Emphysema

destruction and enlargement of the

lung alveoli
 Definition
condition of the lung characterized by abnormal permanent
enlargement of the airspaces distal to the terminal
bronchiole, accompanied by destruction of their walls, and
without obvious fibrosis.
Overinflation- the enlargement of airspaces unaccompanied
by destruction.

airflow limitation caused by lack of elastic

recoil in the lungs.
 Epidemiology
more prevalent in males than females; about
65% of patients with well-defined emphysema
are men and 35% are women.
Higher in heavy smoker men
 Risk Factor
Cigarette smoking
Aging
Senile emphysema results from degenerative
changes; stretching occurs without destruction in
the smooth muscle.
 Causes

Emphysema is usually caused by:

deficiency of alpha1-antitrypsin
cigarette smoking.
 Pathophysiology
Primary emphysema has been linked to an inherited deficiency of the
enzyme alpha1-antitrypsin, a major component of alpha1-globulin.

Alpha1-antitrypsin inhibits the activation of several proteolytic enzymes;

deficiency of this enzyme is an autosomal recessive trait that predisposes
an individual to develop emphysema because proteolysis in lung tissues is
not inhibited.

Homozygous individuals have up to an 80% chance of developing lung

disease; if the individual smokes, he has a greater chance of developing
emphysema.

Patients who develop emphysema before or during their early forties and
those who are nonsmokers are believed to have a deficiency of alpha1-
antitrypsin.
 Pathophysiology
In emphysema, recurrent inflammation is
associated with the release of proteolytic
enzymes from lung cells. This causes
irreversible enlargement of the air spaces
distal to the terminal bronchioles.
Enlargement of air spaces destroys the
alveolar walls, which results in a breakdown of
elasticity and loss of fibrous and muscle tissue,
thus making the lungs less compliant.
 Pathophysiology
In normal breathing, the air moves into and out of the lungs
to meet metabolic needs. A change in airway size
compromises the ability of the lungs to circulate sufficient
air.
In patients with emphysema, recurrent pulmonary
inflammation damages and eventually destroys the alveolar
walls, creating large air spaces.
The alveolar septa are initially destroyed, eliminating a
portion of the capillary bed and increasing air volume in the
acinus.
This breakdown leaves the alveoli unable to recoil normally
after expanding and results in bronchiolar collapse on
expiration.
 The damaged or destroyed alveolar walls cannot support
the airways to keep them open.
The amount of air that can be expired passively is
diminished, thus trapping air in the lungs and leading to
overdistention.
Hyperinflation of the alveoli produces bullae (air spaces)
and air spaces adjacent to the pleura (blebs).
Septal destruction also decreases airway calibration..
Septal destruction may affect only the respiratory
bronchioles and alveolar ducts, leaving alveolar sacs intact
(centriacinar emphysema), or it can involve the entire
acinus (panacinar emphysema), with damage more
random and involving the lower lobes of the lungs.
 Clinical Manifestation
tachypnea related to decreased oxygenation
dyspnea on exertion, which is often the initial symptom
barrel-shaped chest due to the lungs over distending and
overinflating
prolonged expiration and grunting, which occur because the
accessory muscles are used for inspiration and abdominal
muscles are used for expiration
decreased breath sounds due to air-trapping in the alveoli and
destruction of alveoli
 Clinical Manifestation
clubbed fingers and toes related to chronic hypoxic
changes
decreased tactile fremitus on palpation as air moves
through poorly functional alveoli
tactile fremitus-is a relatively rough assessment of tools,
but as a scouting technique, it directs attention to possible
abnormalities.
decreased chest expansion due to hypoventilation
hyperresonance on chest percussion due to
overinflated air spaces
crackles and wheezing on inspiration as bronchioles
collapse.
 Complications

Possible complications of emphysema include:

right ventricular hypertrophy (cor pulmonale)
respiratory failure
recurrent respiratory tract infections.
 Diagnosis

Chest X-rays in advanced disease may show a

flattened diaphragm, reduced vascular markings at
the lung periphery, overaeration of the lungs, a
vertical heart, enlarged anteroposterior chest
diameter, and large retrosternal air space.

Pulmonary function studies indicate increased

residual volume and total lung capacity, reduced
diffusing capacity, and increased inspiratory flow.

Arterial blood gas analysis usually reveals reduced

PaO2 and a normal PaCO2 until late in the disease
process.
 Diagnosis

Electrocardiography may show tall,

symmetrical P waves in leads II, III, and aVF;
vertical QRS axis and signs of right ventricular
hypertrophy are seen late in the disease.
Complete blood count usually reveals an
increased hemoglobin level late in the disease
when the patient has persistent severe
hypoxia.
 Treatment
Correcting this disorder typically involves:
avoiding smoking to preserve remaining alveoli
avoiding air pollution to preserve remaining
alveoli
bronchodilators, such as beta-adrenergic blockers
and albuterol and ipratropium bromide, to
reverse bronchospasms and promote mucociliary
clearance
antibiotics to treat respiratory tract infections
 Treatment
pneumovax to prevent pneumococcal pneumonia
adequate hydration to liquefy and mobilize
secretions
chest physiotherapy to mobilize secretions
oxygen therapy at low settings to correct hypoxia
flu vaccine to prevent influenza
mucolytics to thin secretions and aid in
expectoration of mucus
 Treatment

aerosolized or systemic corticosteroids

transtracheal catheterization to enable the
patient to receive oxygen therapy at home.