Respiratory

Roses are red,
Violets are blue,

Without your lungs
Your blood would be, too.
David D. Ralph, MD
New England Journal of Medicine
MEDICAL-SURGICAL
NURSING
Arni A. Magdamo, MD, MHA,
FPCP
University of the Philippines
College of Medicine, College of Nursing
The Respiratory System

Normal Anatomy and
Physiology
The Respiratory Process
Respiration is the process by which

oxygen enters the body and is utilized
by the cells for their metabolic
processes. It essentially involves five
interdependent steps.
Ventilation refers to the entry of air
containing oxygen and other gases into
the lungs.
Ventilation is followed by the diffusion

of gases from and into the alveoli and
alveolar sacs. Oxygen from the alveoli
passes through the respiratory
membrane and enter the perialveolar
capillaries, while carbon dioxide from
the capillaries diffuses through the
respiratory membrane to leave the
lungs by means of exhalation.
Circulation makes it possible for oxygen

to reach the distant tissues, and for
carbon dioxide to travel from the tissues
back into the lungs.
The fourth component of the respiratory
process involves another diffusion of
gases, this time involving the entry of
oxygen into target tissues, and the
entry of carbon dioxide into the blood
stream for delivery back into the lungs.
Cell metabolism and respiration are the

final steps of the respiratory process
wherein oxygen is utilized by the cells,
and carbon dioxide, along with other
waste products, is produced.
The Upper Respiratory

Tract:
The Nose
The bridge of the nose is bone, and

most of the external nose is cartilage.
The nasal cavity houses one of the most
efficient filtering system of the body.
The external nares is divided by the
nasal septum into right and left
portions.
The paranasal sinuses and the
nasolacrimal duct open into the nasal
cavity.
Hairs inside the external nares trap

Tract:
The Nose
The nasal cavity is lined with

pseudostratified ciliated epithelium that
traps debris and moves it to the
pharynx.
The nasal turbinates or conchae provide
for an additional filtering mechanism by
creating a turbulent airflow within the
nasal cavity that dislodges inhaled
pollutants and make them adhere to the
sticky mucosal surface of the nasal
cavity.

Tract:
The Nose
The superior part of the nasal cavity

contains the sensory cells for the sense
of smell.
A vast network of capillaries, called
Kiesselbachs plexus, line the mucosa of
the nasal cavity.

Tract:
The Nose

Tract:
The Pharynx
The nasopharynx joins the nasal cavity

through the internal nares and contains
the opening to the auditory (Eustachian)
tube and the pharyngeal tonsils.
The oropharynx joins the oral cavity and
contains the palatine and lingual tonsils.
The laryngopharynx opens into the
larynx and the esophagus.

Tract:
The Pharynx

Tract:
The Larynx
The larynx is a set of cartilages

collectively called the voice box.
There are three unpaired cartilages.
The thyroid cartilage and cricoid
cartilage form most of the larynx. The
epiglottis covers the opening of the
larynx during swallowing.
There are six paired cartilages. The
corniculate, the arytenoid, and the
cuneiform cartilages all serve as
attachment sites on which the vocal
cords are anchored.

Tract:
The Larynx
The vocal cords are structures within

the larynx that vibrate to produce.
There are two main groups.
The vocal folds are the true vocal cords,
connective tissues that vibrate when air
passes through them to produce the
audible sound.

Tract:
The Larynx
The vestibular folds are known as the

false vocal cords, because they merely
serve as connective tissue support for
the vocal folds.
The cords produce sounds of different
pitches when their length is varied.

Tract:
The Trachea
The trachea, also known as the wind

pipe, is a hollow tubular structure that
connects the larynx to the lower
respiratory organs (the respiratory
tree).
It is a series of 15 to 20 C-shaped
cartilages that are solid anteriorly, and
supported posteriorly by a layer of
smooth muscles which contract or relax
to bring about dilation or constriction of
the airways.

Tract:
The Trachea
It is lined by pseudostratified ciliated

columnar epithelium which aids in the
filtering of inhaled air.

Tract:
The Trachea
The Lower Respiratory

Tract:
The Respiratory Tree
The primary bronchi extend from the

trachea to each lung. The right primary
bronchus is shorter, wider and is
oriented more vertically, while the left
primary bronchus is longer, narrower
and is oriented more horizontally.
There are two lungs. The right lung has
three lobes and ten lobules, while the
left lung has two lobes and nine lobules.

Tract:
The airway passages of the lungs

branch and decrease in size.
The primary bronchi form the secondary
bronchi, which go to each lobe of the
lungs.
The secondary bronchi form the tertiary
bronchi, which go to each lobule of the
lung.
The tertiary bronchi branch many times
to form the bronchioles.

Tract:
The bronchioles branch to form the

terminal bronchioles, which become the
respiratory bronchioles, from which the
alveoli branch.
The epithelium from the trachea to the
terminal bronchioles is ciliated to
facilitate the removal of debris.
Cartilage helps to hold the tube system
open (from the trachea to the
bronchioles).

Tract:
Smooth muscle controls the diameter f

the tubes (especially the bronchioles).
The alveoli are sacs formed by simple
squamous epithelium, and they
facilitate the diffusion of gases.

Tract:
The Lungs

Tract:
The Alveoli
Mechanics of Breathing
Ventilation is the movement of air into

and out of the lungs. Air moves from an
area of higher pressure to an area of
lower pressure.
Inspiration occurs when the diaphragm
contracts and the external intercostal
muscles lift the ribcage, thus increasing
the volume of the thoracic cavity.
Expiration occurs when the diaphragm
relaxes and the internal intercostal
muscles depress the ribcage, thus
decreasing the volume of the thoracic
Lungs tend to collapse because of the

elastic recoil of the connective tissue,
and surface tension of the fluid lining
the alveoli.
The lungs normally do not collapse
because surfactant reduces the surface
tension of the fluid lining the alveoli,
and the visceral pleura tends to adhere
to the parietal pleura.
Pulmonary Volumes and

Capacities
There are four pulmonary volumes: tidal

volume, inspiratory reserve volume,
expiratory reserve volume, and residual
volume.
The tidal volume refers to the volume of
air that goes into and out of the lungs
during normal respiration (about 500
cc).
The inspiratory reserve volume is the
amount of air that can be inspired
forcefully after inspiration of the normal
tidal volume (about 3000 cc).

Capacities
The expiratory reserve volume is the

additional amount of air that can be
expired forcefully (about 1100 cc).
The residual volume is the volume of air
left in the lungs after maximum
expiration. This is also known as dead
space (about 1200 cc).

