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STRUCTURE OF THE

There are three steps in this


RESPIRATORY SYSTEM
process:
(1) ventilation, the movement of
air into and out of the lungs;
(2) diffusion, the movement of
gases between air spaces in the
lungs and the bloodstream;
(3) perfusion, the movement of
blood into and out of the capillary
beds of the lungs to body organs
and tissues

Nasal passages, sinuses and nasopharynx.

Larynx

Lungs

RESPIRATORY SYSTEM
Sources:
Porths Pathophysiology
Pathophysiology, The Biologic Basis for Disease for Adult and Children
Handbook of Pathophysiology
Fundamentals of Nursing

CONDUCTING AIRWAYS
The conducting airways consist of the
nasal passages, mouth and pharynx,
larynx, trachea, bronchi, and bronchioles.

FUNCTIONS OF THE
RESPIRATORY SYSTEM
The primary function of the respiratory system, which
consists of the airways and lungs, is gas exchange.
In addition to gas exchange, the lungs serve as a host
defense by providing a barrier between the external
environment and the inside of the body.
Finally, the lung is also a metabolic organ that
synthesizes and metabolizes different compounds.

Nasopharyngeal Airways
The nose is the preferred route for the entrance of air into the respiratory tract during normal
breathing
The oropharynx extends posteriorly from the soft palate to the epiglottis. The oropharynx is the only
opening between the nose, mouth, and lungs. Both swallowed food on its way to the esophagus and
air on its way to the larynx pass through it. Obstruction of the oropharynx leads to immediate
cessation of ventilation. The oropharynx is the only opening betweenthe nose, mouth, and lungs.

Larynx

The larynx connects the oropharynx with the trachea. divided into two categories:
1.

those associated with speech and

2.

2.those associated with protecting the lungs fromsubstances other than air.

cavity of the larynx is divided into two pairs:

1.

vestibular folds protective function

2.

vocal folds vibrations

-glottis, the vocal fold elongation, a complex set of muscles responsible for opening and closing.
-epiglottis, located above the larynxDuring swallowing, the larynx is pulled superiorly and the free
edges of the epiglottis move downward to cover the larynx, thus routing liquids and foods into the
esophagus.

. cough reflexWhen confronted with substancesother than air, the laryngeal muscles contract and
close offthe airway. At the same time, the cough reflex is initiated as a means of removing a foreign
substance from the airway

Tracheobronchial Tree The tracheobronchial tree,


which consists of the trachea, bronchi, and
bronchioles, can be viewed as a system of branching
tubes flowing through the lobes of the lungs. There
are approximately 23 levels of branching, beginning
with the conducting airways and ending with the
respiratory airways, where gas exchange takes place.

The trachea, or windpipe, is a continuous tube that


connects the larynx and the major bronchi of the
lungs
expand anteriorly as swallowed food passes through
it. The trachea extends to the superior border of the
fifth thoracic vertebra, where it divides to form the
right and left main or primary bronchi. Between the
main bronchi is a keellike ridge, called the carina.

(A) Anterior view of respiratory


structures, ncluding the lobes of the
lung, the larynx, trachea, and the main
bronchi on the left and the main
pulmonary artery and vein on the right.
(B) The carina is located at the
bifurcation of the right and left
mainstem bronchi.

Porths Pathophysiology

LUNGS AND THE


RESPIRATORY AIRWAYS

The bronchioles terminate in gas-exchange airways,


where oxygen (O2) enters the blood and carbon dioxide
(CO2) is removed from it. The gas-exchange airways
consist of respiratory bronchioles, alveolar ducts,
and alveoli
The lungs are the functional structures of the
respiratory system. In addition to their gas exchange
function, they inactivate vasoactive substances such as
bradykinin, they convert angiotensin I to angiotensin II,
and they serve as a reservoir for blood storage.

LOBULES
Lobules
The gas exchange function of the lung takes place in
the lobules of the lungs, which are the smallest
functional units of the lungs. A branch of a terminal
bronchiole, an arteriole, the pulmonary capillaries, and
a venule supply each lobule
It is here where gas exchange takes place and enters
in the bronchioles the alveolar ducts and sacs.

ALVEOLI
The alveoli are the terminal air spaces of the respiratory tract
and the actual sites of gas exchange between the air and the
blood.
Each alveolus is a small outpouching of respiratory bronchioles,
alveolar ducts, and alveolar sacs.
Alveoli has pores of Kohn which are small holes in the alveolar
walls allowing the mixing of air.
Alveoli are interconnectiong spaces that has no separate walls
as compared to the bronchioles. Bronchioles doesnt mixed air.
The alveolar epithelium is composed of two types of cells: type
I and type II alveolar cells.
The alveoli also contain brush cells and macrophages.

TYPE I AND II ALVEOLAR


CELLS
Type I
The type I alveolar cells, also
known as type I pneumocytes,
are extremely thin squamous
cells with a thin cytoplasm and
flattened nucleus that occupy
about 95% of the surface area of
the alveoli. They are joined to
one another and to other cells by
occluding junctions. These
junctions form an effective
barrier between the air and the
components
of the alveolar wall. Type I
alveolar cells are not capable of
cell division.

Type II

The type II cells synthesize pulmonary surfactant, a


substance that decreases the surface tension in the alveoli
and allows for greater ease of lung inflation. They are also
the progenitor cells for type I cells. After lung injury, they
proliferate and restore both type I and type II alveolar cells.
retain airway patency despite large changes in volume.

Surfactant is a complex material produced by type II


alveolar cells and composed of multiple phospholipids and
specifi c associated proteins. Th e physiologic function of
surfactant is to enhance the anatomic stability of the lungs.
Th e presence of surfactant covering the alveolar epithelial
surface reduces surface tension, allowing expansion of
alveoli with a transpulmonary distending pressure of less
than 5 cm H 2 O.

Alveolar Macrophages The macrophages are present in


both the connective tissue of the septum and in the air
spaces of the alveolus. They are responsible for the
removal of offending substances from the alveoli. In the air
spaces, they scavenge the surface to remove inhaled
particulate matter, such as dust and pollen

Schematic illustration of type I and type II alveolar


cells and their relationship to the alveoli and
pulmonary capillaries. Type I alveolar cells constitute
most of the alveolar surface. Type II alveolar cells,
which produce surfactant, are located at the corners
between adjacent alveoli. Also shown are the
endothelial cells, which line the pulmonary
capillaries, and an alveolar macrophage.

THE PULMONARY CIRCULATION. THE RIGHT AND LEFT PULMONARY VEINS


AND ARTERIES AND THE BRANCHING CAPILLARIES
ARE ILLUSTRATED. NOTE THE PULMONARY ARTERY CARRIES VENOUS
BLOOD, AND THE PULMONARY VEIN CARRIES ARTERIAL BLOOD.

