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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.
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
Chronic Bronchitis
Recurrent or chronic productive cough for
a minimum of 3 months for 2 consecutive
years.
Risk factors
Cigarette smoke
Air pollution
Chronic Bronchitis
Pathophysiology
Chronic inflammation
Hypertrophy &
hyperplasia of
bronchial glands that
secrete mucus
Increase number of
goblet cells
Cilia are destroyed
Chronic Bronchitis
Pathophysiology
Narrowing of airway
Starting w/ bronchi
smaller airways
airflow resistance
work of breathing
Hypoventilation & CO2
retention hypoxemia &
hypercapnea
Chronic Bronchitis
Pathophysiology
Bronchospasm often occurs
End result
Hypoxemia
Hypercapnea
Polycythemia (increase RBCs)
Cyanosis
Cor pulmonale (enlargement of right side of heart)
Chronic Bronchitis:
Clinical Manifestations
In early stages
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”
Bronchospasm
Frequent respiratory infections
Chronic Bronchitis:
Clinical Manifestations
Advanced stages
Dyspnea on exertion Dyspnea at rest
Hypoxemia & hypercapnea
Polycythemia
Cyanosis
Bluish-red skin color
Pulmonary hypertension Cor pulmonale
Chronic Bronchitis:
Diagnostic Tests
PFTs
ABGs
FVC: Forced vital capacity
FEV1: Forcible exhale in 1 second
FEV1/FVC = <70%
PaCO2
PaO2
CBC
Hct
Emphysema
Abnormal distension
of air spaces
Actual cause is
unknown
Emphysema: Pathophysiology
Structural changes
Hyperinflation of alveoli
Destruction of alveolar &
alveolar-capillary walls
Small airways narrow
Lung elasticity decreases
Emphysema: Pathophysiology
Mechanisms of
structural change
Obstruction of small
bronchioles
Proteolytic enzymes destroy
alveolar tissue
Elastin & collagen are
destroyed
Support structure is destroyed
“paper bag” lungs
Emphysema: Pathophysiology
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
TIFF (LZW) decompressor
are needed to see this picture.
Emphysema:
Clinical Manifestations
Early stages
Dyspnea
Non productive cough
Diaphragm flattens
A-P diameter increases
• “Barrel chest”
Hypoxemia may occur
• Increased respiratory rate
• Respiratory alkalosis
Prolonged expiratory phase
Emphysema:
Clinical Manifestations
Later stages
Hypercapnea
Purse-lip breathing
Use of accessory muscles to breathe
Underweight
• No appetite & increase breathing workload
Lung sounds diminished
Emphysema: Clinical
Manifestations
Emphysema: Clinical
Manifestations
Pulmonary function
• residual volume, lung capacity, DECREASED FEV1,
vital capacity maybe normal
Arterial blood gases
Normal in moderate disease
May develop respiratory alkalosis
Later: hypercapnia and respiratory acidosis
Chest x-ray
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
Collaborative Care: Emphysema &
Chronic Bronchitis
Treat respiratory infection
Monitor spirometry and PEFR
Nutritional support
Fluid intake 3 lit/day
O2 as indicated
Collaborative Care: Medications
Anti-inflammatory
Bronchodilators
Corticosteroids
Beta-adrenergic agonist: Proventil
Methylxanthines: Theophylline
Anticholinergics: Atrovent
Mucolytics: Mucomyst
Expectorants: Guaifenisin
Antihistamines: non-drying
Collaborative Care: Emphysema &
Chronic Bronchitis
Client teaching
Support to stop smoking
Conservation of energy
Breathing exercises
• Pursed lip breathing
• Diaphragm breathing
Chest physiotherapy
• Percussion, vibration
• Postural drainage
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
Asthma
Triggers
Allergens
Exercise
Respiratory infections
Drugs and food additives
Nose and sinus problems
GERD
Emotional stress
Asthma: Pathophysiology
QuickTime™ and a
TIFF (LZW) decompressor
are needed to see this picture.
