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N24: Class #8 Obstructive and Inflammatory Lung Disease
Emphysema Chronic Bronchitis Asthma Christine Hooper, Ed.D., RN Spring 2006
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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
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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 Cigarette smoke Air pollution
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Chronic Bronchitis Pathophysiology
Chronic inflammation Hypertrophy & hyperplasia of bronchial glands that secrete mucus Increase number of goblet cells Cilia are destroyed
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Chronic Bronchitis Pathophysiology
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 Hypoxemia Hypercapnea Polycythemia (increase RBCs) Cyanosis Cor pulmonale (enlargement of right side of heart)
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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
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Chronic Bronchitis: Clinical Manifestations
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
PFTs FVC: Forced vital capacity FEV1: Forcible exhale in 1 second FEV1/FVC = <70% ABGs PaCO2 PaO2 CBC Hct
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Emphysema Abnormal distension of air spaces Actual cause is unknown
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Emphysema: Pathophysiology
Structural changes Hyperinflation of alveoli Destruction of alveolar & alveolar-capillary walls Small airways narrow Lung elasticity decreases
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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
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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
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Emphysema: Clinical Manifestations
Later stages Hypercapnea Purse-lip breathing Use of accessory muscles to breathe Underweight No appetite & increase breathing workload Lung sounds diminished
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Emphysema: Clinical Manifestations
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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
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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
Anti-inflammatory Corticosteroids Bronchodilators Beta-adrenergic agonist: Proventil Methylxanthines: Theophylline Anticholinergics: Atrovent Mucolytics: Mucomyst Expectorants: Guaifenisin Antihistamines: non-drying
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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
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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 Triggers Allergens Exercise Respiratory infections
Drugs and food additives Nose and sinus problems GERD Emotional stress
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Asthma: Pathophysiology
Swelling of mucus membranes (edema) Spasm of smooth muscle in bronchioles Increased airway resistance Increased mucus gland secretion
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Asthma: Pathophysiology
Early phase response: 30 – 60 minutes Allergen or irritant activates mast cells Inflammatory mediators are released histamine, bradykinin, leukotrienes, prostaglandins, platelet- activating-factor, chemotactic factors, cytokines Intense inflammation occurs Bronchial smooth muscle constricts Increased vasodilation and permeability Epithelial damage Bronchospasm Increased mucus secretion Edema
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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
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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
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Asthma: Early Clinical Manifestations
Wheezing Chest tightness Dyspnea Cough Prolonged expiratory phase [1:3 or 1:4]
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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
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Endotracheal Intubation
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Classifications of Asthma
Mild intermittent Mild persistent Moderate persistent Severe persistent
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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,
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Asthma: Collaborative Care
Mild intermittent Avoid triggers Premedicate before exercising May not need daily medication Mild persistent asthma Low-dose inhaled corticosteroids
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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
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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
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Asthma Medications: Anti-inflammatory
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 Corticosteroids Not useful for acute attack Beclomethasone: vanceril, beclovent, qvar Cromolyn & nedocromil Inhibits immediate response from exercise and allergens Prevents late-phase response Useful for premedication for exercise, seasonal asthma Intal, Tilade
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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]
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Asthma Medications: Bronchodilators con’t
Methylxanthines Less effective than beta- adrenergics 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 Anticholinergics Inhibit parasympathetic effects on respiratory system Increased mucus Smooth muscle contraction Useful for pts w/adverse reactions to beta-adrenergics or in combination w/beta- adrenergics Ipratropium [atrovent] Ipratropium + albuterol [Combivent]
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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
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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
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