Respiratory system

and
Its diseases
Submitted By:
Constante, Quolette M.
BSN IV-B NCM 104
Submitted to:
Mr. Carlo Hidalgo
Primary Function
 The exchange of gases between the environmental
air and the blood.
– Ventilation
– Diffusion
– Perfusion
Nonrespiratory Functions of the Respiratory
System
 Water loss and heat elimination
 Warms and humidifies inspired air
 Enhances venous return
 Contributes to normal acid-base balance
 Enables speech, singing, etc.
 Defends against inhaled foreign matter.
 Removes, modifies, activates various materials passing through
the pulmonary circulation.
Inactivates prostaglandins
Activates angiotensin II
 Nose - organ of smell
Structure of the Respiratory System
 Respiratory airways
– Nasal passages
– Pharynx
– Trachea
– Bronchi
– Bronchioles
 Lungs - left lung - 2 lobes; right lung - 3 lobes
– Alveoli
• Type I alveolar cells
• Type II alveolar cells
• Alveolar macrophages
• Pores of Kohn
 Alveolar fluid lining
with pulmonary surfactant Alveolar
Type II alveolar cell macrophage

Type I alveolar cell

Interstitial fluid

Alveolus
Pulmonary
capillary

Erythrocyte
 Lungs, contd.
– Pulmonary capillaries
– Elastic connective tissue
– Pleural sac
 Thorax
Respiratory Mechanics
 Air moves from an area of high pressure to an
area of low pressure, following the pressure
gradient.
 Pressure considerations
– Atmospheric pressure
– Intra-alveolar pressure
– Intrapleural pressure
Major Inspiratory Muscles
 Quiet breathing
– Diaphragm
– External intercostal muscles
 Deeper inspirations
– Accessory inspiratory muscles
Expiration
Expiration is normally a passive process.
 Inspiratory muscles relax
 Chest wall and lungs recoil
 Intra-alveolar pressure increases
 Air leaves the lungs

For more complete and rapid emptying:

– Abdominal muscles
– Internal intercostal muscles
Airway Resistance
 Bronchoconstriction - parasympathetic
stimulation
 Bronchodilation - sympathetic stimulation
Lung Elasticity
Elastic recoil and compliance
– Connective tissue
– Alveolar surface tension
Pulmonary Surfactant
 Secreted by Type II alveolar cells
 Reduces alveolar surface tension
– Increased pulmonary compliance
– Reduces the lungs tendency to recoil
Energy Expenditure is Increased When:

 Pulmonary compliance is decreased

 Airway resistance is increased
 Elastic recoil is decreased
 There is need for increased ventilation
Lung Volumes
• Normal range:
– Male - 5.7 liters
– Female - 4.2 liters
• 500 ml of air are inspired and
expired
• At end of quiet expiration, the lungs
still contain 2,200 ml of air
 Gas exchange continues during expiration
– Maintains constant gas content
– Decreased energy utilization
 Tidal volume
 Residual volume
 Vital capacity
 Total lung capacity
 Forced expiratory volume in one second
Alveolar Ventilation
 Pulmonary ventilation
 Respiratory Rate
 Anatomical dead space
 Alveolar ventilation
 Alveolar dead space
Local Regulation
• Goal - Maximally match blood flow to airflow

¯ Airflow in comparison to blood flow   CO2

 relaxation of airway   airflow

 blood flow in comparison to air flow   O2

in alveolus and surrounding tissues 
vasoconstriction of pulmonary arteriole  
blood flow
Gas Exchange
Simple diffusion down partial pressure
gradients
 Partial Pressure
 The individual pressure exerted independently by a
particular gas within a mixture of gases.
 The air we breath exerts a total atmospheric pressure
of 760 mm Hg (at sea level) and is composed of:
– 79% Nitrogen - PN2 = 760 mm Hg x .79 - 600 mm
Hg
– 21% Oxygen - PO2 = 760 mm Hg x .21 = 160 mm Hg
– The partial pressure of CO2 is negligible at 0.03 mm
Hg
Amount of gas that dissolves in blood
depends on:
 Solubility of the gas in blood
 Partial pressure of the gas

The difference in partial pressure between

pulmonary blood and alveolar air is known as
a partial pressure gradient.
Alveolar Air
 Inspired air is humidified - water vapor
 Fresh inspired air mixes with the large volume
of old air and the dead space - at the end of
each inspiration, less than 15% of the air in
the alveoli is fresh air.

The average alveolar PO2 is 100 mm Hg.