Capacities
The pulmonary capacities refer to the

sum of two or more pulmonary volumes.
The vital capacity is the sum of the IRV,
the TV and the ERV. It is the maximum
volume of air that a person can expel
from his respiratory tract after a
maximum inspiration (about 4600 cc).
VC = IRV + TV + ERV

Capacities
The inspiratory capacity is the amount

of air that a person can inspire
maximally after a normal expiration
(about 3500 cc).
IC = TV + IRV
The functional residual capacity is the
amount of air remaining in the lungs at
the end of a normal expiration (about
2300 cc).
FRC = ERV + RV
The total lung capacity is the sum of all

Capacities
MAXIMUM
INSPIRATION
IRV
IC
TOTAL
LUNG
CAPACITY
VC
TV
ERV
MAXIMUM
EXPIRATION
FRC
RV
RV
Pulmonary Pressures
Major factors in determining the extent

of lung expansion and compliance
during the processes of inspiration and
expiration:
Alveolar pressure
Intrapleural pressure
Alveolar surfactant
During inspiration, the thoracic cage

enlarges, enlarging both lungs and
decreasing the pressures.
Pulmonary Pressures
Boyles Law:
During inspiration, the enlargement of
the thoracic cage decreases the
pressure in the alveoli to about 3
mmHg. This negative pressure pulls air
through the respiratory passageways
into the alveoli.
Pulmonary Pressures
Boyles Law:
During expiration, the exact mechanism
and effects occur. Compression of the
thoracic cage around the lungs
increases the alveolar pressure to
approximately +3 mmHg which pushes
the air out of the alveoli into the
atmosphere.
Pulmonary Pressures
Intrapleural Pressures:
Intrapleural space is the space between the

lungs and the outer walls of the thoracic
cavity. The pressure here is ALWAYS a few
mmHg less than in the alveoli for the
following reasons:
Surface tension of the fluid inside the alveoli

always makes the alveoli try to collapse.
Elastic fibers spread in all directions through the
lung tissues and tend to contract the lungs.
These factors pull the lungs away from the

outer walls of the pleural cavity, creating an
average negative pressure of 5 mmHg.
Pulmonary Pressures
Surfactant:
Surface active agent

Detergent that greatly decreases the
surface tension of fluid lining the alveoli.
Essential Requirements for

Ventilation
Adequate atmospheric oxygen

Clean air passages
Adequate pulmonary compliance and
recoil
Compliance is the expansibility or

stretchability of the lungs.
Recoil is the ability to collapse away from
the chest wall due to (1) elastic fibers
present in the lungs, and (2) surface tension
of the fluid lining of the alveoli which
accounts for 2/3 of the recoil phenomenon.
Gas Exchange
The respiratory membranes are thin and

have a large surface area that facilitates
gas exchange.
The components of the respiratory
membrane include a film of water, the
walls of the alveoli, and interstitial
space, and the walls of the perialveolar
capillary.
Gas Exchange
The rate of diffusion depends on the

thickness of the respiratory membrane,
the surface area of the membrane, the
diffusion coefficient of the gas, and the
partial pressure of gases in the alveoli
and in the blood.
Transport of Oxygen and

Carbon Dioxide
97% of oxygen combines loosely with

hemoglobin in the red blood cells and is
carried into the tissues as
oxyhemoglobin. The remaining oxygen
is dissolved and transported in the fluid
of plasma and cells.
The amount of oxygen that the blood
will absorb before it is fully saturated is
about 20 ml per 100 ml of blood (20
vol%).

Carbon Dioxide
As the hemoglobin releases oxygen to

the tissues, it is referred to as reduced
hemoglobin.
Normally, only about 25% of oxygen per
ml of blood is diffused to the tissue (5
vol%). However, this rate of release can
be increased to 75% during periods of
stress or increased exercise.

Carbon Dioxide
Factors that influence the rate of

oxygen transport from the lungs to the
tissues:
Cardiac output
Erythrocyte count
Exercise
Hematocrit
Control of Respiration
The respiratory center in the medulla

oblongata and pons stimulates the
muscles of inspiration to contract.
When stimulation of the muscles of
inspiration stops, expiration occurs
passively.
Receptors present in the respiratory and

cardiovascular system, as well as in
other parts of the body, receive changes
in the internal milieu and send sensory
signals to the respiratory center.
Receptors are classified as:
chemoreceptors, baroreceptors,
proprioceptors, and stretch receptors.
The Hering-Breuer reflex inhibits the

inspiratory center when the lungs are
stretched during inspiration.
Carbon dioxide is the major chemical
regulator of respiration.
It is possible to consciously control
ventilation, but only up to a certain
degree.
The Cough and Sneeze

Reflexes
The Cough and Sneeze

Reflexes
Means for keeping the respiratory

passages clean by forcing air very
rapidly outward using these two
reflexes.
Mediated by respiratory muscles,
voluntary and involuntary, with
regulation by the central nervous
system and sensory receptors lining the
respiratory tract.
The Cough Reflex

Irritant touches the surface of the glottis, trachea or bronchus.
Sensory signals are transmitted to the medulla.
Motor signals are transmitted back to the respiratory system.
The Cough Reflex

Motor signals are transmitted back to the respiratory system.
Respiratory muscles contract rapidly generating

high pressures in the lungs while the vocal cords
remain tightly closed.
Vocal cords open suddenly, allowing pressurized air in the

lungs to flow out in a blast.
The Sneeze Reflex

Irritant comes into contact with sensory receptors in the nose.
Sensory signals are received in the medulla.
Motor signals are generated and transmitted back.
The Sneeze Reflex

Motor signals are generated and transmitted back.
Respiratory muscles contract rapidly generating

high pressures in the lungs while the vocal cords
remain tightly closed.
Vocal cords open suddenly, allowing pressurized air in the

lungs to flow out in a blast through the nose and mouth.
Diagnosis of Pulmonary
Function
Clinical Assessment
Symptoms of Pulmonary
Disease
Dyspnea
Paroxysmal nocturnal dyspnea
Inappropriate breathlessness at night.
Orthopnea
Sensation of breathlessness that is

excessive for any given level of physical
activity.
Dyspnea on recumbency.
Platypnea
Dyspnea on the upright position relieved by

recumbency.
Disease
Persistent cough
Always abnormal
Chronic persistent cough may be caused by
cigarette smoking, asthma, bronchiectasis
or COPD.
May also be caused by drugs, cardiac
disease, occupational agents and
psychogenic factors.
Complications include (1) worsening of
bronchospasm, (2) vomiting, (3) rib
fractures,
(4) urinary incontinence, and (5) syncope.
Disease
Stridor
Crowing sound during breathing.

Caused by turbulent airflow through a
narrowed upper airway.
Inspiratory stridor implies extratracheal
variable airway obstruction.
Expiratory stridor implies intratracheal
variable airway obstruction.
Stertorous breathing is an inspiratory sound
due to vibration in the pharynx during sleep.
Disease
Wheezing
Continuous musical or whistling noises

caused by turbulent airflow through
narrowed intrathoracic airways.
Most, but not all, are due to asthma.
Hemoptysis
Expectoration of blood.
Often the first indication of serious
bronchopulmonary disease.
Massive hemoptysis: coughing up of more
than 600 ml of blood in 24 hours.
Signs of Pulmonary
Disease
Tachypnea
Bradypnea
Slow breathing.
Hyperpnea
Rapid, shallow breathing.

Arbitrarily defined as a respiratory rate in
excess of 18/min.
Rapid, deep breathing.
Hyperventilation
Increase in the amount of air entering the

alveoli.
Signs of Pulmonary
Disease
Kussmaul respiration (air hunger)
Deep, regular sighing respiration, whether

the rate be normal slow or fast.
Occurs in diabetic ketoacidosis and uremia,
as an exaggerated form of bradypnea.
Cheyne-Stokes respiration
Commonest form of periodic breathing.

