Chapter 31

1. Chapter 31 Chronic Respiratory Disorders

2. Learning Objectives • Identify examples of chronic inflammatory, obstructive, and restrictive pulmonary diseases. • Explain the relationship between cigarette smoking and chronic respiratory disorders. • For selected chronic respiratory disorders, describe the pathophysiology, signs and symptoms, complications, diagnostic measures, and medical treatment. • Assist in developing a nursing care plan for the patient who has a chronic respiratory disorder.

3. Asthma

4. Pathophysiology Potentially reversible obstructive airway disorder: airway inflammation and hyperresponsiveness

5. Pathophysiology: Acute Episode Begins when “triggers” activate the inflammatory process Airways constrict and become edematous Mucous secretion increases, forming plugs in the airways, and tenacious sputum is produced Obstruction causes air to be trapped in the alveoli, creating a ventilation-perfusion mismatch Effect is hypoxemia with compensatory hyperventilation Acute episodes begin within 30 to 60 minutes after exposure to trigger and resolve 30 to 90 minutes later

6. Figure 31-1

7. Pathophysiology Late phase Begins 5 to 6 hours after the early phase response Red and white blood cells infiltrate swollen tissues of the airways During this phase, which lasts several hours or days, the airways are hyperreactive (very sensitive) Risk for another episode until phase subsides When no specific trigger can be identified, the patient may be said to have “intrinsic” asthma Asthma with known triggers: “extrinsic” asthma

8. Signs and Symptoms Dyspnea, productive cough, use of accessory muscles of respiration, audible expiratory wheezing, tachycardia, and tachypnea

9. Medical Diagnosis Health history, the physical examination, and the pulmonary function test results

10. Medical Treatment Bronchodilators Anti-inflammatory drugs

11. Figure 31-2

12. Assessment Essential information (medications, allergies, known cardiac disease, sleep disruption); immediately take steps to relieve symptoms Health history Frequency and severity of attacks, the factors known to trigger attacks, effect of condition on patient’s life, strategies used to manage the condition, sources of stress and support, and patient’s knowledge about asthma and its treatment

13. Assessment Physical examination Measurement of vital signs and auscultation of lung sounds Assess skin color and respiratory effort

14. Interventions Ineffective Breathing Pattern Impaired Gas Exchange Anxiety

15. Chronic Bronchitis and Emphysema

16. Pathophysiology Chronic bronchitis Bronchial inflammation; increased production of mucus and chronic cough that persist for at least 3 months of the year for 2 consecutive years and by impaired ciliary action Cause: inhaled irritants, e.g., cigarette smoke Cor pulmonale: right-sided heart failure secondary to pulmonary disease

17. Figure 31-3

18. Pathophysiology Emphysema Degenerative, nonreversible disease: enlargement of the airways beyond the terminal bronchioles Centrilobular emphysema Associated with cigarette smoking; affects mainly the respiratory bronchioles Panlobular emphysema Affects the respiratory bronchioles and the alveoli

19. Figure 31-4

20. Complications Respiratory failure Factors: infection, air pollution, continued smoking, left ventricular failure, myocardial infarction, pulmonary embolism, spontaneous pneumothorax, and adverse effects of drugs

21. Signs and Symptoms Chronic bronchitis Productive cough, exertional dyspnea, and wheezing Emphysema Dyspnea on exertion Increased anteroposterior diameter

22. Figure 31-5

23. Figure 31-6

24. Figure 31-7

25. Medical Diagnosis Patient’s health history and physical examination Pulmonary function tests Computed tomography (CT) scan

26. Medical Treatment Drug therapy Goals: improved ventilation and removal of secretions Bronchodilators Corticosteroids

27. Medical Treatment Oxygen therapy Initial is usually 1 to 3 L/minute Chest physiotherapy Exercise Nutrition Supplementary feedings may be needed Good hydration Treatment of respiratory failure Oxygen therapy, aerosol bronchodilators, chest physiotherapy, and mechanical ventilation

28. Surgical Treatment Lung volume reduction surgery (LVRS) Up to 30% of hyperinflated lung tissue excised to improve mechanics of breathing, enabling patient to breathe more deeply Bullectomy (removal of bullae) Lung transplantation

29. Assessment Describe the presenting symptoms—often dyspnea, cough, chest pain, or a combination of these Obtain a complete medical history List of current medications and drug allergies

30. Assessment Physical examination Posture, color, respiratory effort, and use of accessory muscles of respiration; measure vital signs Hypoxemia: restlessness, confusion, and lethargy Inspect neck for distention of veins Shape of the thorax for the classic barrel chest Auscultate lung fields for diminished breath sounds Inspect the nails for clubbing, pallor, or cyanosis Inspect and palpate the feet and ankles for edema; note muscle wasting

