Chronic Obstructive Pulmonary Disease (COPD)

1. Chronic Obstructive Pulmonary Disease (COPD)

2. COPDDescription • Characterized by presence of airflow obstruction • Caused by emphysema or chronic bronchitis • Generally progressive • May be accompanied by airway hyperreactivity • May be partially reversible

3. EmphysemaDescription • Abnormal permanent enlargement of the air space distal to the terminal bronchioles • Accompanied by destruction of bronchioles

4. Chronic BronchitisDescription • Presence of chronic productive cough for 3 or more months in each of 2 successive years in a patient whom other causes of chronic cough have been excluded

5. COPDCauses • Cigarette smoking • Primary cause of COPD*** • Clinically significant airway obstruction develops in 15% of smokers • 80% to 90% of COPD deaths are related to tobacco smoking • > 1 in 5 deaths is result of cigarette smoking

6. COPDCauses • Cigarette smoking • Nicotine stimulates sympathetic nervous system resulting in: •  HR • Peripheral vasoconstriction •  BP and cardiac workload

7. COPDCauses • Cigarette smoking • Compounds problems in a person with CAD •  Ciliary activity • Possible loss of ciliated cells • Abnormal dilation of the distal air space • Alveolar wall destruction • Carbon monoxide •  O2 carrying capacity • Impairs psychomotor performance and judgment • Cellular hyperplasia • Production of mucus • Reduction in airway diameter • Increased difficulty in clearing secretions

8. COPDCauses • Secondhand smoke exposure associated with: •  Pulmonary function •  Risk of lung cancer •  Mortality rates from ischemic heart disease

9. COPDCauses • Infection • Major contributing factor to the aggravation and progression of COPD • Heredity • -Antitrypsin (AAT) deficiency (produced by liver and found in lungs); accounts for < 1% of COPD cases • Emphysema results from lysis of lung tissues by proteolytic enzymes from neutrophils and macrophages

10. Pathophysiology of Chronic Bronchitis and Emphysema Fig. 28-7

11. EmphysemaPathophysiology • Hyperinflation of alveoli • Destruction of alveolar walls • Destruction of alveolar capillary walls • Narrowed airways • Loss of lung elasticity

12. Emphysema Pathophysiology • Two types: • Centrilobular (central part of lobule) • Most common • Panlobular (destruction of whole lobule) • Usually associated with AAT deficiency

13. Emphysema Pathophysiology • Structural changes are: • Hyperinflation of alveoli • Destruction of alveolar capillary walls • Narrowed, tortuous small airways • Loss of lung elasticity

14. Emphysema Pathophysiology • Small bronchioles become obstructed as a result of • Mucus • Smooth muscle spasm • Inflammatory process • Collapse of bronchiolar walls • Recurrent infections production/stimulation of neutrophils and macrophages release proteolytic enzymes alveolar destruction inflammation, exudate, and edema

15. Emphysema Pathophysiology • Elastin and collagen are destroyed • Air goes into the lungs but is unable to come out on its own and remains in the lung • Causes bronchioles to collapse

16. Emphysema Pathophysiology • Trapped air  hyperinflation and overdistention • As more alveoli coalesce, blebs and bullae may develop • Destruction of alveolar walls and capillaries  reduced surface area for O2 diffusion • Compensation is done by increasing respiratory rate to increase alveolar ventilation • Hypoxemia usually develops late in disease

17. EmphysemaClinical Manifestations • Dyspnea • Progresses in severity • Patient will first complain of dyspnea on exertion and progress to interfering with ADLs and rest

18. Emphysema Clinical Manifestations • Minimal coughing with no to small amounts of sputum • Overdistention of alveoli causes diaphragm to flatten and AP diameter to increase

19. Emphysema Clinical Manifestations • Patient becomes chest breather, relying on accessory muscles • Ribs become fixed in inspiratory position

20. EmphysemaClinical Manifestations • Patient is underweight (despite adequate calorie intake)

21. Chronic BronchitisPathophysiology Pathologic lung changes are: • Hyperplasia of mucus-secreting glands in trachea and bronchi • Increase in goblet cells • Disappearance of cilia • Chronic inflammatory changes and narrrowing of small airways • Altered fxn of alveolar macrophages infections

22. Chronic BronchitisPathophysiology Chronic inflammation • Primary pathologic mechanism causing changes • Narrow airway lumen and reduced airflow d/t • hyperplasia of mucus glands • Inflammatory swelling • Excess, thick mucus

23. Chronic BronchitisPathophysiology • Greater resistance to airflow increases work of breathing • Hypoxemia and hypercapnia develop more frequently in chronic bronchitis than emphysema

24. Chronic BronchitisPathophysiology • Bronchioles are clogged with mucus and pose a physical barrier to ventilation • Hypoxemia and hypercapnia d/t lack of ventilation and O2 diffusion • Tendency to hypoventilate and retain CO2 • Frequently patients require O2 both at rest and during exercise

