Chronic Obstructive Pulmonary Disease (COPD) is characterized by airflow obstruction that is generally progressive and may be partially reversible. It includes emphysema and chronic bronchitis. Cigarette smoking is the primary cause of COPD and damages the lungs through various mechanisms. Pathophysiology involves destruction of lung tissue and narrowing of airways. Symptoms include dyspnea, cough, and limited physical activity. Treatment focuses on smoking cessation, bronchodilators, oxygen therapy, breathing exercises, nutrition management, and pulmonary rehabilitation.

1. Chronic Obstructive
Pulmonary Disease (COPD)

2. COPD
Description
 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. Emphysema
Description
 Abnormal permanent enlargement of the
air space distal to the terminal bronchioles
 Accompanied by destruction of bronchioles

4. Chronic Bronchitis
Description
 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. COPD
Causes
 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. COPD
Causes
 Cigarette smoking
 Nicotine stimulates sympathetic nervous
system resulting in:
  HR
 Peripheral vasoconstriction
  BP and cardiac workload

7. COPD
Causes
 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. COPD
Causes
 Secondhand smoke exposure associated
with:
  Pulmonary function
  Risk of lung cancer
  Mortality rates from ischemic heart
disease

9. COPD
Causes
 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. Emphysema
Pathophysiology
 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. Emphysema
Clinical 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. Emphysema
Clinical Manifestations
 Patient is underweight (despite adequate
calorie intake)

21. Chronic Bronchitis
Pathophysiology
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 Bronchitis
Pathophysiology
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 Bronchitis
Pathophysiology
 Greater resistance to airflow increases
work of breathing
 Hypoxemia and hypercapnia develop
more frequently in chronic bronchitis
than emphysema

24. Chronic Bronchitis
Pathophysiology
 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 Bronchitis
Pathophysiology
 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 Bronchitis
Clinical Manifestations
 Earliest symptoms:
 Frequent, productive cough during
winter
 Frequent respiratory infections

27. Chronic Bronchitis
Clinical 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 Bronchitis
Clinical Manifestations
 Hypoxemia and hypercapnia
 Results from hypoventilation and 
airway resistance + problems with
alveolar gas exchange

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

30. COPD
Diagnostic 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. COPD
Diagnostic Studies
 ABGs
  PaO2
  PaCO2 (especially in chronic bronchitis)
  pH (especially in chronic bronchitis)
  Bicarbonate level found in late stages
COPD

32. COPD
Collaborative Care
 Smoking cessation
 Most significant factor in slowing the
progression of the disease

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

34. COPD
Collaborative Care:
Oxygen Therapy
 O2 therapy
 Raises PO2 in inspired air
 Treats hypoxemia
 Titrate to lowest effective dose

35. COPD
Collaborative Care:
Oxygen Therapy
 Chronic O2 therapy at home
 Improved prognosis
 Improved neuropsychologic function
 Increased exercise tolerance
 Decreased hematocrit
 Reduced pulmonary hypertension

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

37. COPD
Collaborative 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
Fig. 28-16
Positions for Postural Drainage

39. COPD
Collaborative Care
 Encourage patient to remain as active
as possible

40. COPD
Collaborative Care
 Surgical Therapy
 Lung volume reduction surgery
 Lung transplant

41. COPD
Collaborative 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. COPD
Collaborative 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. COPD
Collaborative 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 Management
Nursing Diagnoses
 Ineffective airway clearance
 Impaired gas exchange
 Imbalanced nutrition: less than body
requirements
 Disturbed sleep pattern
 Risk for infection

45. Nursing Management
Nursing 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 Management
Nursing Implementation
Acute Intervention
 Required for complications like pneumonia,
cor pulmonale, and acute respiratory failure

47. Nursing Management
Nursing Implementation
Ambulatory and Home Care
 Pulmonary rehabilitation
 Control and alleviate symptoms of
pathophysiologic complications of
respiratory impairment

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

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

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

51. Nursing Management
Nursing Implementation
Ambulatory and Home Care
 Sexual activity
 Plan during part of day when breathing is best
 Slow, pursed-lip breathing
 Refrain after eating or other strenuous
activity
 Do not assume dominant position
 Do not prolong foreplay

52. Nursing Management
Nursing Implementation
Ambulatory and Home Care
 Sleep
 Nasal saline sprays
 Decongestants
 Nasal steroid inhalers
 Long-acting theophylline
 Decreases bronchospasm and airway obstruction

53. Nursing Management
Nursing Implementation
Ambulatory and Home Care
 Psychosocial considerations
 Guilt
 Depression
 Anxiety
 Social isolation
 Denial
 Dependence
 Use relaxation techniques and support groups

54. Nursing Management
Nursing Implementation
Ambulatory and Home Care
 Discourage moving to places above 4000
ft.