Periods of apnea alternate regularly with
series of respiratory cycles. In each series,
the rate and amplitude increase to a
maximum followed by cessation.
Signs of Pulmonary
Disease
Biot breathing
Uncommon variant of Cheyne-Stokes

respiration.
Periods of apnea alternate irregularly with
series of breaths of equal depth that
terminate abruptly.
Most often seen in meningitis.
Signs of Pulmonary
Disease
Singultus
Sudden, involuntary diaphragmatic

contraction producing an inspiration
interrupted by glottal closure to emit a
characteristic sharp sound.
Causes:
Reflex stimulation without organic disease

Diseases of the central nervous system
Mediastinal disorders
Pleural irritation
Abdominal disorders
Diaphragmatic stimulation
Signs of Pulmonary
Disease
Physical chest deformities
The thorax is usually symmetric, both sides

rise equally on inspiration.
Chest asymmetry at rest:
Scoliosis
Chest wall deformity
Severe fibrothorax
Conditions with unilateral loss of lung volume
Signs of Pulmonary
Disease
Symmetrically reduced chest expansion

during deep inspiration:
Neuromuscular disease
Emphysema
Ankylosis of the spine
Asymmetric chest expansion during

inspiration:
Unilateral airway obstruction

Pleural or pulmonary fibrosis
Splinting due to chest pain
Pleural effusion
Pneumothorax
Signs of Pulmonary
Disease
Expansion on the chest, collapse of the

abdomen on inspiration:
Weakness or paralysis of the diaphragm
Chest collapse, rise of the abdomen on

inspiration:
Airway obstruction
Intercostal muscle paralysis
Flail deformity of the chest
Signs of Pulmonary
Disease
Pulsus paradoxicus
The arterial blood pressure normally falls

about 5 mmHg to a maximum of 10 mmHg
on inspiration.
Exaggeration of the normal response.
Seen in:
Severe asthma or emphysema

Upper airway obstruction
Pulmonary embolism
Pericardial constriction or tamponade
Restrictive cardiomyopathy
Signs of Pulmonary
Disease
Cyanosis
Bluish discoloration of skin or mucous

membranes.
Caused by increased amounts (>5 g/dL) of
unsaturated / reduced hemoglobin.
Presents as either central or peripheral
cyanosis
Signs of Pulmonary
Disease
Digital clubbing
Anteroposterior thickness of the index finger

at the base of the fingernail exceeds the
thickness of the distal interphalangeal joint.
Helpful clues:
Nail bed sponginess

Excessive rounding of the nail plate
Flattening of the angle between the nail plate and
the proximal nail skin fold
Signs of Pulmonary
Disease
Percussion sounds (resonance, dullness,

hyperresonance)
Auscultatory sounds (vesicular,
bronchial, bronchovesicular)
Adventitious sounds
Abnormal sounds on auscultation

May be classified as continuous (wheezes,
rhonchi) or discontinuous (crackles,
crepitations)
Signs of Pulmonary
Disease
Wheezes
High-pitched sounds which results from

bronchospasm, bronchial or bronchiolar
mucosal edema, or airway obstruction by
mucus, tumors, or foreign bodies.
Rhonchi
Low-pitched sounds caused by sputum in

large airways and frequently clear after
coughing.
Signs of Pulmonary
Disease
Crackles
Generated by the snapping open of small

airways during inspiration.
Fine crackles are heard in interstitial
diseases, early pneumonia or pulmonary
edema, patchy atelectasis and in some
patients with asthma or bronchitis.
Coarse crackles are heard late in the course
of pulmonary edema or pneumonia.
Signs of Pulmonary
Disease
Fremitus
Voice vibrations on the chest wall.

Localized reduction in fremitus occurs over
areas of air or fluid accumulation in the
lungs.
Increased fremitus suggests lung
consolidation.
Bronchophony
Increased intensity and clarity of the spoken

word during auscultation.
Heard over areas of consolidation or lung
Signs of Pulmonary
Disease
Whispered pectoriloquy
Extreme form of bronchophony in which

softly spoken words are readily heard by
auscultation.
Egophony
Auscultation of an a sound when the

patient speaks an e sound.
Signs of Pulmonary
Disease
TYPICAL CHEST EXAMINATION FINDINGS IN SELECTED CLINICAL CONDITIONS
CONDITION
Normal
Consolidatio
n or
Atelectasis
(with patent
airway)
Consolidatio
n or
Atelectasis
(with
blocked
Bronchial
airway)
Asthma
PERCUSSIO
N
FREMITUS
BREATH
SOUNDS
VOICE
TRANSMISSIO
N
Normal
ADVENTITIOU
S SOUNDS
Resonant
Normal
Vesicular
Dull
Increased
Bronchial
Bronchophony
, whispered
pectoriloquy,
egophony
Crackles
Dull
Decrease
d
Decreased
Decreased
Absent
Resonant
Normal
Vesicular
Normal
Wheezing
Absent
Signs of Pulmonary
Disease
TYPICAL CHEST EXAMINATION FINDINGS IN SELECTED CLINICAL CONDITIONS
CONDITION
PERCUSSION
FREMITUS
BREATH
SOUNDS
Interstitial
Lung
Disease
Emphysema
Resonant
Normal
Vesicular
Hyperresona
nt
Decrease
d
Hyperresona
nt
Dull
Pneumothor
ax
Pleural
effusion
VOICE
TRANSMISSIO
N
Normal
ADVENTITIOU
S SOUNDS
Decrease
d
Decreased
Absent or
wheezing
Decrease
d
Decrease
d
Decreased
Absent
Decrease
d
Decrease
d
Decreased
Absent or
pleural
friction rub
Crackles
Diagnosis of Pulmonary
Function
Laboratory Assessment
Routine Radiography
Integral part of the diagnostic

evaluation of diseases involving the
pulmonary parenchyma, the pleura, and
to a lesser extent, the airways and the
mediastinum.
Usually involves a postero-anterior view
and a lateral view.
Lateral decubitus views are often useful
for determining whether pleural
deformities represent freely flowing
Routine Radiography
Apicolordotic views visualize disease at

the lung apices better than the standard
posteroanterior view.
Chest Radiography
Chest Radiography
Ultrasonography
Not useful for evaluation of the

pulmonary parenchyma.
Helpful in the detection and localization
of pleural fluid.
Computed Tomography
Offers several advantages over

conventional radiographs.
Use of cross-sectional images makes it
possible to distinguish between
densities.
Better at characterizing tissue densities
and providing accurate size of lesions.
Computed Tomography
Computed Tomography
Magnetic Resonance
Imaging
Pulmonary Function Tests
Objectively measure the ability of the

respiratory system to perform gas
exchange by assessing ventilation,
diffusion and mechanical properties.
Composed of the spirometry test and
ventilation-perfusion (V/Q) test.
Indications:
Evaluation of the type and degree of

pulmonary dysfunction (obstructive or
restrictive)
Evaluation of dyspnea, cough and other
symptoms
Early detection of lung dysfunction
Surveillance in occupational settings
Follow-up or response to therapy
Preoperative evaluation
Disability assessment
Relative contraindications:
Severe acute asthma or respiratory distress

Chest pain aggravated by testing
Pneumothorax
Brisk hemoptysis
Active tuberculosis
Spirometry
Allows for the determination of the presence

and severity of obstructive and restrictive
pulmonary dysfunction.
The hallmark of obstructive pulmonary
dysfunction is reduction of airflow rates.
Restrictive pulmonary dysfunction is
characterized by reduction in pulmonary
volumes.

Capacities
MAXIMUM
INSPIRATION
IRV
IC
TOTAL
LUNG
CAPACITY
VC
TV
ERV
MAXIMUM
EXPIRATION
FRC
RV
RV
Ventilation-Perfusion Lung Scan (V/Q

scan)
Measures the degree of ventilation of the

individual lung segments and the perfusion
of respective segments to detect any
shunting or mismatch.
Finds utility in settings where possible
pulmonary embolism is suspected.

