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.
2.
2.those associated with protecting the lungs fromsubstances other than air.
1.
2.
-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
Porths Pathophysiology
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 II
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
apneustic center.
1.
Irritant Receptors
2.
Stretch Receptors
3.
J-receptors
Chemoreceptors
.
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
-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.
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.
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.
ALVEOLAR CAPILLARY
TRANSFER
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
Range
1. pH = acid or base
7.357.45
3545 mm Hg
3. HCO
3 = bicarbonate
2226 mEq/L
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
ALTERATIONS OF
PULMONARY FUNCTION
SIGNS AND
SYMPTOMS OF
PULMONARY DISEASE
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
CAUSES OF HYPOXEMIA
MECHANISM
Decrease in inspired
oxygen (decreased
Fio2)
High altitude
Low oxygen content of gas mixture
Enclosed breathing spaces (suffocation)
Hypoventilation of the
alveoli
Ventilation-perfusion
mismatch
Alveolocapillary
diffusion abnormality
Edema
Fibrosis
Emphysema
Decreased pulmonary
capillary perfusion
Intracardiac defects
Intrapulmonary arteriovenous malformations
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
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.
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
ATELECTASIS
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.
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
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,
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)
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
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.
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.
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
CLINICAL MANIFESTATIONS
-experiences chest constriction
-expiratory wheezing
-dyspnea
-nonproductive coughing, prolonged expiration
-tachycardia
-tachypnea
-pulsus paradoxus
-status asthmaticus
CHRONIC
OBSTRUCTIVE
PULMONARY DISEASE
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
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.
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
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.
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.)
RESPIRATORY
TRACT
INFECTIONS
ETIOLOGIC MICROORGANISMS
FOR PNEUMONIA IN ADULTS
CAP
HCAP/HAP/VAP
IMMUNOCOMPROMISED
INDIVIDUALS
Streptococcus
pneumoniae
Pseudomonas
aeruginosa
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