PULMONARY VASCULATURE
AND LYMPHATIC SUPPLY
Pulmonary and Bronchial
Circulations, distributes
blood to the conducting
airways and the supporting
structures of the lung
Lymphatic Circulation, Both
of these systems have
numerous interconnections,
and both form networks
that drain into the hilar
lymph nodes at the base of
each lung.

INNERVATION
parasympathetic stimulation, through the vagus nerve, that is responsible
for the slightly constricted smooth muscle tone in the normal resting lung.
Stimulation of the parasympathetic nervous system leads to airway
constriction and increased glandular secretion
preganglionic and postganglionic fibers contain excitatory (cholinergic)
motor neurons that respond to acetylcholine.
Stimulation of the sympathetic nervous system causes airway relaxation,
blood vessel constriction, and inhibition of glandular secretion
Neurotransmitters of the sympathetic nervous system include the
catecholamines norepinephrine and epinephrine.
The lungs are encased in a thin, transparent, double layered serous
membrane called the pleura. A thin film of serous fluid separates the
outer parietal and inner visceral pleural layers, allowing the two layers to
glide over each other and yet hold together, allowing no separation
between the lungs and the chest wall

VENTILATION

VENTILATION
Ventilation is the mechanical movement of gas
or air into and out of the lungs. Ventilation often is
misnamed respiration, which is actually the
exchange of O2 and CO2 during cellular metabolism.
Respiratory rate is actually the ventilatory rate, or
the number of times gas is inspired and expired per
minute.
CO2, the gaseous form of carbonic acid (H2CO3), is a
product of cellular metabolism. The lung eliminates
about 10,000 milliequivalents (mEq) of carbonic acid
per day in the form of CO2, which is produced at the
rate of approximately 200 ml/ minute.

FUNCTIONAL COMPONENTS OF
THE RESPIRATORY SYSTEM

NEUROCHEMICAL
CONTROL OF VENTILATION

The respiratory center in the brainstem controls


respiration by transmitting impulses to the respiratory
muscles, causing them to contract and relax.
The respiratory center is composed of several groups of
neurons located in the brainstem:

the dorsal respiratory group (DRG),


the ventral respiratory group (VRG),

the pneumotaxic center

apneustic center.

Lung Receptors send impulses from the lungs to the dorsal


respiratory group:

1.

Irritant Receptors

2.

Stretch Receptors

3.

J-receptors

Chemoreceptors
.

Chemoreceptors monitor pH, Paco2, and Pao2. Central


chemoreceptors monitor arterial blood indirectly by
sensing changes in the pH of cerebrospinal fluid (CSF).

MECHANICS OF
BREATHING
The mechanical aspects of
inspiration and expiration are
known collectively as the
mechanics of breathing and
involve:
(1) major and accessory
muscles of inspiration and
expiration.
(2) elastic properties of the
lungs and chest wall,
(3) Resistance to airflow
through the conducting
airways

Elastic Properties of the Lung and Chest Wall


Elastic recoil is the tendency of the lungs to return to the
resting state after inspiration. Normal elastic recoil permits
passive expiration, eliminating the need for major muscles
of expiration.
Compliance is the measure of lung and chest wall
distensibility. It represents the relative ease with which
these structures can be stretched.
Airway Resistance.

-Bronchoconstriction
-Bronchodilation
Work of Breathing, The work of breathing is determined
by the muscular effort (and therefore oxygen and energy)
required for ventilation.
Measurement of Gas Pressure

MEASUREMENT OF GAS
PRESSURE
Barometric pressure (PB) (atmospheric pressure) is the
pressure exerted by gas molecules in air at specific
altitudes. At sea level, barometric pressure is 760 of
mercury (mm Hg, or torr) or 14.7 pounds per square
inch(PSI).
A respiratory pressure of +15 mm Hg means that the
pressure is 15 mm Hg above atmospheric pressure,
and a respiratory pressure of 15 mm Hg is 15 mm Hg
less than atmospheric pressure.

GAS TRANSPORT
Gas transport, the delivery of oxygen to the cells of the body and the
removal of CO2, has four steps:
1. Ventilation of the lungs
2. Diffusion of oxygen from the alveoli into the capillary blood
3. Perfusion of systemic capillaries with oxygenated blood
4. Diffusion of oxygen from systemic capillaries into the cells
Steps in the transport of CO2 occur in reverse order:
1. Diffusion of CO2 from the cells into the systemic capillaries
2. Perfusion of the pulmonary capillary bed by venous blood
3. Diffusion of CO2 into the alveoli
4. Removal of CO2 from the lung by ventilation If any step in gas transport is
impaired by a respiratory or cardiovascular disorder, gas exchange at the
cellular level is compromised.

GRAVITY AND THE


ALVEOLAR PRESSURE

PARTIAL PRESSURE OF
RESPIRATORY GASES IN NORMAL
RESPIRATION
The values of Po2, Pco2,
and Pn2 fluctuate from
breath to breath.
-CO2, Carbon dioxide
-O2, oxygen
-Pco2-partial pressure of
carbon dioxide
-Ph2o, partial pressure of
water; -Pn2, partial
pressure of nitrogen
-Po2, partial pressure of
oxygen.

DEAD AIR SPACE


Dead space refers to the air that must be moved with
each breath but does not participate in gas exchange.
The movement of air through dead space contributes
to the work of breathing but not to gas exchange.
There are two types of dead space:
Anatomic dead space: that contained in the
conducting airways.
Alveolar dead space: that contained in the respiratory
portion of the lung

UNDERSTANDING OXYGEN
AND TRANSPORT

OXYGEN TRANSPORT
Oxygen is carried on 2 forms:

1.Dissolved
2.Bound to hemoglobin
Dissolved Oxygen is the only form of that diffuses across cell
members and and produces partial pressure (PO2) which in
turn drives diffusion.
The transport of O2 involves
(1) transfer from the alveoli to the pulmonary capillaries in the
lung.

(2) hemoglobin binding and transport.


(3) the dissociation from hemoglobin in the tissue capillaries.

ALVEOLAR CAPILLARY
TRANSFER

In the lung, O2 moves from the alveoli to the


pulmonary capillaries as a dissolved gas. Its
movement occurs along a concentration gradient. It
moves from the alveoli, where the partial pressure of
PO2 is about 100 mm Hg, to the venous end of the
pulmonary capillaries with their lesser O2
concentration and lower PO2. The dissolved O2
moves rapidly between the alveoli and the
pulmonary capillaries, such that the PO2 at the
arterial end of the capillary is almost, if not exactly,
the same as that in the alveoli.

HEMOGLOBIN BINDING
AND TRANSPORT
Oxygen, which is relatively insoluble
in plasma, relies on hemoglobin for
transport in the blood. Once oxygen
has diffused into the pulmonary
capillary, it moves rapidly into the
red blood cells and reversibly binds
to hemoglobin to form HbO2. The
hemoglobin molecule contains four
heme units, each capable of
attaching an oxygen molecule.
Hemoglobin is 100% saturated when
all four units are occupied and is
usually about 97% saturated in the
systemic arterial blood. The capacity
of the blood to carry O2 is
dependent both on hemoglobin
levels and the ability of the lungs to
oxygenate the hemoglobin.