Tract:
The Lungs
Arterial Blood Gases
Measure of acid and base balance in the

blood.
Also check the saturation of blood with
oxygen.
Biologic Specimen
Collection
Sputum collection
Spontaneous expectoration or sputum

induction
Percutaneous needle aspiration
Usually carried out under CT or ultrasound

guidance.
Potential risks include intrapulmonary
bleeding and creation of a pneumothorax.
Biologic Specimen
Collection
Thoracentesis
Sampling of pleural fluid or for palliation of

dyspnea in patients with pleural effusion.
Analysis of the fluid for cellular composition
and chemical constituents like glucose,
protein and LDH.
Biologic Specimen
Collection
Bronchoscopy
Provides for direct visualization of the

tracheobronchial tree.
Rigid bronchoscopy is performed in an
operating room on a patient under general
anesthesia.
Flexible bronchoscopy may be done under
local anesthesia / sedation.
Diagnostic uses include histologic
identification or neoplasms and
identification of sources of hemoptysis.
Biologic Specimen
Collection
Bronchoscopy
Therapeutic indications are retrieval of

foreign bodies and control of bleeding.
Bronchoalveolar lavage has been used for
the recovery of organisms that are difficult
to isolate in the usual sputum recovery
methods.
Biologic Specimen
Collection
Video-Assisted Thoracic Surgery (VATS)
Operator can biopsy lesions of the pleura

under direct vision for both diagnostic and
therapeutic purposes.
Thoracotomy
Frequently replaced by VATS.

Provides the largest amount of biologic
specimen for histologic study.
Biologic Specimen
Collection
Mediastinoscopy and Mediastinotomy
Both performed under general anesthesia

by a qualified surgeon.
Used for visualization and sampling of
tissues in the mediastinum such as lymph
nodes and neoplasms.
Diseases of the
Respiratory System
Nose, Paranasal Sinuses and
Larynx
Influenza
Influenza viruses, members of the

Orthomyxoviridae family, include types
A, B and C.
Outbreaks occur virtually every year
and communicability is influenced by
antigenic shifts and viral mutations that
confuse the affected patients
immune system.
Influenza:
Clinical Manifestations
Incubation period of 3-6 days.

Acute illness usually resolves over 2-5
days.
Most patients largely recover within 1
week.
Symptoms and Signs:
Abrupt onset of headache

Fever and chills
Myalgia and malaise
Cough, sneezing and sore throat
Influenza:
The major problem posed consists of its

complications:
Primary influenza viral pneumonia

Secondary bacterial pneumonia
Mixed viral and bacterial pneumonia
Extrapulmonary complications:
Reyes syndrome
Myositis, rhabdomyolysis and myoglobinuria
Encephalitis, transverse myelitis
Guillain-Barr syndrome
Influenza: Treatment
Treatment for uncomplicated influenza

is symptomatic
Salicylates should be avoided in children

because of its association with Reyes
syndrome.
Increased oral fluid intake.
Ascorbic acid
Antivirals:
Amantadine (Influenza A)
Rimantadine (Influenza B)
Ribavirin (Influenza A and B)
Influenza: Treatment
Prophylaxis:
Vaccination against Influenza A and B

Amantadine and rimantadine
Viral Rhinitis
The nonspecific symptoms of the

ubiquitous common cold are present in
the early phases of many diseases that
affect the upper aerodigestive tract.
Rhinoviruses, members of the
Picornaviridae family, are a prominent
cause of the common cold, with
seasonal peaks in the early fall and
spring.
Infections highest among infants and
Viral Rhinitis
The infection is spread by contact with

infected secretions or respiratory
droplets or by hand-to-hand contact,
with autoinoculation of the conjunctival
or nasal mucosa.
Viral Rhinitis:
Incubation period of 1 to 2 days.

Illness generally lasts 4 to 9 days and
resolves spontaneously.
Symptoms:
Headache
Nasal congestion
Water rhinorrhea
Sneezing
Scratchy throat
General malaise and occasionally fever
Viral Rhinitis:
Signs:
Reddened, edematous nasal mucosa

Water nasal discharge
Rhinoviruses are not a major cause of

lower respiratory tract disease.
Rhinoviruses may cause exacerbations
of asthma and chronic pulmonary
disease in adults.
Viral Rhinitis:
Complications:
Transient middle ear effusion

Secondary bacterial infection
Because of the mild nature and short

duration of the illness, a specific
diagnosis is not commonly needed;
however, viral cultures can be
performed.
Viral Rhinitis: Treatment
No proven specific treatment.

Supportive measures:
Decongestants should not be used for more

than a week because of rebound congestion
noted after cessation (rhinitis
medicamentosa).
Antipyretics
Liberal fluid intake
Ascorbic acid
Other Viral URTI:

Coronavirus
Account for 10 to 20% of common colds.

Most active in late fall, winter and early
spring a period when the rhinovirus is
relatively inactive.
Symptoms are similar to those of
rhinovirus, but the incubation period is
longer (3 days) and usually lasts 6 to 7
days.
Mutations of the virus brought about the
SARS phenomenon.
Other Viral URTI:

Respiratory Syncytial Virus
Belongs to the Paramyxoviridae family.

Major respiratory pathogen of young
children and is the foremost cause of
lower respiratory disease in infants.
Transmitted by close contact with
fingers or fomites as well as through
coarse (not fine) aerosols produced by
coughing or sneezing.
Incubation period of 4 to 6 days.
Viral shedding may last two weeks in
children but is much shorter in adults.
Other Viral URTI:

Respiratory Syncytial Virus
Clinical Manifestations:
Rhinorrhea
Low-grade fever
Mild systemic symptoms
Cough and wheezing
25-40% with lower respiratory tract
involvement
Treatment:
Antiviral ribavirin for children and infants.

No specific treatment for adults.
Other Viral URTI:

Parainfluenza Virus
Single-stranded RNA virus of the

Paramyxoviridae family.
Important cause of mild illnesses and
croup (laryngotracheobronchitis),
bronchiolitis and pneumonia.
Cold or hoarseness with cough

Acute febrile illness with coryza
Barking cough and frank stridor in children
Other Viral URTI:

Parainfluenza Virus
Treatment:
In mild illness, treatment is symptom-based.

Mild croup may be treated with moisturized
air from a vaporizer.
More severe cases require hospitalization
and close observation for development of
respiratory distress.
No specific antiviral treatment is available.
Other Viral URTI:

Adenovirus
Infections occur frequently in infants

and children with a seasonal distribution
of fall to spring.
Certain serotypes are associated with
outbreaks of acute respiratory disease
in military recruits.
Transmission can take place via
inhalation of aerosolized virus, through
the inoculation of the conjunctival sac,
and probably by the fecal-oral route.
Other Viral URTI:

Adenovirus
Rhinitis
Pharyngoconjunctival fever (bilateral
conjunctivitis, low-grade fever, rhinitis, sore
throat and cervical lymphadenopathy)
In adults, the most frequent syndrome is the
acute respiratory disease seen in military
recruits, with prominent sore throat, fever
on the second or third day of illness, cough,
coryza and regional lymphadenopathy.
Other Viral URTI:

Adenovirus
Diagnosis and Treatment:
Diagnosis is established by isolation of the

virus.
No specific antiviral therapy is available.
A live oral vaccine is available and used
widely to prevent outbreaks among military
recruits.
Acute Bacterial Sinusitis
Symptoms of rhinitis plus clinical signs

and symptoms that indicate
involvement of the affected sinus or
sinuses such as pain and tenderness
over the involved sinus.
Occurs when an undrained collection of
pus accumulates in a sinus.
Typical Pathogens:
Streptococcus pneumoniae
Other streptococci
Haemophilus influenzae
Staphylococcus aureus
Moraxella catarrhalis
Symptoms and Signs:
Pain on pressure over the cheeks (maxillary

sinuses are the most common sinuses
affected).
Discolored nasal discharge and poor
response to decongestants.
Headache in the middle of the head or in
the forehead.
Imaging:
Transillumination
Caldwell view (frontal)
Waters view (maxillary)
Lateral view (sphenoid)
Submentovertical view (ethmoid)
CT scan for recurrent sinusitis
MRI if malignancy in suspected
Acute Bacterial Sinusitis:

Treatment
Uncomplicated:
Outpatient management
Oral decongestants and nasal decongestant
sprays
Appropriate oral antibiotics for at least two
weeks
* Amoxicillin provides better sinus
penetration than ampicillin.
Complicated:
Failure of sinusitis to resolve after a

completed course of antibiotic treatment.
Complications:
Lower respiratory tract infections

Osteomyelitis and mucocoele
Intracranial complications
Malignancy (?)
Allergic Rhinitis
Allergic Rhinitis
Hay fever
Symptoms mimic that of viral rhinitis
but more persistent and show seasonal
variation.
Symptoms:
Watery rhinorrhea
Eye irritation, pruritus, erythema and
tearing
Signs:
Pale or violaceous turbinates
Allergic Rhinitis:
Treatment
Symptomatic in most cases.

