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

 Elastinand 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 O both at
2
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

 Earliestsymptoms:
 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 FEV /FVC and  residual
1
volume and total lung capacity
COPD
Diagnostic Studies
 ABGs
  PaO
2

 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
Positions for Postural
for Postural Drainage
Drainage

Fig. 28-16
COPD
Collaborative Care

 Encourage patient to remain as active

as possible
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

Management

 Ineffective airway clearance

 Impaired gas exchange
 Imbalanced nutrition: less than body
requirements
 Disturbed sleep pattern
 Risk for infection
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
Acute Intervention
 Required for complications like pneumonia,
cor pulmonale, and acute respiratory
failure
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
n Ambulatory and Home Care
n Explore alternative methods of ADLs
 Encourage patient to sit while
performing activities
 Coordinated walking