OXYGEN DISSOCIATION IN
THE TISSUES

The dissociation or release of O2


from hemoglobin occurs in the
tissue capillaries where the PO2 is
less than that of the arterial blood.
As
oxygen
dissociates
from
hemoglobin, it dissolves in the
plasma and then moves into the
tissues where the PO2 is less than
that in the capillaries. The affinity
of hemoglobin for O2 is influenced
by the carbon dioxide (PCO2)
content of the blood and its pH
temperature
and
2,3diphosphoglycerate (2,3-DPG), a
by-product of glycolysis in red
blood cells. Under conditions of
high metabolic demand, in which
the PCO2 is increased and the pH
is decreased, the binding affinity of
hemoglobin is decreased. During
decreased
metabolic
demand,
when the PCO2 is decreased and
the pH is increased, the affinity is
increased.

OXYGEN AND CARBON


DIOXIDE
TRANSPORT
Arterial Blood Gas Ranges
Parameter

Range

1. pH = acid or base

7.357.45

2. PCO2 = partial pressure of


carbon dioxide

3545 mm Hg

3. HCO
3 = bicarbonate

2226 mEq/L

4. PO2 = partial pressure of


oxygen

80100 mm Hg

OXYGEN TRANSPORT
Steep O2 released to Hgb
Plateau O2 loaded Hgb

OxyHemoglobin
Dissociation Curve

OXYGEN TRANSPORT /
PULMONARY VENTILATION
Effect of Anemia

A. Spirogram
B. Lung Capacities

AGING AND THE PULMONARY


SYSTEM

Normal alterations include:


(1) loss of elastic recoil,
(2)stiffening of the chest wall,
(3) changes in gas exchange, and
(4)increases in flow resistance

ALTERATIONS OF
PULMONARY FUNCTION

SIGNS AND
SYMPTOMS OF
PULMONARY DISEASE

Dyspnea is a subjective experience of breathing


discomfort that is comprised of qualitatively distinct sensations
that vary in intensity.
Cough is a protective reflex that helps clear the airways
by an explosive expiration. Inhaled particles, accumulated
mucus, inflammation, or the presence of a foreign body initiates
the cough reflex by stimulating irritant receptors in the airway.
Abnormal Breathing Patterns
-Kussmaul respirations are characterized by a slightly increased
ventilatory rate, very large tidal volume, and no expiratory
pause.
-

Labored breathing occurs whenever there is an


increased work of breathing, especially if the airways
are obstructed, as in chronic obstructive pulmonary
disease (COPD).
Cheyne-Stokes respirations are characterized by
alternating periods of deep and shallow breathing.
Apnea lasting 15 to 60 seconds is followed by
ventilations that increase in volume until a peak is
reached, after which ventilation (tidal volume)
decreases again to apnea.
Hypoventilation is inadequate alveolar
ventilation in relation to metabolic demands
Hyperventilation is alveolar ventilation that
exceeds metabolic demands

Clubbing
Clubbing is the selective bulbous enlargement of
the end (distal segment) of a digit (finger or toe) (Figure
35-1) whose severity can be graded from 1 to 5 based on
the extent of nail bed hypertrophy and the amount of
changes in the nails themselves. It is usually painless.
Clubbing is commonly associated with diseases that
interfere with oxygenation, such as bronchiectasis, cystic
fibrosis, pulmonary fibrosis, lung abscess, and congenital
heart disease.
Pain caused by pulmonary disorders originates in
the pleurae airways, or chest wall.
i.e., Infection and infllammation of the parietal pleura
(Pleuritiis or pleurisy) Pericardial friction rub
- Costochondritis - Caused by pressing on the sternum or
ribs.

CONDITIONS CAUSED BY
PULMONARY DISEASE OR
INJURY
Hypercapnia, or increased CO2 concentration in the arterial
blood (increased Paco2), is caused by hypoventilation of the alveoli.

Causes:
-depression of the respiratory center by drugs
diseases of the medulla, including infections of the central nervous
system or trauma
abnormalities of the spinal conducting pathways, as in spinal cord
disruption or poliomyelitis;
diseases of the neuromuscular junction or of the respiratory muscles
themselves, as in myasthenia gravis or muscular dystrophy;
thoracic cage abnormalities, as in chest injury or congenital deformity;
large airway obstruction, as in tumors or sleep apnea increased work
of breathing or physiologic dead space, as in emphysema

Hypoxemia, or reduced oxygenation of arterial blood


(reduced Pao2), is caused by respiratory alterations,
whereas hypoxia, or reduced oxygenation of cells in
tissues, may be caused by alterations of other systems as
well.
Hypoxemia results from problems with one or more of the
major mechanisms of oxygenation:
1. Oxygen delivery to the alveoli
a. Oxygen content of the inspired air (Fio2)
2. Ventilation of the alveoli
3. Diffusion of oxygen from the alveoli into the blood
a. Balance between alveolar ventilation and perfusion ( V/Q
mismatch)
b. Diffusion of oxygen across the alveolocapillary membrane
4. Perfusion of pulmonary capillaries

CAUSES OF HYPOXEMIA
MECHANISM

COMMON CLINICAL CAUSES

Decrease in inspired
oxygen (decreased
Fio2)

High altitude
Low oxygen content of gas mixture
Enclosed breathing spaces (suffocation)

Hypoventilation of the
alveoli

Lack of neurologic stimulation of the respiratory


center (oversedation, drug overdose,
neurologic damage)
Defects in chest wall mechanics (neuromuscular
disease, trauma, chest deformity, air trapping)
Large airway obstruction (laryngospasm, foreign
body aspiration, neoplasm)
Increased work of breathing (emphysema, severe
asthma)

Ventilation-perfusion
mismatch

Asthma, Chronic bronchitis ,Pneumonia


Acute respiratory distress syndrome
AtelectasisPulmonary embolism

Alveolocapillary
diffusion abnormality

Edema
Fibrosis
Emphysema

Decreased pulmonary
capillary perfusion

Intracardiac defects
Intrapulmonary arteriovenous malformations

O2 is dependent into two factors


- The amount of oxygen, measured by the fraction of air that is
composed of O2, called FiO2.
-Alveolar minute minute ventilation (tidal volume respiratory
rate)
Diffusion of oxygen from the alveoli:
-Balance between the air perfusing into the alveoli (V)
-Amount of blood perfusing around the capillaries of the alveoli
(Q)
alveolocapillary barrier inadequacy, if this is thickened that
happens in edema(Tissue swelling) and fibrosis (formation of
fibrous lesions).
These factors could result in compensatory hyperventilation and
resulting respiratory alkalosis(dec. PaO2 Inc. pH)

VENTILATION-PERFUSION ABNORMALITIES.
(DATA FROM GLENNY RW:
ADV PHYSIOL EDUC 32[3]:192195, 2008 .)