Oral decongestants
Antihistamines
Nasal corticosteroid sprays
Maintaining an allergen-free
environment
Air purifiers and dust filters
Desensitization
Epistaxis
Bleeding from Kiesselbachs plexus

Predisposing factors:
Nasal trauma (nose picking, foreign bodies,

forceful nose blowing)
Rhinitis
Drying of the nasal mucosa from low
humidity
Nasal septal deviation
Alcohol use
Antiplatelet medications
Bleeding diathesis
Epistaxis
Treatment:
Direct pressure on the bleeding site.

Venous pressure is reduced in the sitting
position, and leaning forward lessens the
swallowing of blood.
Short-acting nasal decongestant sprays
Cautery
Treatment of other possible underlying
causes of bleeding
Acute Laryngitis
Most common cause of vocal

hoarseness.
May persist for a week or so after
symptoms of upper airway infection
have cleared.
Etiologies:
Viral
Bacterial (Moraxella catarrhalis,
Haemophilus influenzae)
Treatment:
Diseases of the
Respiratory System
Diseases of the Airways
Diseases of the
Respiratory System
Obstructive Airway Diseases
Asthma
Increased responsiveness of lower

airways to multiple stimuli.
Episodic and with reversible obstruction.
May range in severity from mild without
limitation of patients activity, to severe
and life-threatening.
Men and women are equally affected.
Afflicts children more commonly than
adults.
Asthma
Airway narrowing results from:
Smooth muscle spasm

Airway edema and inflammation
Mucus plugging
Variants:
Exercise-induced asthma
Triad asthma
Cardiac asthma
Asthmatic bronchitis
Drug-induced asthma
Asthma
Asthma
Pathogenesis:
Common denominator is nonspecific

hyperirritability of the tracheobronchial tree.
Airway reactivity increased by:
Allergenic
Pharmacologic
Environmental, occupational
Infectious
Emotional
Activity-related
Asthma
Symptoms and Signs:
Episodic wheezing
Chest tightness
Dyspnea and cough
Tachycardia and tachypnea with prolonged
expiation
Ominous signs: fatigue, pulsus paradoxicus,
diaphoresis, inaudible breath sounds with
diminished wheezing, inability to maintain
recumbency, and cyanosis
Asthma
Laboratory Findings:
Increased WBC count with eosinophilia

Viscid sputum on gross examination
Curschmanns spirals on microscopic
examination of sputum
Charcot-Leyden crystals
Obstructive pattern on the pulmonary
function tests
Diminished peak expiratory flow rate
(normal: 450-650 L/min in men; 350-500
L/min in women)
Respiratory alkalosis and mild hypoxemia in
Asthma
Asthma
Asthma
Asthma
Asthma
Complications:
Exhaustion
Dehydration
Airway infection
Cor pulmonale
Tussive syncope
Pneumothorax (rare)
Asthma
Prevention:
Comprehensive patient education

Pharmacologic intervention
Environment control
Early treatment of chest infections
Recognition and effective management of
nasal and paranasal disorders
Discontinuance of cigarette smoking
Pneumococcal and yearly influenza
immunization for patients with moderate to
severe asthma
Asthma: Classifications
Mild asthma:
Intermittent brief symptoms up to two times

weekly.
Absence of symptoms between
exacerbations.
Brief symptoms with activity.
Nocturnal symptoms less than twice a
month.
PEFR or FEV1 of 80% or more, with less than
20% variability on exacerbations.
Moderate asthma:
Symptoms more than one to two times

weekly.
Exacerbations affecting sleep and level of
activity.
Exacerbations lasting several days.
Requirement for occasional emergency
care.
PEFR values 60-80% of predicted, with 2030% variability during exacerbations and
greater than 30% on worst exacerbations.
Severe asthma:
Continuous symptoms
Frequent exacerbations
Limitations of physical activities
Frequent nocturnal symptoms
Requirement for frequent emergency care
PEFR less than 60% of predicted, with
variability of 20-30% on treatment, and
greater than 50% on severe exacerbations
Prolonged asthma refractory to conventional
modes of therapy (status asthmaticus)
Asthma: Treatment
Mild ambulatory asthma:
Short-acting inhaled 2-agonist drug
Moderate ambulatory asthma:
Daily maintenance therapy with inhaled

corticosteroids
Cromolyn or nedocromil
Short-acting inhaled 2-agonist drugs for
breakthrough wheezing
Oral theophylline
Asthma: Treatment
Asthma: Treatment
Severe ambulatory asthma:
Daily maintenance therapy with inhaled

corticosteroids
Daily oral sustained-release theophylline or
oral 2-agonist drugs
Long-acting inhaled 2-agonist drug
(salmeterol)
Inhaled anti-cholinergic drug (ipratropium
bromide)
Short-acting inhaled 2-agonist drug for
breakthrough wheezing
Asthma: Treatment
Status asthmaticus:
Supplemental oxygen, 1-3 L/min

Monitoring with oximetry
Inhaled 2-agonist agents
Intravenous aminophylline
Subcutaneous terbutaline
Intravenous corticosteroids
Inhaled corticosteroids
Oral corticosteroids
Supportive: hydration, physical therapy, MV
Asthma: Prognosis
Outlook is excellent because of the

availability of medications.
Better prognosis in those who develop
asthma early in life.
Chronic Obstructive
Pulmonary Disease (COPD)
Characterized by airflow obstruction due

to chronic bronchitis or emphysema.
Classifications:
Chronic Bronchitis
Excessive secretion of bronchial mucus.

Productive cough for 3 months or more in at least
2 consecutive years.
Emphysema
Abnormal and permanent enlargement of air