O2 and CO2 Exchange
 Only small fluctuations occur in alveolar PO2
throughout both inspiration and expiration.
– Small proportion of total air exchanged
– Oxygen rapidly moves down its partial pressure
gradient
– Pulmonary blood PO2 equilibrates with
alveolar PO2
– PO2 of arterial blood is fairly constant
O2 and CO2 Exchange – Alveoli Level

 Alveolar PCO2 also remains fairly constant at 40

mm Hg.
 Partial pressures of gases favor the movement
of O2 from the alveoli into the blood and CO2
from the blood into the alveoli.
O2 and CO2 Exchange
 O2 uptake matches O2 use even when O2
consumption increases due to increased
metabolism.
Rate of Diffusion
 Surface area
 Thickness of the membrane
 Diffusion coefficient of the particular gas.

These factors are relatively constant under

resting conditions, therefore the partial
pressure is the primary factor that determines
rate of exchange.
O2 and CO2 Exchange – Tissue Level
Partial pressures of gases favor the
movement of O2 from the blood into the
adjacent cells and CO2 from the cells into
the capillary blood.
Gas Transport
 Oxygen
– Dissolved oxygen (1.5%)
– Chemically bound to hemoglobin (98.5%)

The PO2 of the blood is a measurement only

of the dissolved oxygen.
Hemoglobin
 Four polypeptide chains
 Four iron-containing heme groups that are
able to combine with an O2 molecule.

If Hb is carrying its maximum O2 load, it is

considered to be fully saturated.
Storage for oxygen
Maintains a low PO2
At the tissue level, as the PO2 falls the Hb
unloads some of its stored oxygen.
Oxyhemoglobin Dissociation Curve
Plateau portion
– Range that exists at the pulmonary
capillaries.

Note: Minimal reduction of oxygen

transported until the PO2 falls below 60
mm Hg.
Steep portion of the curve
– Range that exists at the systemic
capillaries

A small drop in systemic capillary PO2 can

result in the release of large amounts of
oxygen for the metabolically active cells.
Factors that Affect the Binding of
Hemoglobin and Oxygen
 Carbon dioxide
 Acidity
 Temperature

Bohr effect – Reduction in the affinity of

hemoglobin for oxygen in response to an
increase in blood carbon dioxide and a
decrease in pH.
Gas Transport
 Carbon Dioxide
– Dissolved CO2 (10%)
– Carbamino hemoglobin (30%)
– Bicarbonate (60%)
– Chloride shift

Haldane effect – the ability of hemoglobin to pick

up CO2 and CO2-generated H+.
Control of Respiration
 Neural control
 Chemical stimuli
Neural Control
 Respiratory control centers housed in the
brain stem
– Inspiratory and expiratory neurons in the
medullary respiratory center
• Dorsal respiratory group
• Ventral respiratory group
• Rostral ventromedial medulla
 Respiratory control centers housed in the
brain stem, contd.
– Apneustic
– Pneumotaxic center
 Stretch receptors in the lung (Hering Breuer
reflex)
– Prevents overinflation of the lung
 Ventilation is matched to the body’s needs for
oxygen uptake and carbon dioxide removal
– Medullary respiratory center receives input
– Appropriate signals sent to motor neurons
– Rate and depth of ventilation adjusted
Chemical Stimuli
 Arterial PO2
 Arterial PCO2
 Arterial H+
Arterial PO2
 Monitored by peripheral chemoreceptors
 PO2 must fall below 60 mm Hg to stimulate
increased respiration
 Peripheral chemoreceptors respond to the PO2
and not the total oxygen content.
 Major regulator of ventilation under resting
conditions.
 CO2 crosses the blood-brain barrier forming H+
Arterial H +

 Monitored by aortic and carotid body

peripheral chemoreceptors
 Plays a role in adjusting ventilation in response
to alterations in arterial H+ concentrations
unrelated to fluctuations in PCO2
Diagnosis of Pulmonary Function