ACUTE RESPIRATORY
FAILURE
Respiratory (lung) failure is defined as inadequate gas
exchange, that is, hypoxemia, in which Pao2 is 50 mmHg, or
hypercapnia, in which Paco2 is 50 mmHg with a pH of 7.25.
If in hypercapneic the condition is usually of inadequate
alveolar ventilation. And ventilatory support must be given:
i.e., bag valve mask, intubation etc.
Respiratory failure is a potential complication of major surgical
procedures that involves the CNS, Thorax and upper abdomen.
Common complications: atelectasis, pneumonia, pulmonary
edema, and pulmonary emboli.
Prevention includes frequent turning and position changes,
deep breathing exercise, early ambulation these prevents
atelectasis and accumulation of secretions, humudification.

DISORDERS OF THE
CHEST WALL
Chest wall restriction
-Obesity and kyphoscoliosis(lateral bending and rotation of
the spinal column with distortion of the thoracic cage) are risk factors.
Diagnosis of chest
restriction is made by pulmonary function testing (reduction in forced
vital capacity [FVC]), arterial blood gas measurement (hypercapnia), and
radiographs
-Flail chest results from the fracture of several consecutive ribs in
more than one place, or the fracture of the sternum and several
consecutive ribs. These multiple fractures result in instability of a portion
of the chest wall, causing paradoxical movement of the chest with
breathing.
Treatment is internal fixation by controlled mechanical ventilation until
the chest wall has stabilized.

FLAIL CHEST

Flail chest. Normal respiration: A, inspiration; B,


expiration. Paradoxical motion: C, inspiration,
area of lung underlying unstable chest wall
sucks in on inspiration; D, expiration, unstable
area balloons out. Note movement of
ediastinum toward opposite lung during inspiration.

PLEURAL
ABNORMALITIES
Pneumothorax is the
presence of air or gas in the
pleural space caused by a
rupture in the visceral pleura
(which surrounds the lungs) or
the parietal pleura and chest
wall.
As air separates the visceral
and parietal pleurae, it
destroys the negative pressure
of the pleural space. This
disrupts the state of
equilibrium that normally exists
between elastic recoil forces of
the lung and chest wall.

Primary (spontaneous) pneumothorax, which


occurs unexpectedly in healthy individuals (usually
men) between ages 20 and 40 years, is most often
caused by the spontaneous rupture of blebs (blisterlike formations) on the visceral pleura, although there
may be underlying pleural disease with emphysemalike changes.

Secondary (traumatic) pneumothorax can be


caused by chest trauma, such as a rib fracture,
stab or bullet wounds, or a surgical procedure that
tears the pleura

Iatrogenic pneumothorax is most commonly


caused by transthoracic needle aspiration

tension pneumothorax, Tension Pneumothorax. Air


in the pleural space causes the lung to collapse
around the hilus and may shift trachea and
mediastinal contents (heart and great vessels)
toward the other lung.

Pleural effusion is the presence of fluid in the pleural space.


The source of the fluid is usually blood vessels or lymphatic vessels
lying beneath either pleura, but occasionally an abscess or other
lesion may drain into the pleural space.
Empyema Empyema (infected pleural effusion) is the
presence of pus in the pleural space. It is thought to develop
when the pulmonary lymphatics become blocked, leading to an
outpouring of contaminated lymphatic fluid into the pleural space.
Commonly documented infectious microorganisms include
Staphylococcus aureus
Escherichia coli
anaerobic bacteria
Klebsiella pneumoniae.

PULMONARY
DISORDERS
Restrictive Lung Disorders

ASPIRATION
Aspiration is the passage of fluid and solid particles into
the lung. It tends to occur in individuals whose normal swallowing
mechanism and cough reflex are impaired by a decreased level of
consciousness or central nervous system abnormalities.
Predisposing Factors

-altered level of consciousness caused by substance abuse,


sedation, or anesthesia.
-seizure disorders
-cerebrovascular accident
-neuromuscular disorders that cause dysphagia

Aspiration of oral or pharyngeal secretions can lead


to aspiration pneumonia, especially if the oral cavity
is colonized with bacteria.

Clinical manifestations of aspiration include:


1. sudden onset of choking and intractable cough with or
without vomiting
2. Fever
3. Dyspnea
4. Wheezing

Treatment of aspiration, pneumonia, or pneumonitis,


Include:
-supplemental oxygen and may require mechanical
ventilation with positive end-expiratory pressure
(PEEP).
-Fluids are restricted to decrease blood volume and
minimize pulmonary edema.
-Corticosteroids may be administered during the first 72
hours after aspiration.
-Antibiotics

ATELECTASIS

Atelectasis is the collapse of lung tissue. There


are three types of atelectasis: compression,
absorption, and surfactant impairment:
1. Compression atelectasis is caused by the
external pressure exerted on lung tissue, such as
occurs with tumors, or by fluid or air in the pleural
space.
2. Absorption atelectasis results from gradual
absorption of air from obstructed or hypoventilated
alveoli or from inhalation of concentrated oxygen or
anesthetic agents.

3. Surfactant impairment results from decreased


production or inactivation of surfactant, which is
necessary to reduce surface tension in the alveoli and

Clinical manifestations of atelectasis are similar to


those of pulmonary infection: dyspnea, cough, fever,
and leukocytosis.
Prevention and treatment of postoperative atelectasis
usually include deep breathing exercises

BRONCHIECTASIS
Bronchiectasis is persistent abnormal dilation of the
bronchi. It
usually occurs in conjunction with other respiratory
conditions
that are associated with chronic bronchial inflammation, such
as obstruction of an airway with mucous plugs, atelectasis,
aspiration
of a foreign body, infection, cystic fibrosis, tuberculosis,
congenital weakness of the bronchial wall, or impaired
defense
mechanisms.

PORES OF KOHN. A, ABSORPTION ATELECTASIS


CAUSED BY LACK OF COLLATERAL VENTILATION
THROUGH PORES OF KOHN. B, RESTORATION OF
COLLATERAL VENTILATION DURING DEEP
BREATHING.

