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 CO 2
Frequently patients require O 2 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
Treats

PO2 in inspired air

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

Acute
Intervention
Nursing
Implementation
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

Ambulatory
Home Care
Nursingand
Implementation
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.