spaces distal to the terminal bronchiole, with
destruction of their walls, and without obvious
fibrosis.
Chronic Obstructive
EMPHYSEMA VS CHRONIC BRONCHITIS
EMPHYSEMA
HISTORY
After age 50
CHRONIC
BRONCHITIS
After age 35
Progressive,
constant, severe
Intermittent, mild to
moderate
Cough
Absent or mild
Persistent, severe
Sputum production
Absent or mild
Copious
Sputum
appearance
Clear, mucoid
Mucopurulent or
purulent
Other features
Weight loss
pink puffer
Airway infections,
right heart failure,
obesity
blue bloater
Onset of
symptoms
Dyspnea
Chronic Obstructive
EMPHYSEMA
PHYSICAL
EXAMINATION
Thin, wasted
CHRONIC
BRONCHITIS
Stocky, obese
Central cyanosis
Absent
Present
Plethora
Absent
Present
Hypertrophied
Unremarkable
Increased
Normal
Hyperresonant
Normal
Diminished breath
sounds
Wheezes, rhonchi
Body habitus
Accessory
respiratory
muscles
Anteroposterior
chest diameter
Percussion note
Auscultation
Chronic Obstructive
EMPHYSEMA
CHEST X-RAY
CHRONIC
BRONCHITIS
Absent
Bullae, blebs
Present
Overall
appearance
Decreased
markings in the
periphery
Present
Dirty lungs
Normal or small,
vertical
Large, horizontal
Low, flat
Normal, rounded
Hyperinflation
Heart size
Hemidiaphragms
Absent
Chronic Obstructive
EMPHYSEMA
LABORATORY
INDICES
Hematocrit
Normal
ECG
Normal
CHRONIC
BRONCHITIS
Increased
Absent, mild
RAD, RVH, P
pulmonale
Moderate, severe
Hypercapnia
Absent
Moderate, severe
Respiratory
acidosis
Total lung capacity
Absent
Present
Increased
Normal
Static lung
compliance
Increased
Normal
Diffusing capacity
Decreased
Normal
Hypoxemia
Chronic Obstructive
Causes:
Cigarette smoking
Air pollution
Airway infection
Familial factors
Allergies
Chronic Obstructive
Symptoms and Signs:
5th or 6th decade of life

Excessive cough and sputum production
Shortness of breath that have often been
present for 10 years or more
Laboratory findings:
Secondary polycythemia
Presence of microorganisms in the sputum
Spirometry shows obstructive pattern
Hyperinflation on radiographs
Chronic Obstructive
Complications:
Pneumonia and acute bronchitis

Pulmonary embolization
Left ventricular heart failure
Pulmonary hypertension
Chronic respiratory failure
Spontaneous pneumothorax
Chronic Obstructive
Prevention:
Smoking cessation
Early treatment of airway infections
Vaccination against pneumococcal
pneumonia and influenza.
Chronic Obstructive
Treatment:
Discontinuance of cigarette smoking

Patient education
Relief of bronchospasm
Ipratropium bromide
Maintenance therapy with oral theophylline
Oral corticosteroids
Aerosol therapy
Chest physiotherapy
Treatment of complications
Home oxygen therapy
Bronchiectasis
Permanent normal dilatation and

destruction of bronchial walls.
May be caused by recurrent infection or
inflammation.
Symptoms:
Chronic cough
Copious sputum production, often purulent
Hemoptysis
Recurrent pneumonia
Bronchiectasis
Signs:
Persistent crackles at the base of the lungs.

Clubbing is infrequent.
Copious foul-smelling sputum that
separates into three layers in a cup.
Crowded bronchial markings on chest x-ray.

Small cystic spaces near the bronchi on
chest CT scan.
Bronchiectasis
Treatment:
Antibiotics
Daily chest physiotherapy with postural
drainage and chest percussion
Inhaled bronchodilators
Surgical resection
Diagnostic and therapeutic bronchoscopy
Complications:
Cor pulmonale
Amyloidosis
Visceral abscesses at distant sites like the
brain
Diseases of the
Respiratory System
Lower Respiratory Tract
Infections
Community-Acquired
Pneumonia
Major health problem despite the

availability of potent antimicrobial
drugs.
Symptoms and Signs:
Fever and shaking chills

Purulent sputum production
Consolidation on physical examination
Adventitious breath sounds on auscultation
Community-Acquired
Pneumonia:
Pathophysiology
Community-Acquired
Pneumonia:
Pathophysiology
Community-Acquired
Pneumonia
Leukocytosis
Patchy infiltrates on chest radiographs
Atypical pneumonia clinico-radiographic
dissonance; often caused by Mycoplasma or
Chlamydia pneumoniae; less striking
symptoms and physical findings with nonpurulent sputum production and absence of
leukocytosis despite significant infiltrates on
chest radiography; OR severe symptoms in
the absence of significant radiographic
findings
Community-Acquired
Pneumonia
Community-Acquired
Pneumonia:
Community-Acquired
Pneumonia: Management
Guidelines for Management:
Criteria for hospitalization:
Age over 65 years old

Co-existing illness
Alteration in vital signs
Leukopenia or marked leukocytosis
Respiratory failure
Septic appearance
Absence of supportive care at home
Prevention:
Pneumococcal vaccine
Influenza vaccine
Community-Acquired
Most common pathogens:
Out-patient, without co-morbidity, < 60

years old
Mycoplasma pneumoniae
Respiratory viruses
Chlamydia pneumoniae
Legionella
Mycobacterium tuberculosis
Community-Acquired
Out-patient, with co-morbidity, age > 60

years old
Respiratory viruses
Moraxella catarrhalis
Hospitalized patients with CAP
Legionella
Chlamydia pneumoniae
Community-Acquired
Treatment:
Should be directed towards the elimination

of the suspected causative organism.
Respiratory support
Isolation from immunocompromised, or
potentially immunocompromised patients.
Hospital-Acquired
Pneumonia
Essentials of Diagnosis:
Occurs more than 48 hours after admission

to the hospital.
One or more clinical findings (fever, cough,
purulent sputum) in most patients.
Frequent in patients requiring intensive care
and mechanical ventilation.
Pulmonary infiltrates on chest x-ray.
Hospital-Acquired
Pneumonia
Pseudomonas aeruginosa
Enterobacter sp.
Klebsiella pneumoniae
Escherichia coli
Treatment:
Empiric therapy must be started as soon as

pneumonia is suspected.
Respiratory support
Pulmonary Tuberculosis
Infection beings when aerosolized

droplets containing viable organisms
are inhaled by a person susceptible to
the disease.
Symptoms and Signs:
Constitutional symptoms of fatigue, weight

loss, anorexia, low-grade fever, and night
sweats
Cough
Patients often appear chronically ill.
Post-tussive apical rales.
Pathogenesis:
After entry into the lungs in aerosolized

droplets, tubercle bacilli are ingested by
macrophages and transported to regional
lymph nodes, and from there, they
disseminate widely.
Lesions are contained by a delayed-type
hypersensitivity response (DTH; the tissuedamaging response), and the cell-mediated
macrophage-activating response.
The development of host immunity and DTH
is evidenced by acquisition of skin-test
reactivity to tuberculin purified protein
Pathogenesis (contd):
Granulomatous lesions form and organisms

survive within macrophages or necrotic
material but do not spread further.
Reactivation may occur at a later time. In
some cases, the immune response is
inadequate to contain the infection, and
symptomatic, progressive primary disease
develops.
Recovery of Mycobacterium tuberculosis

from cultures, or identification of organisms
by DNA probe
Acid-fast bacilli in the sputum
Serologic diagnosis by ELISA
Apical infiltrates on chest radiographs
Ghon and Ranke signs
Tuberculin skin test
Sputum examination for acid-fast bacilli