A TYPES OF BRONCHIECTASIS.
B, LEFT POSTERIOR OBLIQUE PROJECTION OF A LEFT
BRONCHOGRAM SHOWING CYLINDRICAL BRONCHIECTASIS
AFFECTING THE ENTIRE LOWER LOBE EXCEPT FOR THE
SUPERIOR SEGMENT. FEW SIDE BRANCHES FILL. THE BASAL
AIRWAYS ARE CROWDED TOGETHER, INDICATING VOLUME LOSS
OF THE OWER LOBE, A COMMON FEATURE IN BRONCHIECTASIS

TREATMENT
Bronchiectasis is treated with sputum culture
antibiotics, bronchodilators, anti-inflammatory drugs,
chest physiotherapy, and supplemental oxygen. In
selected individuals with localized areas of
involvement, surgery may be indicated to remove the
affected portion of the lung

BRONCHIOLITIS
Bronchiolitis is diffuse inflammation of the small airways or
bronchioles. It is most common in children
but can occur in otherwise healthy individuals in association with an
upper or lower airway viral infection (e.g., respiratory syncytial virus
[RSV]).
Clinical manifestations include:
1. rapid ventilatory rate
2. marked use of accessory muscles
3. low-grade fever;
4. dry, nonproductive
5. Cough
6. hyperinflated chest

Diagnosis is made by spirometry and bronchoscopy


with biopsy
Bronchiolitis is treated with appropriate antibiotics,
steroids, and chest physical therapy (humidified air,
coughing and deep breathing, postural drainage).

BRONCHIOLITIS
OBLITERANS
Bronchiolitis obliterans is a late-stage fibrotic
process that occludes the airways and causes
permanent scarring of the lungs. This process can
occur in all causes of bronchiolitis Bronchiolitis
obliterans can be further complicated by the
development of pneumonia (called
bronchiolitis obliterans organizing pneumonia
[BOOP]) in which the alveoli and bronchioles become
filled with plugs of connective tissue.

PULMONARY
FIBROSIS
Pulmonary fibrosis is an excessive amount of fibrous or
connective tissue in the lung. When no specific cause for the
development of fibrosis is known, it is called idiopathic pulmonary
fibrosis. The fibrotic process results from chronic inflammation,
alveolar epithelialization, and myofibroblast proliferation. Fibrosis
causes a marked loss of lung compliance. The lung becomes stiff
and difficult to ventilate, and the diffusing capacity of the
alveolocapillary membrane may decrease, causing hypoxemia.
Diffuse pulmonary fibrosis has a poor prognosis. Specific Causes:
1. include inhalation of harmful substances
2. inorganic dusts
3. organic dusts
4. underlyingautoimmune systemic disorders,

IDIOPATHIC PULMONARY FIBROSIS.


IDIOPATHIC PULMONARY FIBROSIS (IPF)
The median survival is only 2 to 4 years after
diagnosis
Chronic inflammation and fibroproliferation of the
interstitial lung tissue occur around the alveoli with
disruption of the alveolocapillary basement
membrane.
This causes decreased oxygen diffusion across the
alveolocapillary membrane and hypoxemia. As the
disease progresses decreased lung compliance leads
to increased work of breathing, decreased tidal
volume, and resultant hypoventilation with
hypercapnia.

The primary symptom of IPF is:


-increasing dyspnea on exertion
diagnosis is confirmed by pulmonary function testing
(decreased FVC), high-resolution CT, and lung biopsy.
Treatment with corticosteroids alone causes remission
in approximately 50% of individual

Exposure to Toxic Gases. Inhalation of gaseous


irritants can cause significant respiratory
dysfunction. Commonly encountered toxic gases
include ammonia, hydrogen chloride, sulfur dioxide,
chlorine, phosgene, and nitrogen dioxide.
Prolonged exposure to high concentrations of
supplemental oxygen can result in a relatively rare
iatrogenic condition known as oxygen toxicity. The
basic underlying mechanism of injury is a severe
inflammatory response mediated primarily by oxygen
free radicals.

PNEUMOCONIOSIS
Pneumoconiosis represents any change in the lung caused
by inhalation of inorganic dust particles, which usually occurs in
the workplace. As in all cases of environmentally acquired lung
disease, the individuals history of exposure is important in
determining the diagnosis
The dusts of silica, asbestos, and coal are the most common
causes of pneumoconiosis
Clinical manifestations with advancement of disease may include
cough, sputum production, dyspnea, decreased lung volumes,
and hypoxemia. In most cases, diagnosis is made by performing
chest x-ray or CT and by obtaining careful occupational history
Treatment is usually palliative and focuses on preventing further
exposure and improving working conditions.

SILICOSIS
is a type of pneumoconiosis resulting from the inhalation of free
silica (silicon dioxide) and silica-containing compounds as occurs
in mining and industries involved with the extraction and
processing of ores; preparation and use of sand; and manufacture
of pipe, building, and roofing materials.
clinical manifestations do appear, they include cough and
dyspnea. although corticosteroids may produce some
improvement in the early, more acute stages.
Coal worker pneumoconiosis (coal miner lung, black lung)
is caused by coal dust deposits in the lung. Although coal
dust itself is relatively well tolerated by the lung, it is frequently
inhaled as a mixture of coal, silica, and quartz, which is strongly
inflammatory.
Individuals usually are seen with a productive cough and wheezing

ASBESTOSIS
Asbestos exposure affects not only factory
workers but also individuals who live in areas of
asbestos emission. Asbestos exposure can result in a
type of pulmonary fibrosis called asbestosis, but can
also cause lung cancer, mesothelioma (cancer of the
pleura), or pleural plaques, especially in those also
exposed to cigarette smoke

HYPERSENSITIVITY
PNEUMONITIS.
is an allergic, inflammatory disease of the lungs caused by inhalation of
organic particles or fumes.
Many allergens (antigens) can cause this disorder, including grains, silage,
bird droppings or feathers, wood dust (particularly redwood and maple), cork
dust, animal pelts, coffee beans, fish meal, mushroom compost, grain molds,
mists from standing water, and fumes from paints and resins.
initiated by alveolar macrophages and results in immunoglobulin G (IgG)
antibody production
Allergic alveolitis can be acute, subacute, or chronic. The
acute form causes a fever, cough, dyspnea, and chills a few hours
after exposure that resolve without treatment in 1 to 3 days.
Chronic allergic alveolitis causes weight loss, fever, fatigue, and gradually
progressive respiratory failure.
Treatment consists of avoidance of the offending agent and corticosteroid
administration.