Clinical Assessment
Symptoms of Pulmonary Disease
 Dyspnea
– Sensation of breathlessness that is excessive for any given
level of physical activity.
 Paroxysmal nocturnal dyspnea
– Inappropriate breathlessness at night.
 Orthopnea
– Dyspnea on recumbency.
 Platypnea
– Dyspnea on the upright position relieved by recumbency.
 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.
 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.
 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
– Rapid, shallow breathing.
– Arbitrarily defined as a respiratory rate in excess of
18/min.
 Bradypnea
– Slow breathing.
 Hyperpnea
– Rapid, deep breathing.
 Hyperventilation
– Increase in the amount of air entering the alveoli.
 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.
 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.
 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
 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
 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
 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
 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
 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
 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
 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)
 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.
 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.
 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 compression.
 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.
 TYPICAL CHEST EXAMINATION FINDINGS IN SELECTED CLINICAL CONDITIONS
CONDITION PERCUSSION FREMITUS BREATH VOICE ADVENTITIOUS
SOUNDS TRANSMISSION SOUNDS
Normal Resonant Normal Vesicular Normal Absent
Consolidation Dull Increased Bronchial Bronchophony, Crackles
or Atelectasis whispered
(with patent pectoriloquy,
airway) egophony
Consolidation Dull Decreased Decreased Decreased Absent
or Atelectasis
(with blocked
airway)
Bronchial Resonant Normal Vesicular Normal Wheezing
Asthma
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 fluid.
 Apicolordotic views visualize disease at the lung apices
better than the standard posteroanterior view.
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.
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.
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.
 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
 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
 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)
 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 young children and
decrease with age.
 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.
 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
 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.
 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.
 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.
 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
 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.
 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.
 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
 Signs and Symptoms:
 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
 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.
 Hospitalization for intravenous antibiotics.
 Complications:
– Lower respiratory tract infections
– Osteomyelitis and mucocoele
– Intracranial complications
– Malignancy (?)
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
 Occasional polyposis
 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
 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
Diseases of the Respiratory System

Diseases of the Airways

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.
 Pathogenesis:
Common denominator is nonspecific
hyperirritability of the tracheobronchial tree.
Airway reactivity increased by:
• Allergenic
• Pharmacologic
• Environmental, occupational
• Infectious
• Emotional
• Activity-related
 Signs and Symptoms:
– 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
 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 ABGs.
 Complications:
Exhaustion
Dehydration
Airway infection
Cor pulmonale
Tussive syncope
Pneumothorax (rare)
 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
 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 20-30% 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)
 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
 Oral steroids
 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
 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.
 EMPHYSEMA VS CHRONIC BRONCHITIS

EMPHYSEMA CHRONIC BRONCHITIS

HISTORY Onset of symptoms After age 50 After age 35

Dyspnea Progressive, constant, Intermittent, mild to

severe moderate

Cough Absent or mild Persistent, severe

Sputum production Absent or mild Copious

Sputum appearance Clear, mucoid Mucopurulent or purulent

Other features Weight loss Airway infections, right

“pink puffer” heart failure, obesity
“blue bloater”
 EMPHYSEMA VS CHRONIC BRONCHITIS

EMPHYSEMA CHRONIC BRONCHITIS

CHEST X-RAY Bullae, blebs Present Absent

Overall appearance Decreased markings in “Dirty lungs”

the periphery

Hyperinflation Present Absent

Heart size Normal or small, vertical Large, horizontal

Hemidiaphragms Low, flat Normal, rounded

 Causes:
 Cigarette smoking
 Air pollution
 Airway infection
 Familial factors
 Allergies
 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
 Complications:
Pneumonia and acute bronchitis
Pulmonary embolization
Left ventricular heart failure
Pulmonary hypertension
Chronic respiratory failure
Spontaneous pneumothorax
 Prevention:
Smoking cessation
Early treatment of airway infections
Vaccination against pneumococcal pneumonia
and influenza.
 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
 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.
 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
Pathophysiology
 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 non-
purulent sputum production and absence of leukocytosis
despite significant infiltrates on chest radiography; OR
severe symptoms in the absence of significant radiographic
findings
 Management
 Guidelines for Management:
Criteria for hospitalization: Prevention:
• Age over 65 years old Pneumococ
• Co-existing illness cal vaccine
• Alteration in vital signs Influenza
vaccine
• Leukopenia or marked
leukocytosis
• Respiratory failure
• Septic appearance
• Absence of supportive care at
home
 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
 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
 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.
 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.
 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 tissue-
damaging 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 derivative (PPD).
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.
 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
 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.
After the third breath, cough hard and try to bring
up sputum from deep in the lungs.
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 just
saliva. Repeat the process if necessary.
 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 x-rays.
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
 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.
 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.
 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
 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).
 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
 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
 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
Horner’s syndrome
Pancoast’s syndrome
Recurrent laryngeal nerve palsy with
diaphragmatic hemiparesis
Paraneoplastic syndromes
 PARANEOPLASTIC SYNDROMES IN LUNG CANCER