(AFB) or direct microscopy is the most
important diagnostic test to request for
a patient clinically suspected to have
PTB.
Sputum collection:
Best obtained on three consecutive

mornings.
Clean and thoroughly rinse the mouth with
water.
Breathe deeply 3 times.
Sputum collection (contd):
Best obtained on three consecutive

mornings.
Clean and thoroughly rinse the mouth with
water.
Breathe deeply 3 times.
After the third breath, cough hard and try to
bring up sputum from deep in the lungs.
Expectorate the sputum into a sterile
container with a well-fitted cap.
Collect at least 1 teaspoonful.
Examine the specimen to see that it is not
Sputum collection (contd):
Supervised nebulization with a warm,

sterile, hypertonic (3%) saline solution is
useful for obtaining specimens from
patients highly suspected of having PTB. It
should be attempted for all cooperative
patients who are smear-negative or unable
to expectorate sputum spontaneously.
Sputum TB culture and sensitivity tests:
Smear (-) patients with a strong clinical

possibility of PTB and suggestive chest xrays.
Smear (+) or (-) patients suspected of
multi-drug resistant PTB.
Smear (+) patients demonstrating the rise
fall phenomenon.
All cases of relapse.
All cases of re-treatment.
All cases of treatment failure.
PTB Classifications:
Class I: exposure, no symptoms, no

radiographic evidence
Class II: exposure, (+) symptoms, no
radiographic evidence
Class III: active PTB; exposure, (+)
symptoms, (+) radiographic evidence
Class IV: treated PTB
Class V: indeterminate
Pulmonary Tuberculosis:
Treatment
Newly diagnosed PTB:
At present, there is a lack of current

evidence or clear trends in favor of efficacy
and superiority of 4 drugs over 3.
The use of four drugs daily in the intensive
phase treatment adds an additional
assurance against treatment failure should
there be unexpected drug resistance and
assuming adherence to the treatment
regimen, also helps the loss of additional
drugs.
Treatment
Newly diagnosed PTB:
Intensive Phase: 2HRZE(S)/4HR(E)
First 2 months: Isoniazid, Rifampicin,

Pyrazinamide and Ethambutol + Streptomycin
(IM)
Next 4 months: Isoniazid and Rifampicin +
Ethambutol
Maintenance Phase: 3/6HR
Next 3 months: Isoniazid and Rifampicin

Check clinical profile. May discontinue after a
total of 9 months, or may continue as clinical
evidence dictates.
Treatment
Areas with high resistance rates:
National Capital Region, including Laguna

Cebu
Davao
Zamboanga
Cavite
Pampanga
Areas with low resistance rates:
Palawan
Mountain Province and Benguet
Treatment
Empiric therapy for MDR-TB suspect:
Use of at least some second-line drugs.

Prescribe drugs which the patient has not
previously taken.
The initial regimens should consist of at
least three drugs, preferably four or five, to
which the bacilli are likely to be fully
sensitive (injectable aminoglycoside and
pyrazinamide, even if previously used,
because resistance is usually unlikely).
Treatment
Hospitalization is not necessary in most

patients, but should be considered if the
patient is incapable of self-care.
Preventive therapy:
Should be given if the patient is under 35

years of age with a positive tuberculin test
(>10 mm) in the following conditions:
Foreign-born persons from countries with high

prevalence of TB.
Medically underserved, low-income groups
Residents of long-term care facilities
Treatment
Preventive therapy:
Isoniazid preventive therapy for 6 to 12

months.
Vaccine:
BCG should be given to tuberculin-negative

persons.
Children who are repeatedly exposed to
individuals with untreated or ineffectively treated
TB also benefit from BCG vaccination.
Diseases of the
Respiratory System
Bronchogenic Carcinoma
Suspected etiologies:
Cigarette smoking
Ionizing radiation
Asbestos
Heavy metals
Industrial agents
Lung scars
Air pollution
Genetic predisposition
Squamous cell carcinoma and

adenocarcinoma are the most common
types (30 to 35% of primary tumors
each).
Small cell carcinoma and large cell
carcinoma account for about 20 to 25%
and 15% of cases, respectively.
10 to 25% of patients are
asymptomatic, especially during the
early course of the disease.
Initial Symptoms:
Cough
Weight loss
Dyspnea
Chest pain
Hemoptysis
Change in the patterns of the symptoms
Physical findings vary and may be

totally absent:
Superior vena cava syndrome

Horners syndrome
Pancoasts syndrome
Recurrent laryngeal nerve palsy with
diaphragmatic hemiparesis
Paraneoplastic syndromes
PARANEOPLASTIC SYNDROMES IN LUNG CANCER
CLASSIFICATION
ENDOCRINE AND
METABOLIC
SYNDROME
COMMON HISTOLOGIC TYPE
Cushings syndrome
Small cell
SIADH
Small cell
Hypercalcemia
Squamous cell
Gynecomastia
Large cell
CONNECTIVE TISSUE
AND OSSEOUS
Clubbing and hypertrophic

pulmonary osteodystrophy
Squamous cell, large cell

and adenocarcinoma
NEUROMUSCULAR
Peripheral neuropathy
Small cell
Subacute cerebellar
degeneration
Myasthenia (Eaton-Lambert
syndrome)
Small cell
Dermatomyositis
All
Small cell
PARANEOPLASTIC SYNDROMES IN LUNG CANCER
CLASSIFICATION
CARDIOVASCULAR
HEMATOLOGIC
CUTANEOUS
SYNDROME
COMMON HISTOLOGIC TYPE
Thrombophlebitis
Adenocarcinoma
Nonbacterial verrucous
(marantic) endocarditis
Adenocarcinoma
Anemia
All
Disseminated intravascular
coagulation
All
Eosinophilia
All
Thrombocytosis
All
Acanthosis nigricans
All
Erythema gyratum repens
All
Cytologic examination of sputum permits

definitive diagnosis of lung cancer in 40 to
60% of cases.
CT scan and other imaging techniques.
Treatment:
Surgery
Chemotherapy
Radiotherapy
Combination therapy
Immunomodulation
Prognosis:
Over-all five-year survival rate is 10 to 15%.

Determinants of survival:
Stage of disease at time of presentation

Patients general health
Age
Histologic type of tumor
Tumor growth rate
Type of therapy
Diseases of the
Respiratory System
Ventilation and Perfusion
Disorders
Pulmonary
Thromboembolism
Pulmonary emboli arise from thrombi in

the venous circulation or right side of
the heart, from tumors that have
invaded the venous circulation, or from
other sources.
More than 90% originate as clots in the
deep veins of the lower extremities.
Pulmonary
Thromboembolism
Physiologic risk factors:
Venous stasis
Venous endothelial injury
Hypercoagulability
Oral contraceptives
Cancer
Protein C or S deficiency
Antithrombin III deficiency
Pulmonary
Thromboembolism
Clinical risk factors:
Prolonged bed rest or inactivity

Surgery
Childbirth
Advanced age
Stroke
Myocardial infarction
Congestive heart failure
Obesity
Fractures of the hip or femur
Pulmonary
Thromboembolism
Symptoms:
Pleuritic chest pain (74%)

Non-pleuritic chest pain (14%)
Dyspnea (84%)
Apprehension (59%)
Cough (53%)
Hemoptysis (30%)
Sweats (27%)
Syncope (13%)
Pulmonary
Thromboembolism
Signs:
Tachypnea (92%)
Crackles (58%)
Accentuated split second heart sound (53%)
Tachycardia (44%)
Fever > 37.8C (43%)
Phlebitis (32%)
Diaphoresis (36%)
Edema (24%)
Murmur (23%)
Cyanosis (19%)
Pulmonary
Thromboembolism
Results of routine laboratory tests are not

helpful in diagnosing pulmonary
thromboembolism.
Imaging and special examinations:
Chest radiography
Lung scanning
Venous thrombosis studies
Pulmonary angiography
Pulmonary
Thromboembolism
Prevention:
Critically important
Identification of those at risk
Prophylaxis
Treatment:
Anticoagulation
Thrombolytic therapy
Inferior vena cava filter
Pulmonary
Thromboembolism
Prognosis:
May cause sudden death.

Depends on the underlying disease and on
proper diagnosis and treatment.
Pulmonary hypertension may be a
complication.
Inhalation of Air Pollutants
Clinical Findings:
Exposure to low levels is inconsequential.

Exposure to high levels produces lower and
upper respiratory tract irritation.
Treatment:
Healthy individuals exposed to the usual

ambient levels of air pollution need not
observe special precautions.
Patients with COPD or severe asthma should
be advised to stay indoors and not engage
in strenuous activity in areas of high
Prognosis:
Depends on the severity and type of

exposure.
Also depends on the patients preexisting
pulmonary status.