SYSTEMIC DISORDERS
AND THE LUNGS

PULMONARY EDEMA
Pulmonary edema is excess water in the lung. The
normal lung contains very little fluid. It is kept dry by
lymphatic drainage and a balance among capillary
hydrostatic pressure, capillary oncotic pressure, and
capillary permeability.
The most common cause of pulmonary edema is left-sided
heart disease.
filling pressures on the left side of the heart increase and
cause a concomitant increase in pulmonary capillary
hydrostatic pressure. When the hydrostatic pressure
exceeds oncotic pressure, fluid moves into the
interstitium, or interstitial space (the space within the
alveolar septum between alveolus and capillary)

Another cause of pulmonary edema is capillary injury


that increases capillary permeability.
Pulmonary edema also can result from obstruction of
the
lymphatic system.
Postobstructive pulmonary edema (POPE, or
negative pressure pulmonary edema)

ACUTE LUNG INJURY/ACUTE


RESPIRATORY DISTRESS
SYNDROME
Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) represents a spectrum of
acute lung inflammation and diffuse alveolocapillary injury.
Common predisposing factors :
1. genetic factors
2. Sepsis
3. multiple trauma
4. Pneumonia
5. Burns
6. Aspiration
7. cardiopulmonary bypass surgery
8. Pancreatitis
9. drug overdose
10. Smoke or noxious gas inhalation

11. Oxygentoxicity
12. radiation therapy and DIC

PATHOPHYSIOLOGY
All disorders that result in ARDS cause acute injury to the
alveolocapillary membrane producing massive pulmonary
inflammation, increased capillary permeability, severe
pulmonary edema, shunting, V/Q mismatch, and hypoxemia.
The alveolocapillary injury can occur directly, aspiration of
highly acidic gastric contents or the inhalation of toxic gases; or
indirectly, as from circulating inflammatory mediators released
in response systemic disorders, such as sepsis and trauma
Lung inflammation and injury damages the alveolar epithelium
and the vascular endothelium. Because the pulmonary edema
is not secondary to heart failure, ARDS is often referred to as
noncardiogenic pulmonary edema. ARDS progresses through
three overlapping phases characterized by histologic changes
in the lung: exudative (inflammatory), proliferative, and fibrotic

EXUDATIVE (INFLAMMATORY)
PHASE (WITHIN 72 HOURS)
The initial lung injury damages the alveolocapillary
membrane. Lung injury activates neutrophils,
platelets, macrophages, lung epithelial and endothelial
cells, and uncontrolled inflammation.
The role of neutrophils is central to the development
and progression of ARDS. Activated neutrophils
release a battery of harmful inflammatory mediators,
among them proteolytic enzymes, oxygen free
radicals (superoxide radicals, hydrogen peroxide,
hydroxyl radicals), arachidonic acid metabolites

ACUTE RESPIRATORY DISTRESS


SYNDROME (ARDS).

CROSS-SECTIONAL

VIEW OF ALVEOLI IN ARDS. (MODIFIED FROM DES JARDINS T, BURTON GG: CLINICAL
MANIFESTATIONS AND ASSESSMENT OF RESPIRATORY DISEASE, ED 3, ST LOUIS, 1995, MOSBY.

FIBROTIC PHASE (14 TO 21


DAYS).

About 2 to 3 weeks after the initial injury, remodeling


and fibrosis occur. The fibrosis progressively
obliterates the alveoli, respiratory bronchioles, and
interstitium, leading to a decrease in functional
residual capacity (FRC) and continuing V/Q
mismatch with severe right-to-left shunt. The result of
this overwhelming inflammatory response by the
lungs is acute respiratory failure.

CLINICAL MANIFESTATIONS. THE CLINICAL MANIFESTATIONS OF ARDS

ARE PROGRESSIVE AS FOLLOWS

Dyspnea and hypoxemia with poor response to oxygen


supplementation

Hyperventilation and respiratory alkalosis

Decreased tissue perfusion, metabolic acidosis, and organ


dysfunction

Increased work of breathing, decreased tidal volume, and


hypoventilation

Hypercapnia, respiratory acidosis, and worsening hypoxemia

Decreased cardiac output, hypotension, and death


EVALUATION AND TREATMENT:
-early detection and management of contributing etiologies
-supportive therapy to prevent progression of lung injury, and
prevention of complications such
as pneumonia and stress ulcer.
Traditional therapy includes:
-mechanical ventilation with PEEP and high oxygen concentrations.
-Alternative modalities of ventilation are being evaluated, including
low-volume ventilation, noninvasive positive-pressure
-ventilation
- permissive hypercapnia
-prone positioning
-extracorporeal gas exchange
- partial liquid ventilation

OBSTRUCTIVE
PULMONARY DISEASE
Asthma,chronic bronchitis, and emphysema.

ASTHMA
Asthma is a chronic inflammatory disorder of the
bronchial mucosa that causes bronchial
hyperresponsiveness, constriction of the airways, and
variable airflow obstruction that is reversible.59 Asthma
occurs at all ages, with approximately half of all cases
developing during childhood.
Asthma is most commonly a familial disorder and more
than 100 genes have been identified that may play a role
in the susceptibility and pathogenesis of asthma,
including those that influence the production of IL-4, IL-5,
and IL-13; IgE; eosinophils; mast cells; adrenergic
receptors; leukotrienes; nitric oxide; and transmembrane
proteins in the endoplasmic reticulum.

PATHOHYSIOLOGY
Many cells and cellular elements contribute to the
persistent inflammation of the bronchial mucosa and
hyperresponsiveness of the airways, including
macrophages (dendritic cells), T helper 2 (Th2)
lymphocytes, B lymphocytes, mast cells, neutrophils,
eosinophils, and basophils. There is both an
immediate (early asthmatic response) and a late
(delayed) response.

Early asthmatic response


CD4+ T cells Differentiation - IL-4, IL-5, IL-8, IL-13, IL-17, and
IL-22. IL-4 stimulates B-cell activation This produces IgE.
. IL-5 stimulates the activation, migration, and proliferation
of eosinophils, which cause direct tissue injury and release
of toxic neuropeptides that contribute to increased bronchial
hyperresponsiveness fibroblast proliferation epithelial
injury, and airway scarring
IL-8 activates neutrophils that contribute to a more
exaggerated inflammatory response
IL-13 impairs mucociliary clearance, enhances fibroblast
secretion, and contributes to bronchoconstriction and airway
remodeling
IL-17 increases neutrophilic inflammation
IL-22 stimulates airway epithelial cells, which play
an important role in stimulating further innate and adaptive
immune responses.

IgE binds to receptors on the surface of mast cells.


Once bound to antigen, the IgE causes the mast cells
to degranulate, releasing a large number of
inflammatory mediators
Together these mediators cause vasodilation,
increased capillary permeability, mucosal edema,
bronchial smooth muscle contraction (bronchospasm),
and tenacious mucus secretion from mucosal goblet
cells with narrowing of the airways and o bstruction to
airflow

The late asthmatic response begins 4 to 8 hours after the early response
Chemotactic recruitment of lymphocytes, eosinophils, and neutrophils during the acute response
causes a latent release of inflammatory mediators
Eosinophil mediators cause direct tissue injury with fibroblast proliferation and airway scarring.
toxic neuropeptides contribute to increased bronchial hyperresponsiveness.


A decrease in the number or function of T regulatory (Treg) cells are associated with asthma.
Untreated inflammation can lead to long-term airway damage that is irreversible, known as airway
remodeling (subepithelial fibrosis, smooth muscle and mucous gland hypertrophy).

Airway obstruction increases resistance to airflow and decreases flow rates, especially expiratory flow.
Impaired expiration causes air trapping, hyperinflation distal to obstructions and increased work of
breathing.

Hyperventilation is triggered by lung receptors responding to increased lung volume and obstruction.
The result is early hypoxemia without CO2 retention.

