients may not recognize early symptoms
Symptoms progress slowly
May not be diagnosed until severe episode with a
cold or flu
Productive cough
• Especially in the morning
• Typically referred to as “cigarette cough”
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Bronchospasm
Frequent respiratory infections
Chronic Bronchitis:
Clinical Manifestations
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Advanced stages
Dyspnea on exertion Dyspnea at rest
 Hypoxemia & hypercapnea
 Polycythemia
 Cyanosis
 Bluish-red skin color
 Pulmonary hypertension Cor pulmonale
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Chronic Bronchitis:
Diagnostic Tests
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PFTs
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ABGs
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FVC:  Forced vital capacity
FEV1:  Forcible exhale in 1 second
FEV1/FVC = <70%
 PaCO2
 PaO2
CBC
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 Hct
Emphysema
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Abnormal distension
of air spaces
Actual cause is
unknown
Emphysema: Pathophysiology
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Structural changes
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Hyperinflation of alveoli
Destruction of alveolar &
alveolar-capillary walls
Small airways narrow
Lung elasticity decreases
Emphysema: Pathophysiology
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Mechanisms of
structural change
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Obstruction of small
bronchioles
Proteolytic enzymes destroy
alveolar tissue
Elastin & collagen are
destroyed
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Support structure is destroyed
“paper bag” lungs
Emphysema: Pathophysiology
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The end result:
Alveoli lose elastic recoil,
then distend, &
eventually blow out.
Small airways collapse or
narrow
Air trapping
Hyperinflation
Decreased surface area
for ventilation
QuickTime™ and a
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Emphysema:
Clinical Manifestations
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Early stages
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Dyspnea
Non productive cough
Diaphragm flattens
A-P diameter increases
• “Barrel chest”
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Hypoxemia may occur
• Increased respiratory rate
• Respiratory alkalosis
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Prolonged expiratory phase
Emphysema:
Clinical Manifestations
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Later stages
Hypercapnea
 Purse-lip breathing
 Use of accessory muscles to breathe
 Underweight
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• No appetite & increase breathing workload
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Lung sounds diminished
Emphysema: Clinical
Manifestations
Emphysema: Clinical
Manifestations
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Pulmonary function
•  residual volume,  lung capacity, DECREASED FEV1,
vital capacity maybe normal
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Arterial blood gases
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Normal in moderate disease
May develop respiratory alkalosis
Later: hypercapnia and respiratory acidosis
Chest x-ray
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Flattened diaphragm
hyperinflation
Goals of Treatment: Emphysema
& Chronic Bronchitis
Improved ventilation
 Remove secretions
 Prevent complications
 Slow progression of signs & symptoms
 Promote patient comfort and participation
in treatment
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Collaborative Care: Emphysema &
Chronic Bronchitis
Treat respiratory infection
 Monitor spirometry and PEFR
 Nutritional support
 Fluid intake 3 lit/day
 O2 as indicated
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Collaborative Care: Medications
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Anti-inflammatory
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Bronchodilators
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Corticosteroids
Beta-adrenergic agonist: Proventil
Methylxanthines: Theophylline
Anticholinergics: Atrovent
Mucolytics: Mucomyst
Expectorants: Guaifenisin
Antihistamines: non-drying
Collaborative Care: Emphysema &
Chronic Bronchitis
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Client teaching
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Support to stop smoking
Conservation of energy
Breathing exercises
• Pursed lip breathing
• Diaphragm breathing
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Chest physiotherapy
• Percussion, vibration
• Postural drainage
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Self-manage medications
• Inhaler & oxygen equipment
Asthma
Reversible inflammation & obstruction
 Intermittent attacks
 Sudden onset
 Varies from person to person
 Severity can vary from shortness of
breath to death
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Asthma
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Triggers
Allergens
 Exercise
 Respiratory infections
 Drugs and food additives
 Nose and sinus problems
 GERD
 Emotional stress
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Asthma: Pathophysiology
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QuickTime™ and a
TIFF (LZW) decompressor
are needed to see this picture.