MAJOR AIR POLLUTANTS, SOURCES AND ADVERSE EFFECTS
NOXIOUS AGENT
OXIDES OF
NITROGEN
HYDROCARBONS
OZONE
SOURCES
ADVERSE EFFECTS
Automobile exhaust;
gas stoves and
heaters; woodburning stoves;
kerosene
space
Automobile
exhaust,
heaters
cigarette smoke
Respiratory tract irritation,

bronchial hyperreactivity,
impaired lung defense,
bronchiolitis obliterans
Automobile exhaust,
high altitude aircraft
cabins
Cough, substernal
discomfort,
bronchoconstriction,
decreased exercise
performance, respiratory
tract irritation
Lung cancer

MAJOR AIR POLLUTANTS, SOURCES AND ADVERSE EFFECTS
NOXIOUS AGENT
SULFUR DIOXIDE
SOURCES
Power plants,
smelters, oil
refineries, kerosene
space heaters
ADVERSE EFFECTS
Exacerbation of asthma
and chronic obstructive
pulmonary disease,
respiratory tract irritation,
hospitalization may be
necessary, and death may
occur in severe exposure
Pulmonary Aspiration
Syndromes
Aspiration of inert materials:
Aspiration of toxic materials:
May cause asphyxia if amount aspirated is

massive.
Most patients suffer no serious sequelae.
Results in clinically evident pneumonia.
Treatment is supportive
Caf coronary
Acute obstruction of upper airways by food

that occurs in intoxicated individuals.
Heimlich maneuver may be life-saving.
Pulmonary Aspiration
Syndromes
Retention of an aspirated foreign body

Chronic aspiration of gastric contents
Mendelsons syndrome
Disorders of Ventilation
Obesity-hypoventilation syndrome
(Pickwickian syndrome)
Sleep-related breathing disorders
Obstructive sleep apnea
Hyperventilation syndrome
Acute Respiratory Failure
Clinical Findings:
Signs and symptoms of the underlying

disease
Hypoxemia and hypercapnia
Dyspnea is the chief symptom.
Cyanosis
Restlessness, confusion, anxiety, delirium
Tachypnea
Tachycardia, hypertension, cardiac
arrhythmias
Tremors
Acute Respiratory Failure:

Treatment
Non-ventilatory respiratory support

Ventilatory respiratory support
Tracheal intubation
Hypoxemia
Upper airway obstruction
Impaired airway protection
Poor handling of secretions
Facilitation of mechanical ventilation

Treatment
Ventilatory respiratory support
Mechanical ventilation
Apnea
Acute hypercapnia
Severe hypoxemia
Progressive patient fatigue

Treatment
General supportive care
Nutritional support
Maintenance of fluid and electrolyte balance
Psychological and emotional support
Skin care to avoid decubitus ulcers
Meticulous avoidance of nosocomial
infections
Prevention of stress ulcers
Pleural Effusion
Essentials of Diagnosis:
Asymptomatic in many cases; pleuritic

chest pain if pleuritis is present; dyspnea if
effusion is large.
Decreased tactile and vocal fremiti; dullness
to percussion; distant breath sounds;
egophony if effusion is large.
Radiographic evidence of pleural effusion.
Diagnostic findings on thoracentesis
Pleural Effusion
Classifications:
Exudative effusion (at least one of the

following features):
Pleural fluid protein to serum protein ratio > 0.5

Pleural fluid LDH to serum LDH ration > 0.6
Pleural fluid LDH greater than 2/3 of the upper
limit of the serum LDH.
Transudative effusion
Very low protein content

Often seen in non-inflammatory states
Pleural Effusion:
Approach to Management
PLEURAL EFFUSION
Perform diagnostic thoracentesis

Measure pleural fluid protein and LDH
Any of the following met?

PF/serum protein > 0.5
PF/serum LDH > 0.6
PF LDH > 2/3 upper normal serum limit
Yes
No
EXUDATE
TRANSUDATE
Further diagnostic procedures
Treat CHF, cirrhosis, nephrosis
Pleural Effusion:
EXUDATE
Further diagnostic procedures
Measure PF glucose, amylase

Obtain PF cytology
Obtain differential cell count
Culture, stain PF
Amylase elevated
Consider: esophageal rupture,
Pancreatic pleural effusion
Malignancy
Glucose < 60 mg/dL

Consider: Malignancy
Bacterial infections
Rheumatoid pleuritis
NO DIAGNOSIS
Pleural Effusion:
NO DIAGNOSIS
Negative
Needle biopsy of
pleura
Negative
Consider pulmonary embolus

(lung scan or pulmonary arteriogram)
Positive:
Treat for TB or CA
Negative
PPD
No: Consider
Thoracoscopy or
Open pleural biopsy
Positive:
Treat for PE
SYMPTOMS IMPROVING
Positive: Treat
for TB
Yes
Observe
Pleural Effusion
Treatment:
Treatment of the underlying condition

Removal if the effusion is large (therapeutic
thoracentesis or tube thoracostomy)
Pleurodesis
Pneumothorax
Types:
Spontaneous
Traumatic
Essentials of diagnosis:
Acute onset of ipsilateral chest pain and

dyspnea, often of several days duration.
Minimal physical findings in mild cases;
unilateral chest expansion, decreased
tactile and vocal fremiti, hyperresonance,
diminished breath sounds, mediastinal shift,
cyanosis in tension pneumothorax.
Presence of pleural air on chest x-ray.
Pneumothorax
Treatment:
Depends on the severity of the condition.

Supportive and oxygen supplementation if
needed.
Tube thoracostomy and pleurodesis.

Respiratory

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Respiratory

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Roses are red,

Violets are blue,

The Respiratory System

The Respiratory Process

Respiration is the process by which

The Respiratory Process

Ventilation is followed by the diffusion

The Respiratory Process

Circulation makes it possible for oxygen

The Respiratory Process

Cell metabolism and respiration are the

The Upper Respiratory

The bridge of the nose is bone, and

The Upper Respiratory

The nasal cavity is lined with

The Upper Respiratory

The superior part of the nasal cavity

The Upper Respiratory

The Upper Respiratory

The nasopharynx joins the nasal cavity

The Upper Respiratory

The Upper Respiratory

The larynx is a set of cartilages

The Upper Respiratory

The vocal cords are structures within

The Upper Respiratory

The vestibular folds are known as the

The Upper Respiratory

The trachea, also known as the wind

The Upper Respiratory

It is lined by pseudostratified ciliated

The Upper Respiratory

The Lower Respiratory

The primary bronchi extend from the

The Lower Respiratory

The airway passages of the lungs

The Lower Respiratory

The bronchioles branch to form the

The Lower Respiratory

Smooth muscle controls the diameter f

The Lower Respiratory

The Lower Respiratory

Ventilation is the movement of air into

Lungs tend to collapse because of the

Pulmonary Volumes and

There are four pulmonary volumes: tidal

Pulmonary Volumes and

The expiratory reserve volume is the

Pulmonary Volumes and

The pulmonary capacities refer to the

Pulmonary Volumes and

The inspiratory capacity is the amount

Pulmonary Volumes and

Major factors in determining the extent

During inspiration, the thoracic cage

Intrapleural space is the space between the

Surface tension of the fluid inside the alveoli

These factors pull the lungs away from the

Surface active agent

Essential Requirements for

Adequate atmospheric oxygen

Compliance is the expansibility or

The respiratory membranes are thin and

The rate of diffusion depends on the