Hypoxemia further increases hyperventilation through stimulation of the respiratory center, causing
Paco2 to decrease and pH to increase (respiratory alkalosis)

With progressive obstruction of expiratory airflow, air trapping becomes more severe and the lungs
and thorax become hyperexpanded

This leads to a fall in tidal volume with increasing CO2 retention and respiratory acidosis. Respiratory
acidosis signals respiratory failur

PATHOPHYSIOLOGY OF ASTHMA. ALLERGEN OR IRRITANT EXPOSURE RESULTS IN A CASCADE OF


INFLAMMATORY EVENTS LEADING TO ACUTE AND CHRONIC AIRWAY DYSFUNCTION. IGE,
IMMUNOGLOBULIN E; IL, INTERLEUKIN

CLINICAL MANIFESTATIONS
-experiences chest constriction
-expiratory wheezing
-dyspnea
-nonproductive coughing, prolonged expiration
-tachycardia
-tachypnea
-pulsus paradoxus
-status asthmaticus

Evaluation and Treatment


- immediate administration of oxygen and inhaled betaagonist bronchodilators
- leukotriene antagonists can be considered. In more
severe asthma, long-acting beta agonists can be used
to control persistent bronchospasm
long-acting beta agonists (LABAs) (salmeterol and
formoterol) are recommended to be used in
onjunction with inhaled corticosteroids as step 3
therapy for persistent asthma
Immunotherapy has been shown to be an important
tool in reducing asthma exacerbations and can now be
given sublingually. Monoclonal antibodies to IgE
(omalizumab) have been found to be helpful in
selected individuals.

CHRONIC
OBSTRUCTIVE
PULMONARY DISEASE

Chronic obstructive pulmonary disease (COPD) is defined as a


preventable and treatable disease with some significant
extrapulmonary effects that may contribute to the severity in
individual patients. Its pulmonary component is characterized by
airflow limitation that is not fully reversible Its pulmonary component
is characterized by airflow limitation that is not fully reversible. The
airflow limitation is usually progressive and associated with an
abnormal inflammatory response of the lung to noxious particles or
gases.
The clinical phenotypes of COPD are chronic bronchitis and
emphysema An inherited mutation in the 1-antitrypsin gene results
in the development of COPD (emphysema) at an early age, even in
nonsmokers The pathologic changes of COPD occur in large central
airways, small peripheral airways, and the lung parenchyma, the
dominant features of chronic bronchitis and emphysema.

Risk factors for COPD include:


tobacco smoke (cigarette, pipe, cigar, and environmental
tobacco smoke)
occupational dusts and chemicals (vapors, irritants, and
fumes)
indoor air pollution from biomass fuel used for cooking and
heating (in poorly vented dwellings), outdoor air pollution
any factor that affects lung growth during gestation and
childhood (low birth weight, respiratory tract infections).
Genetic susceptibilities have been identified, including
polymorphisms of genes that code for tumor necrosis factor,
surfactant, proteases, antiproteases, and risks for lung
cancer.

CHRONIC
BRONCHITIS
Chronic bronchitis is defined as hypersecretion of mucus and chronic
productive cough that continues for at least 3 months of the year (usually the
winter months) for at least 2 consecutive years.

PATHOPHYSIOLOGY.
Inspired irritants result in airway inflammation with infiltration of neutrophils,
macrophages, and lymphocytes into the bronchial wall. Tobacco smoke directly
injures airway epithelial cells. Continual bronchial inflammation causes bronchial
edema and increases the size and number of mucous glands and goblet cells in
the airway epithelium. Thick, tenacious mucus is produced and cannot be
cleared because of impaired ciliary function The lungs defense mechanisms are,
therefore, compromised, increasing susceptibility to pulmonary infection, which
contributes to airway injury Frequent infectious exacerbations are complicated
by bronchospasm with dyspnea and productive cough.
Initially chronic bronchitis affects only the larger bronchi, but eventually all
airways are involved. The thick mucus and hypertrophied bronchial smooth
muscle narrow the airways and lead to obstruction, particularly during expiration
when the airways are constricted. Obstruction eventually leads to ventilationperfusion mismatch with hypoxemia. The airways collapse early in expiration,
trapping gas in the distal portions of the lung. Air trapping expands the thorax,
putting the respiratory muscles at a mechanical disadvantage. This leads to
decreased tidal volume, hypoventilation, and hypercapnia

CHRONIC BRONCHITIS. INFLAMMATION AND THICKENING OF MUCOUS


MEMBRANE WITH ACCUMULATION OF MUCUS AND PUS LEADING TO
OBSTRUCTION CHARACTERIZED BY PRODUCTIVE COUGH. (MODIFIED FROM
DES JARDINS T, BURTON GG: CLINICAL MANIFESTATIONS AND ASSESSMENT OF
RESPIRATORY DISEASE, ED 3, ST LOUIS, 1995, MOSBY.)

Pathogenesis of Chronic Bronchitis and Emphysema (Chronic


Obstructive Pulmonary Disease [COPD])

CLINICAL MANIFESTATIONS:
-decreased exercise tolerance
-wheezing, and shortness of breath
-Individuals usually have a productive cough (smokers
cough)
-of airway obstruction (decreased FEV1) is shown by
spirometry
-Marked hypoxemia leads to polycythemia
(overproduction of erythrocytes) and cyanosis
-If not reversed, hypoxemia leads to pulmonary
hypertension and eventually results in cor pulmonale
and can lead to severe disability or death.

EVALUATION AND TREATMENT. Diagnosis is based


on history of symptoms, physical examination, chest
radiograph, pulmonary function tests, and blood gas
analyses; these tests reflect the progressive nature of
the disease. Prevention of chronic bronchitis is the
best treatment because pathologic changes are not
reversible. By the time an individual seeks medical
care for symptoms, considerable airway damage is
present. If the individual stops smoking, disease
progression can be halted. Bronchodilators (longacting inhaled anticholinergics or long-acting inhaled
beta agonists for symptomatic persons with COPD and
FEV1 <60% predicted) and expectorants are
prescribed to reduce dyspnea and control cough.
Chest physical therapy may be helpful and includes
deep breathing and postural drainage.

Clinical Manifestations:
CLINICAL MANIFESTATIONS OF CHRONIC
PULMONARY
DISEASE
CLINICAL
MANIFESTATI
ONS

CHRONIC
BRONCHITIS

EMPHYSEMA

Productive
cough

Classic sign

Late in course
with infection

Dyspnea

Late in course

Common

Wheezing

Intermittent

Minimal

History of
smoking

Common

Common

Barrel chest

Occasionally

Classic

Prolonged
expiration

Always present

Always present

Cyanosis

Common

Uncommon

Chronic
hypoventilation

Common

Late in course

Polycythemia

Common

Late in course

MECHANISMS OF AIR TRAPPING IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD).


