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. The primary cause is cigarette smoking which damages the lungs over many years through destruction of lung tissue and increased inflammation. Symptoms include dyspnea, cough, and limited physical activity. Treatment focuses on smoking cessation and medications to relieve symptoms along with respiratory therapy and oxygen as needed.
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
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
α-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
12. Emphysema
Pathophysiology
Two types:
Centrilobular (central part of lobule)
Most common
Panlobular (destruction of whole lobule)
Usually associated with AAT deficiency
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
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
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 O2diffusion
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
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
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
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
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
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
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