Swelling of mucus
membranes (edema)
Spasm of smooth
muscle in bronchioles
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Increased airway
resistance
Increased mucus
gland secretion
Asthma: Pathophysiology
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Early phase response: 30 – 60 minutes
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Allergen or irritant activates mast cells
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Inflammatory mediators are released
• histamine, bradykinin, leukotrienes, prostaglandins, plateletactivating-factor, chemotactic factors, cytokines
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Intense inflammation occurs
• Bronchial smooth muscle constricts
• Increased vasodilation and permeability
• Epithelial damage
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Bronchospasm
• Increased mucus secretion
• Edema
Asthma: Pathophysiology
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Late phase response: 5 – 6 hours
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Characterized by inflammation
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Eosinophils and neutrophils infiltrate
Mediators are released
mast cells release
histamine and additional mediators
Self-perpetuating cycle
Lymphocytes and monocytes invade as well
Future attacks may be worse because of increased
airway reactivity that results from late phase
response
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• Individual becomes hyperresponsive to specific allergens
and non-specific irritants such as cold air and dust
• Specific triggers can be difficult to identify and less
stimulation is required to produce a reaction
Asthma: Early Clinical
Manifestations
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Expiratory & inspiratory wheezing
Dry or moist non-productive cough
Chest tightness
Dyspnea
Anxious &Agitated
Prolonged expiratory phase
Increased respiratory & heart rate
Decreased PEFR
Asthma: Early Clinical
Manifestations
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Wheezing
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Chest tightness
Dyspnea
 Cough
 Prolonged expiratory phase [1:3 or 1:4]
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Asthma: Severe Clinical
Manifestations
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Hypoxia
Confusion
Increased heart rate & blood pressure
Respiratory rate up to 40/minute & pursed lip
breathing
Use of accessory muscles
Diaphoresis & pallor
Cyanotic nail beds
Flaring nostrils
Endotracheal Intubation
Classifications of Asthma
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Mild intermittent
Mild persistent
 Moderate persistent
 Severe persistent
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Asthma: Diagnostic Tests
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Pulmonary Function Tests
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FEV1 decreased
• Increase of 12% - 15% after bronchodilator indicative of asthma
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PEFR decreased
Symptomatic patient
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eosinophils > 5% of total WBC
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Increased serum IgE
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Chest x-ray shows hyperinflation
ABGs
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Early: respiratory alkalosis, PaO2 normal or near-normal
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severe: respiratory acidosis, increased PaCO2,
Asthma: Collaborative Care
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Mild intermittent
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Avoid triggers
Premedicate before exercising
 May not need daily medication
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Mild persistent asthma
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Avoid triggers
Premedicate before exercising
 Low-dose inhaled corticosteroids
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Asthma: Collaborative Care
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Moderate persistent asthma
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Low-medium dose inhaled corticosteroids
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Long-acting beta2-agonists
Can increase doses or use theophylline or
leukotriene-modifier [singulair, accolate, zyflo]
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Severe persistent asthma
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High-dose inhaled corticosteroids
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Long-acting inhaled beta2-agonists
Corticosteroids if needed
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Asthma: Collaborative Care
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Acute episode
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FEV1, PEFR, pulse oximetry compared to baseline
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O2 therapy
Beta2-adrenergic agonist
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• via MDI w/spacer or nebulizer
• Q20 minutes – 4 hours prn
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Corticosteroids if initial response insufficient
• Severity of attack determines po or IV
• If poor response, consider IV aminophylline
Asthma Medications: Antiinflammatory
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Corticosteroids
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Not useful for acute attack
Beclomethasone: vanceril,
beclovent, qvar
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Leukotriene modifiers
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Interfere with synthesis or
block action of leukotrienes
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Have both bronchodilation
and anti-inflammatory
properties
Not recommended for acute
asthma attacks
Should not be used as only
therapy for persistent
asthma
Accolate, Singulair, Zyflo
Cromolyn & nedocromil
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Inhibits immediate response
from exercise and allergens
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Prevents late-phase response
Useful for premedication for
exercise, seasonal asthma
Intal, Tilade
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Asthma Medications:
Bronchodilators
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2-adrenergic agonists
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Rapid onset: quick relief of bronchoconstriction
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Treatment of choice for acute attacks
If used too much causes tremors, anxiety, tachycardia, palpitations,
nausea
Too-frequent use indicates poor control of asthma
Short-acting
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• Albuterol[proventil]; metaproterenol [alupent]; bitolterol [tornalate];
pirbuterol [maxair]
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Long-acting
• Useful for nocturnal asthma
• Not useful for quick relief during an acute attack
• Salmeterol [serevent]
Asthma Medications:
Bronchodilators con’t
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Methylxanthines
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Anticholinergics
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Less effective than betaadrenergics
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Inhibit parasympathetic
effects on respiratory system
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Useful to alleviate
bronchoconstriction of early
and late phase, nocturnal
asthma
Does not relieve
hyperresponsiveness
Side effects: nausea,
headache, insomnia,
tachycardia, arrhythmias,
seizures
Theophylline, aminophylline
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Increased mucus
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Smooth muscle contraction
Useful for pts w/adverse
reactions to beta-adrenergics
or in combination w/betaadrenergics
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Ipratropium [atrovent]
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Ipratropium + albuterol
[Combivent]
Asthma: Client Teaching
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Correct use of medications
Signs & symptoms of an attack
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Dyspnea, anxiety, tight chest, wheezing, cough
Relaxation techniques
When to call for help, seek treatment
Environmental control
Cough & postural drainage techniques
Asthma: Nursing Diagnoses
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Ineffective airway clearance r/t bronchospasm,
ineffective cough, excessive mucus
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Anxiety r/t difficulty breathing, fear of suffocation
Ineffective therapeutic regimen management r/t
lack of information about asthma
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