Chronic Obstructive
Pulmonary Disease (COPD)
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

Emphysema
Description

Abnormal permanent enlargement of the
air space distal to the terminal bronchioles

Accompanied by destruction of bronchioles
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
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
COPD
Causes

Cigarette smoking
 Nicotine stimulates sympathetic nervous
system resulting in:



 HR
Peripheral vasoconstriction
 BP and cardiac workload
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
COPD
Causes

Secondhand smoke exposure associated
with:
  Pulmonary function
  Risk of lung cancer
  Mortality rates from ischemic heart
disease
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
Pathophysiology of Chronic Bronchitis
and Emphysema
Fig. 28-7
Emphysema
Pathophysiology
 Hyperinflation
of alveoli
 Destruction of alveolar walls
 Destruction of alveolar capillary walls
 Narrowed airways
 Loss of lung elasticity
Emphysema
Pathophysiology
 Two
types:
 Centrilobular (central part of lobule)
 Most common

Panlobular (destruction of whole lobule)
 Usually associated with AAT deficiency
Emphysema
Pathophysiology

Structural changes are:
 Hyperinflation of alveoli
 Destruction of alveolar capillary walls
 Narrowed, tortuous small airways
 Loss of lung elasticity
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
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
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

Emphysema
Clinical Manifestations
 Dyspnea
Progresses in severity
 Patient will first complain of dyspnea
on exertion and progress to interfering
with ADLs and rest

Emphysema
Clinical Manifestations
 Minimal
coughing with no to small
amounts of sputum
 Overdistention
of alveoli causes
diaphragm to flatten and AP diameter to
increase
Emphysema
Clinical Manifestations
 Patient
becomes chest breather, relying
on accessory muscles
 Ribs become fixed in inspiratory
position
Emphysema
Clinical Manifestations
 Patient
is underweight (despite adequate
calorie intake)
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
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
Chronic Bronchitis
Pathophysiology
 Greater
resistance to airflow increases
work of breathing
 Hypoxemia
and hypercapnia develop
more frequently in chronic bronchitis
than emphysema
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

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
Chronic Bronchitis
Clinical Manifestations
 Earliest
symptoms:
 Frequent, productive cough during
winter
 Frequent respiratory infections
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
Chronic Bronchitis
Clinical Manifestations
 Hypoxemia
and hypercapnia
 Results from hypoventilation and 
airway resistance + problems with
alveolar gas exchange
COPD
Complications
Pulmonary hypertension (pulmonary vessel
constriction d/t alveolar hypoxia & acidosis)
 Cor pulmonale (Rt heart hypertrophy + RV
failure)
 Pneumonia
 Acute Respiratory Failure

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

COPD
Diagnostic Studies

ABGs
  PaO2
  PaCO2 (especially in chronic bronchitis)
  pH (especially in chronic bronchitis)
  Bicarbonate level found in late stages
COPD
COPD
Collaborative Care

Smoking cessation
 Most significant factor in slowing the
progression of the disease
COPD
Collaborative Care: Drug Therapy

Bronchodilators – as maintenance therapy
 -adrenergic agonists (e.g. Ventolin)

MDI or nebulizer preferred
 Anticholinergics
(e.g. Atrovent)
COPD
Collaborative Care:
Oxygen Therapy

O2 therapy
 Raises PO2 in inspired air
 Treats hypoxemia
 Titrate to lowest effective dose
COPD
Collaborative Care:
Oxygen Therapy
 Chronic
O2 therapy at home
Improved prognosis
 Improved neuropsychologic function
 Increased exercise tolerance
 Decreased hematocrit
 Reduced pulmonary hypertension

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
COPD
Collaborative Care: Respiratory
Therapy
Huff coughing (Table 28-21)
 Chest physiotherapy – to bring secretions
into larger, more central airways
 Postural drainage
 Percussion
 Vibration

Positions
for Postural
Positions
for Postural
Drainage
Drainage
Fig. 28-16
COPD
Collaborative Care
 Encourage
as possible
patient to remain as active
COPD
Collaborative Care

Surgical Therapy
 Lung volume reduction surgery
 Lung transplant
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

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
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

Nursing Management
Nursing Diagnoses
Ineffective airway clearance
 Impaired gas exchange
 Imbalanced nutrition: less than body
requirements
 Disturbed sleep pattern
 Risk for infection

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
Nursing Management
Nursing Implementation
Acute Intervention
 Required for complications like pneumonia,
cor pulmonale, and acute respiratory failure
Nursing Management
Nursing Implementation
Ambulatory and Home Care
 Pulmonary rehabilitation
 Control and alleviate symptoms of
pathophysiologic complications of
respiratory impairment
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
Nursing Management
Nursing Implementation
n
n
Ambulatory and Home Care
Explore alternative methods of ADLs
Encourage patient to sit while
performing activities
 Coordinated walking

Nursing Management
Nursing Implementation
Ambulatory and Home Care
 Slow, pursed-lip breathing
 After exercise, wait 5 minutes before
using -adrenergic agonist MDI
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
Nursing Management
Nursing Implementation
Ambulatory and Home Care
 Sleep
Nasal saline sprays
 Decongestants
 Nasal steroid inhalers
 Long-acting theophylline


Decreases bronchospasm and airway obstruction
Nursing Management
Nursing Implementation
Ambulatory and Home Care
 Psychosocial considerations
 Guilt
 Depression
 Anxiety
 Social isolation
 Denial
 Dependence
 Use relaxation techniques and support groups
Nursing Management
Nursing Implementation
Ambulatory and Home Care
 Discourage moving to places above 4000
ft.