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
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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
FVC: Forced vital capacity FEV1: Forcible exhale in 1 second FEV1/FVC = <70% PaCO2 PaO2 Hct
ABGs
CBC
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
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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
Flattened diaphragm hyperinflation
Chest x-ray
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
Corticosteroids Beta-adrenergic agonist: Proventil Methylxanthines: Theophylline Anticholinergics: Atrovent
Bronchodilators
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
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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] High-dose inhaled corticosteroids Long-acting inhaled beta2-agonists Corticosteroids if needed
Severe persistent asthma
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
Leukotriene modifiers
Not useful for acute attack Beclomethasone: vanceril, beclovent, qvar Inhibits immediate response from exercise and allergens Prevents late-phase response Useful for premedication for exercise, seasonal asthma Intal, Tilade
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
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 cont
Methylxanthines
Anticholinergics
Less effective than betaadrenergics 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
Inhibit parasympathetic effects on respiratory system 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