31. Interventions Impaired Gas Exchange Ineffective Airway Clearance Anxiety Imbalanced Nutrition: Less Than Body Requirements Risk for Infection Activity Intolerance Decreased Cardiac Output

32. Figure 31-8

33. Bronchiectasis Abnormal dilation/distortion of bronchi and bronchioles; usually confined to one lung lobe or segment Follows recurrent inflammatory conditions, infections, or obstructions but is sometimes congenital Signs: coughing, production of large amounts of purulent sputum Also fever, hemoptysis, nasal stuffiness, sinus drainage, fatigue, and weakness Goals: control symptoms and prevent spread Treatment: antibiotic therapy, bronchodilators, chest physiotherapy, and oxygen therapy

34. Cystic Fibrosis Hereditary disorder characterized by dysfunction of the exocrine glands and production of thick, tenacious mucus Cough is the first pulmonary symptom Becomes productive of thick, purulent sputum; obstructs airways Results in obstruction of the pancreatic ducts so that pancreatic enzymes cannotbe delivered to the GI tract

35. Cystic Fibrosis Stools become bulky and foul smelling Lose more salt in sweat than normal; at risk for salt depletion, especially in hot environments Over years, symptoms progress: increased dyspnea, decreased exercise tolerance, and weight loss Airway obstruction and decreased resistance to infections lead to chronic bacterial infections, emphysema, atelectasis, and respiratory failure

36. Cystic Fibrosis Treatment Pancreatic enzyme replacement, chest physiotherapy, and aerosol and nebulizer treatments to reduce mucus viscosity Infections treated with antibiotics

37. Cystic Fibrosis Nursing care To clear airway: administer prescribed medications, maintain hydration, and perform chest physiotherapy Prevent infection with medical asepsis and protect patient from others with infections Maintain adequate nutrition: administer pancreatic enzymes as ordered, allow for rest around mealtimes, and encourage to consume adequate nutrients

38. Tuberculosis

39. Etiology and Risk Factors An infection caused by Mycobacterium tuberculosis, an acid-fast aerobic bacterium Spread by droplets from infected people during coughing, laughing, sneezing, and singing Anyone may become infected, but most healthy people not through brief contact At increased risk: elderly, economically disadvantaged and homeless, substance abusers, children younger than 5 years, the immunosuppressed, racial and ethnic groups

40. Pathophysiology Most people do not acquire active (symptomatic, progressive) tuberculosis Body’s immune response attempts to destroy the infecting organisms, but some may escape into the lymph nodes or throughout the body The site of the primary infection may undergo necrotic degeneration

41. Pathophysiology Cavities develop that are filled with infectious material, which eventually liquefies and is coughed up as sputum In some, infectious process progresses, and active tuberculosis develops It is possible for inactive bacteria to be reactivated, causing illness later

42. Signs and Symptoms Cough, night sweats, chest pain and tightness, fatigue, anorexia, weight loss, and low-grade fever

43. Medical Diagnosis History and physical examination Sputum cultures, acid-fast smears of potentially infected body fluids, tuberculin skin tests, and chest radiographs

44. Medical Treatment Common preventive treatment is isoniazid therapy for 9 to 12 months Individuals with inactive tuberculosis may be treated with INH alone, INH with rifampin, or rifampin with pyrazinamide

45. Assessment A complete health history and a physical examination

46. Interventions Impaired Gas Exchange Social Isolation Risk for Injury Fatigue Imbalanced Nutrition: Less Than Body Requirements Ineffective Therapeutic Regimen Management

47. Interstitial Lung Disease Inflammation of the lower respiratory tract and thickening and fibrosis of the alveolar walls; render the alveoli nonfunctional May be caused by inhaled substances or connective tissue disorders; sometimes no specific cause identified Examples: idiopathic pulmonary fibrosis (occupational lung diseases), sarcoidosis

48. Idiopathic Pulmonary Fibrosis Pathophysiology Formation of scar tissue in lung tissue after inflammation or irritation Cigarette smoking, frequent aspiration, or exposure to environmental or occupational substances Complications Pulmonary hypertension, cor pulmonale, and ventilatory failure

49. Idiopathic Pulmonary Fibrosis Signs and symptoms Nonproductive cough and progressive dyspnea Inspirational crackles heard in the lungs on auscultation Clubbing of the fingertips

50. Idiopathic Pulmonary Fibrosis Medical treatment Corticosteroids, bronchodilators, and oxygen therapy Also cytotoxic drugs and antifibrotic agents Interventions Similar to those described for the patient with COPD