Obstructive and Inflammatory Lung Disease

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 Bronchitis Emphysema Chronic 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    FVC:  Forced vital capacity FEV1:  Forcible exhale in 1 second FEV1/FVC = <70%  PaCO2  PaO2  ABGs    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  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   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] 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 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 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  