25. Chronic BronchitisPathophysiology • Cough is often ineffective to remove secretions because the person cannot breathe deeply enough to cause air flow distal to the secretions • Bronchospasm frequently develops • More common with history of smoking or asthma

26. Chronic BronchitisClinical Manifestations • Earliest symptoms: • Frequent, productive cough during winter • Frequent respiratory infections

27. Chronic BronchitisClinical Manifestations • Bronchospasm at end of paroxysms of coughing • Cough • Dyspnea on exertion • History of smoking • Normal weight or heavyset • Ruddy (bluish-red) appearance d/t • polycythemia (increased Hgb d/t chronic hypoxemia)) • cyanosis

28. Chronic BronchitisClinical Manifestations • Hypoxemia and hypercapnia • Results from hypoventilation and  airway resistance + problems with alveolar gas exchange

29. COPDComplications • Pulmonary hypertension (pulmonary vessel constriction d/t alveolar hypoxia & acidosis) • Cor pulmonale (Rt heart hypertrophy + RV failure) • Pneumonia • Acute Respiratory Failure

30. COPDDiagnostic Studies • Chest x-rays early in the disease may not show abnormalities • History and physical exam • Pulmonary function studies • reduced FEV1/FVC and  residual volume and total lung capacity

31. COPDDiagnostic Studies • ABGs •  PaO2 •  PaCO2 (especially in chronic bronchitis) •  pH (especially in chronic bronchitis) •  Bicarbonate level found in late stages COPD

32. COPDCollaborative Care • Smoking cessation • Most significant factor in slowing the progression of the disease

33. COPDCollaborative Care:Drug Therapy • Bronchodilators – as maintenance therapy • -adrenergic agonists (e.g. Ventolin) • MDI or nebulizer preferred • Anticholinergics (e.g. Atrovent)

34. COPDCollaborative Care: Oxygen Therapy • O2 therapy • Raises PO2 in inspired air • Treats hypoxemia • Titrate to lowest effective dose

35. COPDCollaborative Care: Oxygen Therapy • Chronic O2 therapy at home • Improved prognosis • Improved neuropsychologic function • Increased exercise tolerance • Decreased hematocrit • Reduced pulmonary hypertension

36. COPDCollaborative Care: Respiratory Therapy • Breathing retraining • Pursed-lip breathing • Prolongs exhalation and prevents bronchiolar collapse and air trapping • Diaphragmatic breathing • Focuseson using diaphragm instead of accessory muscles to achieve maximum inhalation and slow respiratory rate • See text re how to teach

37. COPDCollaborative Care: Respiratory Therapy • Huff coughing (Table 28-21) • Chest physiotherapy – to bring secretions into larger, more central airways • Postural drainage • Percussion • Vibration

38. Positions for Postural Drainage Positions for Postural Drainage Fig. 28-16

39. COPDCollaborative Care • Encourage patient to remain as active as possible

40. COPDCollaborative Care • Surgical Therapy • Lung volume reduction surgery • Lung transplant

41. COPDCollaborative Care • Nutritional therapy • Full stomachs press on diaphragm causing dyspnea and discomfort • Difficulty eating and breathing at the same time leads to inadequate amounts being eaten

42. COPDCollaborative Care • Nutritional therapy • To decrease dyspnea and conserve energy • Rest at least 30 minutes prior to eating • Use bronchodilator before meals • Select foods that can be prepared in advance • 5-6 small meals to avoid bloating • Avoid foods that require a great deal of chewing • Avoid exercises and treatments 1 hour before and after eating

43. COPDCollaborative Care • Nutritional therapy • Avoid gas-forming foods • High-calorie, high-protein diet is recommended • Supplements • Avoid high carbohydrate diet to prevent increase in CO2 load

44. Nursing ManagementNursing Diagnoses • Ineffective airway clearance • Impaired gas exchange • Imbalanced nutrition: less than body requirements • Disturbed sleep pattern • Risk for infection

45. Nursing ManagementNursing Implementation Health Promotion • STOP SMOKING!!! • Avoid or control exposure to occupational and environmental pollutants and irritants • Early detection of small-airway disease • Early diagnosis of respiratory tract infections

46. Nursing ManagementNursing Implementation Acute Intervention • Required for complications like pneumonia, cor pulmonale, and acute respiratory failure

47. Nursing ManagementNursing Implementation Ambulatory and Home Care • Pulmonary rehabilitation • Control and alleviate symptoms of pathophysiologic complications of respiratory impairment

48. Nursing ManagementNursing Implementation Ambulatory and Home Care • Teach patient how to achieve optimal capability in carrying out ADLs • Physical therapy • Nutrition • Education • Activity considerations • Exercise trainingof upper extremities to help improve function and relieve dyspnea

49. Nursing ManagementNursing Implementation • Ambulatory and Home Care • Explore alternative methods of ADLs • Encourage patient to sit while performing activities • Coordinated walking

50. Nursing ManagementNursing Implementation Ambulatory and Home Care • Slow, pursed-lip breathing • After exercise, wait 5 minutes before using -adrenergic agonist MDI