Swelling of mucus
membranes (edema)
Spasm of smooth
muscle in bronchioles
Increased airway
resistance
Increased mucus
gland secretion
Asthma: Pathophysiology
Early phase response: 30 – 60 minutes
Allergen or irritant activates mast cells
Inflammatory mediators are released
• histamine, bradykinin, leukotrienes, prostaglandins, plateletactivating-factor, chemotactic factors, cytokines
Intense inflammation occurs
• Bronchial smooth muscle constricts
• Increased vasodilation and permeability
• Epithelial damage
Bronchospasm
• Increased mucus secretion
• Edema
Asthma: Pathophysiology
Late phase response: 5 – 6 hours
Characterized by inflammation
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
• 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
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
Wheezing
Chest tightness
Dyspnea
Cough
Prolonged expiratory phase [1:3 or 1:4]
Asthma: Severe Clinical
Manifestations
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
Mild intermittent
Mild persistent
Moderate persistent
Severe persistent
Asthma: Diagnostic Tests
Pulmonary Function Tests
FEV1 decreased
• Increase of 12% - 15% after bronchodilator indicative of asthma
PEFR decreased
Symptomatic patient
eosinophils > 5% of total WBC
Increased serum IgE
Chest x-ray shows hyperinflation
ABGs
Early: respiratory alkalosis, PaO2 normal or near-normal
severe: respiratory acidosis, increased PaCO2,
Asthma: Collaborative Care
Mild intermittent
Avoid triggers
Premedicate before exercising
May not need daily medication
Mild persistent asthma
Avoid triggers
Premedicate before exercising
Low-dose inhaled corticosteroids
Asthma: Collaborative Care
Moderate persistent asthma
Low-medium dose inhaled corticosteroids
Long-acting beta2-agonists
Can increase doses or use theophylline or
leukotriene-modifier [singulair, accolate, zyflo]
Severe persistent asthma
High-dose inhaled corticosteroids
Long-acting inhaled beta2-agonists
Corticosteroids if needed
Asthma: Collaborative Care
Acute episode
FEV1, PEFR, pulse oximetry compared to baseline
O2 therapy
Beta2-adrenergic agonist
• via MDI w/spacer or nebulizer
• Q20 minutes – 4 hours prn
Corticosteroids if initial response insufficient
• Severity of attack determines po or IV
• If poor response, consider IV aminophylline
Asthma Medications: Antiinflammatory
Corticosteroids
Not useful for acute attack
Beclomethasone: vanceril,
beclovent, qvar
Leukotriene modifiers
Interfere with synthesis or
block action of leukotrienes
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
Inhibits immediate response
from exercise and allergens
Prevents late-phase response
Useful for premedication for
exercise, seasonal asthma
Intal, Tilade
Asthma Medications:
Bronchodilators
2-adrenergic agonists
Rapid onset: quick relief of bronchoconstriction
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
• Albuterol[proventil]; metaproterenol [alupent]; bitolterol [tornalate];
pirbuterol [maxair]
Long-acting
• Useful for nocturnal asthma
• Not useful for quick relief during an acute attack
• Salmeterol [serevent]
Asthma Medications:
Bronchodilators con’t
Methylxanthines
Anticholinergics
Less effective than betaadrenergics
Inhibit parasympathetic
effects on respiratory system
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
Increased mucus
Smooth muscle contraction
Useful for pts w/adverse
reactions to beta-adrenergics
or in combination w/betaadrenergics
Ipratropium [atrovent]
Ipratropium + albuterol
[Combivent]
Asthma: Client Teaching
Correct use of medications
Signs & symptoms of an attack
Dyspnea, anxiety, tight chest, wheezing, cough
Relaxation techniques
When to call for help, seek treatment
Environmental control
Cough & postural drainage techniques
Asthma: Nursing Diagnoses
Ineffective airway clearance r/t bronchospasm,
ineffective cough, excessive mucus
Anxiety r/t difficulty breathing, fear of suffocation
Ineffective therapeutic regimen management r/t
lack of information about asthma