Respiratory

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“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.

The Respiratory Process


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.

The Respiratory Process




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.

The Respiratory Process


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

The Upper Respiratory
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.

The Upper Respiratory
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
Kiesselbach’s plexus, line the mucosa of
the nasal cavity.

The Upper Respiratory
Tract:
The Nose

The Upper Respiratory
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.

The Upper Respiratory
Tract:
The Pharynx

The Upper Respiratory
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.

The Upper Respiratory
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.

The Upper Respiratory
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.

The Upper Respiratory
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.

The Upper Respiratory
Tract:
The Trachea


It is lined by pseudostratified ciliated
columnar epithelium which aids in the
filtering of inhaled air.

The Upper Respiratory
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.

The Lower Respiratory
Tract:
The Respiratory Tree








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.

The Lower Respiratory
Tract:
The Respiratory Tree






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).

The Lower Respiratory
Tract:
The Respiratory Tree




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.

The Lower Respiratory
Tract:
The Lungs

The Lower Respiratory
Tract:
The Alveoli

Mechanics of Breathing

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

Mechanics of Breathing

Mechanics of Breathing




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).

Pulmonary Volumes and
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).

Pulmonary Volumes and
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

Pulmonary Volumes and
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

Pulmonary Volumes and
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


Boyle’s 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


Boyle’s 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%).

Transport of Oxygen and
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.

Transport of Oxygen and
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.

Control of Respiration


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.

Control of Respiration






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.

Symptoms of Pulmonary
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.

Symptoms of Pulmonary
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.

Symptoms of Pulmonary
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


Physical chest deformities


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


Physical chest deformities


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.

Pulmonary Function Tests


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

Pulmonary Function Tests


Relative contraindications:






Severe acute asthma or respiratory distress
Chest pain aggravated by testing
Pneumothorax
Brisk hemoptysis
Active tuberculosis

Pulmonary Function Tests


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.

Pulmonary Volumes and
Capacities
MAXIMUM
INSPIRATION

IRV
IC
TOTAL
LUNG
CAPACITY

VC
TV
ERV
MAXIMUM
EXPIRATION

FRC
RV

RV

Pulmonary Function Tests


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.

The Lower Respiratory
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 patient’s
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:
Clinical Manifestations


The major problem posed consists of its
complications:





Primary influenza viral pneumonia
Secondary bacterial pneumonia
Mixed viral and bacterial pneumonia
Extrapulmonary complications:





Reye’s syndrome
Myositis, rhabdomyolysis and myoglobinuria
Encephalitis, transverse myelitis
Guillain-Barré syndrome

Influenza: Treatment


Treatment for uncomplicated influenza
is symptomatic







Salicylates should be avoided in children
because of its association with Reye’s
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:
Clinical Manifestations





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:
Clinical Manifestations


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:
Clinical Manifestations


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.
Clinical Manifestations:




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


Clinical Manifestations:





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.

Acute Bacterial Sinusitis


Typical Pathogens:






Streptococcus pneumoniae
Other streptococci
Haemophilus influenzae
Staphylococcus aureus
Moraxella catarrhalis

Acute Bacterial Sinusitis


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.

Acute Bacterial Sinusitis


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.

Acute Bacterial Sinusitis


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 Kiesselbach’s 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 patient’s 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
Curschmann’s 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.

Asthma: Classifications


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.

Asthma: Classifications


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 β2-agonist drug

Moderate ambulatory asthma:







Daily maintenance therapy with inhaled
corticosteroids
Cromolyn or nedocromil
Short-acting inhaled β2-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 β2-agonist drugs
Long-acting inhaled β2-agonist drug
(salmeterol)
Inhaled anti-cholinergic drug (ipratropium
bromide)
Short-acting inhaled β2-agonist drug for
breakthrough wheezing

Asthma: Treatment


Status asthmaticus:










Supplemental oxygen, 1-3 L/min
Monitoring with oximetry
Inhaled β2-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
Pulmonary Disease (COPD)
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
Pulmonary Disease (COPD)
EMPHYSEMA VS CHRONIC BRONCHITIS
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
Pulmonary Disease (COPD)
EMPHYSEMA VS CHRONIC BRONCHITIS
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
Pulmonary Disease (COPD)
EMPHYSEMA VS CHRONIC BRONCHITIS
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
Pulmonary Disease (COPD)


Causes:






Cigarette smoking
Air pollution
Airway infection
Familial factors
Allergies

Chronic Obstructive
Pulmonary Disease (COPD)


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
Pulmonary Disease (COPD)


Complications:







Pneumonia and acute bronchitis
Pulmonary embolization
Left ventricular heart failure
Pulmonary hypertension
Chronic respiratory failure
Spontaneous pneumothorax

Chronic Obstructive
Pulmonary Disease (COPD)


Prevention:




Smoking cessation
Early treatment of airway infections
Vaccination against pneumococcal
pneumonia and influenza.