CLASSIFICATION SYNDROME COMMON HISTOLOGIC TYPE

ENDOCRINE AND Cushing’s syndrome Small cell

METABOLIC
SIADH Small cell

Hypercalcemia Squamous cell

Gynecomastia Large cell

CONNECTIVE TISSUE AND Clubbing and hypertrophic Squamous cell, large cell and
OSSEOUS pulmonary osteodystrophy adenocarcinoma

NEUROMUSCULAR Peripheral neuropathy Small cell

Subacute cerebellar degeneration Small cell

Myasthenia (Eaton-Lambert Small cell

syndrome)

Dermatomyositis All
 PARANEOPLASTIC SYNDROMES IN LUNG CANCER

CLASSIFICATION SYNDROME COMMON HISTOLOGIC TYPE

CARDIOVASCULAR Thrombophlebitis Adenocarcinoma

Nonbacterial verrucous (marantic) Adenocarcinoma

endocarditis

HEMATOLOGIC Anemia All

Disseminated intravascular All

coagulation

Eosinophilia All

Thrombocytosis All

CUTANEOUS Acanthosis nigricans All

Erythema gyratum repens All

 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
 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.
 Physiologic risk factors:
Venous stasis
Venous endothelial injury
Hypercoagulability
• Oral contraceptives
• Cancer
• Protein C or S deficiency
• Antithrombin III deficiency
 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
 Symptoms:
Pleuritic chest pain (74%)
Non-pleuritic chest pain (14%)
Dyspnea (84%)
Apprehension (59%)
Cough (53%)
Hemoptysis (30%)
Sweats (27%)
Syncope (13%)
 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%)
 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
 Prevention:
Critically important
Identification of those at risk
Prophylaxis
 Treatment:
Anticoagulation
Thrombolytic therapy
Inferior vena cava filter
 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 pollution level.
 Prognosis:
Depends on the severity and type of
exposure.
Also depends on the patient’s preexisting
pulmonary status.
 MAJOR AIR POLLUTANTS, SOURCES AND ADVERSE EFFECTS

NOXIOUS AGENT SOURCES ADVERSE EFFECTS

OXIDES OF NITROGEN Automobile exhaust; gas Respiratory tract irritation,

stoves and heaters; wood- bronchial hyperreactivity,
burning stoves; kerosene impaired lung defense,
space heaters bronchiolitis obliterans

HYDROCARBONS Automobile exhaust, Lung cancer

cigarette smoke

OZONE Automobile exhaust, high Cough, substernal discomfort,

altitude aircraft cabins bronchoconstriction, decreased
exercise performance, respiratory
tract irritation
 MAJOR AIR POLLUTANTS, SOURCES AND ADVERSE EFFECTS

NOXIOUS AGENT SOURCES ADVERSE EFFECTS

SULFUR DIOXIDE Power plants, smelters, oil Exacerbation of asthma and

refineries, kerosene space chronic obstructive pulmonary
heaters disease, respiratory tract
irritation, hospitalization may be
necessary, and death may occur
in severe exposure
Pulmonary Aspiration Syndromes
 Aspiration of inert materials:
 May cause asphyxia if amount aspirated is massive.
 Most patients suffer no serious sequelae.
 Aspiration of toxic materials:
 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.
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
 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
 Ventilatory respiratory support
Mechanical ventilation
• Apnea
• Acute hypercapnia
• Severe hypoxemia
• Progressive patient fatigue
 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
 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
 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
 EXUDATE
Further diagnostic procedures

Measure PF glucose, amylase

Obtain PF cytology
Obtain differential cell count
Culture, stain PF

Amylase elevated Glucose < 60 mg/dL

Consider: esophageal rupture, Consider: Malignancy
Pancreatic pleural effusion Bacterial infections
Malignancy Rheumatoid pleuritis

NO DIAGNOSIS
 NO DIAGNOSIS
Negative

Needle biopsy of Consider pulmonary embolus Positive:

pleura (lung scan or pulmonary arteriogram) Treat for PE

Negative Positive:
Treat for TB or CA

Negative
Positive: Treat
PPD for TB

No: Consider SYMPTOMS IMPROVING

Yes
Thoracoscopy or
Observe
Open pleural biopsy
 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.
 Treatment:
Depends on the severity of the condition.
Supportive and oxygen supplementation if
needed.
Tube thoracostomy and pleurodesis.
Thank you…