destruction and enlargement of the lung alveoli

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.
 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
 Cigarette smoking
Aging
Senile emphysema results from degenerative
changes; stretching occurs without destruction in
the smooth muscle.
Emphysema is usually caused by:

deficiency of alpha1-antitrypsin
cigarette smoking.
 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.
 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.
 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.
 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
 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.
Possible complications of emphysema include:
right ventricular hypertrophy (cor pulmonale)
respiratory failure
recurrent respiratory tract infections.
 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.
 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.
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
 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
 aerosolized or systemic corticosteroids
transtracheal catheterization to enable the
patient to receive oxygen therapy at home.