1 / 42

N24: Class #8 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.

teneil
Télécharger la présentation

N24: Class #8 Obstructive and Inflammatory Lung Disease

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. N24: Class #8Obstructive and Inflammatory Lung Disease • Emphysema • Chronic Bronchitis • Asthma Christine Hooper, Ed.D., RN Spring 2006

  2. 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.

  3. Chronic Obstructive Pulmonary Disease: COPD Disease of airflow obstruction that is not totally reversible • Chronic Bronchitis • Emphysema

  4. COPD: Etiology • Cigarette smoking #1 • Recurrent respiratory infection • Alpha 1-antitrypsin deficiency • Aging

  5. Chronic Bronchitis • Recurrent or chronic productive cough for a minimum of 3 months for 2 consecutive years. • Risk factors • Cigarette smoke • Air pollution

  6. Chronic Bronchitis Pathophysiology • Chronic inflammation • Hypertrophy & hyperplasia of bronchial glands that secrete mucus • Increase number of goblet cells • Cilia are destroyed

  7. Chronic Bronchitis Pathophysiology • Narrowing of airway • Starting w/ bronchi  smaller airways • airflow resistance • work of breathing • Hypoventilation & CO2 retention  hypoxemia & hypercapnea

  8. Chronic Bronchitis Pathophysiology • Bronchospasm often occurs • End result • Hypoxemia • Hypercapnea • Polycythemia (increase RBCs) • Cyanosis • Cor pulmonale (enlargement of right side of heart)

  9. 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

  10. Chronic Bronchitis: Clinical Manifestations • Advanced stages • Dyspnea on exertion Dyspnea at rest • Hypoxemia & hypercapnea • Polycythemia • Cyanosis • Bluish-red skin color • Pulmonary hypertension Cor pulmonale

  11. Chronic Bronchitis: Diagnostic Tests • PFTs • FVC:  Forced vital capacity • FEV1:  Forcible exhale in 1 second • FEV1/FVC = <70% • ABGs •  PaCO2 •  PaO2 • CBC •  Hct

  12. Emphysema • Abnormal distension of air spaces • Actual cause is unknown

  13. Emphysema: Pathophysiology • Structural changes • Hyperinflation of alveoli • Destruction of alveolar & alveolar-capillary walls • Small airways narrow • Lung elasticity decreases

  14. 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

  15. 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

  16. 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

  17. Emphysema: Clinical Manifestations • Later stages • Hypercapnea • Purse-lip breathing • Use of accessory muscles to breathe • Underweight • No appetite & increase breathing workload • Lung sounds diminished

  18. Emphysema: Clinical Manifestations

  19. 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

  20. Goals of Treatment: Emphysema & Chronic Bronchitis • Improved ventilation • Remove secretions • Prevent complications • Slow progression of signs & symptoms • Promote patient comfort and participation in treatment

  21. Collaborative Care: Emphysema & Chronic Bronchitis • Treat respiratory infection • Monitor spirometry and PEFR • Nutritional support • Fluid intake 3 lit/day • O2 as indicated

  22. Collaborative Care: Medications • Anti-inflammatory • Corticosteroids • Bronchodilators • Beta-adrenergic agonist: Proventil • Methylxanthines: Theophylline • Anticholinergics: Atrovent • Mucolytics: Mucomyst • Expectorants: Guaifenisin • Antihistamines: non-drying

  23. 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

  24. Asthma • Reversible inflammation & obstruction • Intermittent attacks • Sudden onset • Varies from person to person • Severity can vary from shortness of breath to death

  25. Asthma • Triggers • Allergens • Exercise • Respiratory infections • Drugs and food additives • Nose and sinus problems • GERD • Emotional stress

  26. Asthma: Pathophysiology • Swelling of mucus membranes (edema) • Spasm of smooth muscle in bronchioles • Increased airway resistance • Increased mucus gland secretion

  27. 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

  28. 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

  29. 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

  30. Asthma: Early Clinical Manifestations • Wheezing • Chest tightness • Dyspnea • Cough • Prolonged expiratory phase [1:3 or 1:4]

  31. 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

  32. Endotracheal Intubation

  33. Classifications of Asthma • Mild intermittent • Mild persistent • Moderate persistent • Severe persistent

  34. 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,

  35. 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

  36. 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

  37. 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

  38. 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 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 Asthma Medications: Anti-inflammatory

  39. 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]

  40. 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] Asthma Medications: Bronchodilators con’t

  41. 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

  42. Asthma: Nursing Diagnoses • Ineffective airway clearancer/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

More Related