Chronic Obstructive
Pulmonary Disease (COPD)


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.

Laboratory findings:



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


Laboratory findings:




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
Pneumonia: Management


Most common pathogens:


Out-patient, without co-morbidity, < 60
years old









Streptococcus pneumoniae
Mycoplasma pneumoniae
Respiratory viruses
Chlamydia pneumoniae
Haemophilus influenzae
Legionella
Staphylococcus aureus
Mycobacterium tuberculosis

Community-Acquired
Pneumonia: Management


Most common pathogens:


Out-patient, with co-morbidity, age > 60
years old







Streptococcus pneumoniae
Respiratory viruses
Haemophilus influenzae
Moraxella catarrhalis

Hospitalized patients with CAP






Streptococcus pneumoniae
Haemophilus influenzae
Legionella
Staphylococcus aureus
Chlamydia pneumoniae

Community-Acquired
Pneumonia: Management


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


Most common pathogens:








Pseudomonas aeruginosa
Staphylococcus aureus
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.

Pulmonary Tuberculosis


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

Pulmonary Tuberculosis


Pathogenesis (cont’d):




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.

Pulmonary Tuberculosis


Laboratory findings:








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

Pulmonary Tuberculosis

Pulmonary Tuberculosis

Pulmonary Tuberculosis

Pulmonary Tuberculosis

Pulmonary Tuberculosis

Pulmonary Tuberculosis

Pulmonary Tuberculosis

Pulmonary Tuberculosis

Pulmonary Tuberculosis




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.

Pulmonary Tuberculosis


Sputum collection (cont’d):












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

Pulmonary Tuberculosis


Sputum collection (cont’d):


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.

Pulmonary Tuberculosis


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.

Pulmonary Tuberculosis


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.

Pulmonary Tuberculosis:
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.

Pulmonary Tuberculosis:
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

Pulmonary Tuberculosis:
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).

Pulmonary Tuberculosis:
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

Pulmonary Tuberculosis:
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

Bronchogenic Carcinoma


Suspected etiologies:









Cigarette smoking
Ionizing radiation
Asbestos
Heavy metals
Industrial agents
Lung scars
Air pollution
Genetic predisposition

Bronchogenic Carcinoma






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.

Bronchogenic Carcinoma


Initial Symptoms:







Cough
Weight loss
Dyspnea
Chest pain
Hemoptysis
Change in the patterns of the symptoms

Bronchogenic Carcinoma


Physical findings vary and may be
totally absent:







Superior vena cava syndrome
Horner’s syndrome
Pancoast’s syndrome
Recurrent laryngeal nerve palsy with
diaphragmatic hemiparesis
Paraneoplastic syndromes

Bronchogenic Carcinoma
PARANEOPLASTIC SYNDROMES IN LUNG CANCER
CLASSIFICATION
ENDOCRINE AND
METABOLIC

SYNDROME

COMMON HISTOLOGIC TYPE

Cushing’s 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

Bronchogenic Carcinoma
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

Bronchogenic Carcinoma


Laboratory findings:






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

Bronchogenic Carcinoma


Prognosis:



Over-all five-year survival rate is 10 to 15%.
Determinants of survival:







Stage of disease at time of presentation
Patient’s 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 > 37.8°C (43%)
Phlebitis (32%)
Diaphoresis (36%)
Edema (24%)
Murmur (23%)
Cyanosis (19%)

Pulmonary
Thromboembolism


Laboratory findings:




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

Inhalation of Air Pollutants


Prognosis:




Depends on the severity and type of
exposure.
Also depends on the patient’s preexisting
pulmonary status.

Inhalation of Air Pollutants
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

Inhalation of Air Pollutants
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

“Café 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
Mendelson’s 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

Acute Respiratory Failure:
Treatment


Ventilatory respiratory support


Mechanical ventilation





Apnea
Acute hypercapnia
Severe hypoxemia
Progressive patient fatigue

Acute Respiratory Failure:
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:
Approach to Management
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:
Approach to Management
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.

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