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

  O
O22carrying
carrying capacity
capacity
 Impairs
Impairs psychomotor
psychomotor performance
performance and
and judgment
judgment

 Cellular hyperplasia
 Production
Production of
of mucus
mucus
 Reduction
Reduction in
in airway
airway diameter
diameter
 Increased
Increased difficulty in clearing
difficulty in clearing secretions
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
Emphysema results
results from
from lysis
lysis of
of lung
lung tissues
tissues by
by proteolytic
proteolytic
enzymes
enzymes from
from neutrophils
neutrophils and
and macrophages
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
(destruction of
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
Mucus

 Smooth
Smooth muscle
muscle spasm
spasm

 Inflammatory
Inflammatory process
process

 Collapse
Collapse of
of bronchiolar
bronchiolar walls
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 O22 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 O22 diffusion
 Tendency to hypoventilate and retain
CO22
 Frequently patients require O 2 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

 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
polycythemia (increased
(increased Hgb
Hgb d/t
d/t chronic
chronic hypoxemia))
hypoxemia))

 cyanosis
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
1
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
 O22 therapy
 Raises PO2 in inspired air
2
 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

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 Ambulatory and Home Care

n 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.