MUCOUS PLUGS AND NARROWED AIRWAYS CAUSE AIR TRAPPING AND HYPERINFLATION
ON EXPIRATION. DURING INSPIRATION THE AIRWAYS ARE PULLED OPEN, ALLOWING GAS
TO FLOW PAST THE OBSTRUCTION. DURING EXPIRATION DECREASED ELASTIC RECOIL OF
THE BRONCHIAL WALLS RESULTS IN COLLAPSE OF THE AIRWAYS AND PREVENTS NORMAL
EXPIRATORY AIRFLOW.

EMPHYSEMA
Emphysema is abnormal permanent enlargement of gas-exchange airways
(acini) accompanied by destruction of alveolar walls without obvious
fibrosis. The major mechanism of airflow limitation in emphysema is loss of
elastic recoil. Some degree of emphysema is considered normal in older
adults, but results in a slow and predictable decline in lung function with
aging.
Primary emphysema, which accounts for 1% to 3% of all cases of
emphysema, is commonly linked to an inherited deficiency of the enzyme
1-antitrypsin.
Normally 1-antitrypsin inhibits the action of many proteolytic enzymes
(enzymes that break down proteins). Individuals who have 1-antitrypsin
deficiency (an autosomal recessive trait) have an increased likelihood of
developing emphysema, because proteolysis in lung tissues is not inhibited.
The major cause of secondary emphysema is the inhalation of cigarette
smoke, although air pollution, occupational exposures, and childhood
respiratory tract infections are known to be contributing factors. Not all
smokers develop emphysema, but approximately 15% to 20% are especially
susceptible and develop significant lung damage, if they continue to smoke.

PATHOPHYSIOLOGY. Emphysema is characterized by


destruction of alveoli through the breakdown of elastin within the
septa by an imbalance between proteases and antiproteases,
oxidative stress, and apoptosis of lung structural cells.
Cellular apoptosis and early cellular senescence contribute to
loss of alveolar cells and reduced surface area for gas exchange.
Alveolar destruction also produces large air spaces within the
lung parenchyma (bullae) and air spaces adjacent to pleurae
(blebs)
Bullae and blebs are not effective in gas exchange and combined
with loss of portions of the pulmonary capillary bed, there is
significant ventilation-perfusion ( V/Q ) mismatching and
hypoxemia.
Expiration becomes difficult because loss of elastic recoil reduces
the volume of air that can be expired passively and air is trapped
in the lungs

Air trapping causes hyperexpansion of the chest, which


puts the muscles of respiration at a mechanical
disadvantage. This results in increased work of breathing,
so that many individuals will develop ypoventilation and
hypercapnia late in the course of the disease.
Chronic inflammation also can have significant systemic
effects including weight loss, muscle weakness, and
increased susceptibility to comorbidities, such as
infection.
Emphysema can be centriacinar (centrilobular) or
panacinar (panlobular) , depending on the site of
involvement.

CLINICAL MANIFESTATIONS. Dyspnea on exertion


that later progresses to marked dyspnea, even at rest,
is the most common symptom of emphysema. Little
coughingand very little sputum are produced Often
the individual is thin, has tachypnea with prolonged
expiration, and must use accessory muscles for
ventilation. The anteroposterior diameter of the chest
is increased (barrel chest), and the chest has a
hyperresonant sound with percussion. To increase lung
capacity, the individual often leans forward with arms
extended and braced on knees when sitting. In
addition, people with emphysema often exhale
through pursed lips which helps prevent expiratory
airway collapse.

EVALUATION AND TREATMENT. Emphysema is usually


diagnosed and staged by pulmonary function measures. In
COPD, pulmonary function tests indicate obstruction to
gas flow during expiration with a marked decrease in
FEV1. Airway collapse and air trapping in distal portions of
the lung lead to a decrease in FVC (but less so than FEV1)
and an increase in FRC, residual volume (RV), and total
lung capacity (TLC). Diffusing capacity is decreased
because of destruction of the alveolocapillary membranes.
On radiographs the diaphragm appears flattened and the
lung fields appear overdistended. In individuals for whom
pulmonary function testing is not definitive for the
diagnosis, high-resolution CT scanning may be indicated.
Arterial blood gas measurements reveal varying degrees
of hypoxemia and/ or hypercapnia. The disease course is
usually prolonged, with increasing dyspnea and
intermittent bouts of infection that culminate in failure of
the right side of the heart (cor pulmonale) and death.

EMPHYSEMA. ENLARGEMENT AND DESTRUCTION OF ALVEOLAR WALLS WITH LOSS OF ELASTICITY AND
TRAPPING OF AIR. A, PANLOBULAR EMPHYSEMA SHOWING ABNORMAL WEAKENING AND
ENLARGEMENT OF ALL AIR SPACES DISTAL TO THE TERMINAL BRONCHIOLES (NORMAL ALVEOLI SHOWN
FOR COMPARISON ONLY); B, CENTRILOBULAR EMPHYSEMA SHOWING ABNORMAL WEAKENING AND
ENLARGEMENT OF THE RESPIRATORY BRONCHIOLES IN THE PROXIMAL PORTION OF THE ACINUS.
(MODIFIED FROM DES JARDINS T, BURTON GG: CLINICAL MANIFESTATIONS AND ASSESSMENT OF
RESPIRATORY DISEASE, ED 3, ST LOUIS, 1995, MOSBY.)

MICROGRAPHS OF TYPES OF EMPHYSEMA. A, CENTRIACINAR EMPHYSEMA. B,


PANACINAR EMPHYSEMA. (MICROGRAPHS FROM DAMJANOV I, LINDER J,
EDITORS: ANDERSONS PATHOLOGY, ED 10, ST LOUIS, 1996, MOSBY.)

RESPIRATORY
TRACT
INFECTIONS

ETIOLOGIC MICROORGANISMS
FOR PNEUMONIA IN ADULTS
CAP

HCAP/HAP/VAP

IMMUNOCOMPROMISED
INDIVIDUALS

Streptococcus
pneumoniae

Pseudomonas
aeruginosa

Pneumocystis jiroveci (formerly


P. carinii)

Haemophilus
influenzae

Staphylococcus aureus
(including methicillinresistant
strains)

Mycobacterium tuberculosis

Staphylococcus
aureus

Klebsiella
pneumoniae

Atypical mycobacteria

Mycoplasma
pneumoniae

Enterobacter
species

Respiratory viruses

Chlamydia
pneumoniae

Protozoa

Moraxella
catarrhalis

Parasites

Legionella
pneumophila

the common cold, pharyngitis (sore throat), and


laryngitis involve only the upper airways. Although
the lungs have direct contact with the atmosphere,
they remain sterile under most circumstances.
Infections of the lower respiratory tract occur most
often in the very young, the very old, or individuals
with impaired immunity or underlying disease. In all
cases the bodys normal defense mechanisms are
impaired.

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