PATHOPHYSIOLOGY II-NURS 340

Prepared by C. Bascombe-Mc Cave

Upper Respiratory Tract
 Respiratory Mucosa  Pharynx
 lined with ciliated mucus
 3 parts: Nasopharynx,
producing cells
Oropharynx, Laryngopharynx
 125cc/ day
 Tonsils(3 pairs)
 purifies air
 pharyngeal (adenoids)
 is contiguous with all
structures  palatine

 Nose
 paranasal sinuses
 frontal, maxillary,
sphenoid, ethmoid
 lighten skull
 sound resonant chambers
 Larynx
 conchae (3 pairs)
 warm & humidify air
 lacrimal ducts
 olfactory receptors
 lingual
 Eustachian (auditory) tubes
open into nasopharynx
 equalizes pressure between
middle ear & the outside
 composed of pieces of cartilage
Thyroid cartilage= Adam’s
apple
 epiglottis & glottis
 Lower Respiratory Tract
 Trachea
 composed of C- shaped cartilaginous rings
 called windpipe
 Bronchi, Bronchioles, Alveolar Duct,
Alveoli
 gas exchange occurs in alveoli
 occurs via Passive Diffusion
 Respiratory Membrane
 2 cell layers thick

 surfactant = reduces surface tension

to keep alveoli distended
 lining of alveolus (alveolar
epithelium)
 lining of capillary ( capillary
endothelium)
 Lungs & Pleura
 right lung = 3 lobes; left lung = 2 lobes
 lower part of lung resting on diaphragm = Base of lung
 upper part of lung under clavicle = Apex of lung
 pleura = serous membrane (i.e. secretes some fluid)
 parietal pleura lines thoracic cavity
 visceral pleura lines organs (viscera)

 Mechanics of Breathing
 air moves by differences in air pressure
 Inspiration
 active process; get contraction of diaphragm & external
intercostal muscles
 results in increase in size of chest cavity

 Expiration
 passive process with normal expiration

 active process with forced expiration; get contraction of

abdominal & internal intercostal muscles
 results in decrease in size of chest cavity which increases
pressure & forces air out
COMMON MANIFESTATIONS
 Dyspnea
 Cough- protective reflex that cleanses the airways
 Abnormal breathing patterns
 Hypoventilation/Hyperventilation
 Cough
 Cyanosis
 Pain
 Clubbing
 Abnormal sputum
Types of disorders
 Infectious diseases
 Upper Respiratory Tract Infections
 The common cold
 Rhinosinusitis
 Croup
 Epiglottitis
 Flu (Influenza)
 Lower Respiratory Tract Infections
 Bronchiolitis
 Pneumonia
 TB
 Fungal diseases
TYPES OF DISORDERS (Cont’d)
 Obstructive lung diseases
 Cystic fibrosis
 Cancer
 Bronchial Asthma
 Chronic Obstructive Pulmonary Disease (COPD)
 Bronchiectasis
 Restrictive lung diseases
 Chest wall abnormalities (deformities, kyphoscoliosis,
ankylosing spondylosis)
 Connective tissue abnormalities (interstitial lung disease)
 Respiratory muscle weakness (Guillian Barre, myasthenia
gravis)
TYPES OF DISORDERS (Cont’d)
 Interstitial lung diseases
_ Occupational lung disease ( Pneumoconioses)
_ Sarcoidosis
 Pulmonary Vascular disorders
 Pulmonary edema
 Pulmonary embolism
 Pulmonary Hypertension
 Acute Respiratory Distress Syndrome
TYPES OF DISORDERS (Cont’d)
 Expansion disorders/Disorders of Lung Inflation
 Atelectasis
 Pleural effusion
 Pneumothorax disorders of the pleura
 Pleural Pain
UPPER RESPIRATORY TRACT INFECTIONS
 The Common Cold
 a viral infection
 spread through respiratory droplets:
 is directly inhaled or spread by secretions on hands or
contaminated objects
 Is highly infectious because the virus is:
Shed in large numbers from the infected nasal
mucosa during the first days
They can survive several hours outside the body
UPPER RESPIRATORY TRACT INFECTIONS(cont’d)
 Influenza (Flu)
 Influenza is a viral infection that may affect both the
upper and lower respiratory tracts.
 There are three types of flu virus:
Type A (the most common)
Type B
Type C
 The viruses mutate constantly preventing effective
immune defense
Influenza
 Flu differs from the common cold in that it usually has
a sudden, acute onset with fever, fatigue and aching
pains in the body
 It may also cause a viral pneumonia
 A mild case of flu may be complicated by secondary
problems like bacterial pneumonia
 Prevention by vaccination recommended
RHINOSINUSITIS
 Inflammation of nasal mucosa and paranasal sinuses
 Most commonly caused by obstruction of sinus
openings(nasal swelling,polyps) and impaired
mucociliary function (URTI, allergic rhinitis)
 Infections with Haemophilus influenzae or
Streptococcus pneumoniae
 Could be acute or chronic
 Treated with antibiotics, oral decongestants,
antihistamines,corticosteroids, mucolytic agents and
surgery
LOWER RESPIRATORY TRACT INFECTIONS

 PNEUMONIA
- Inflammation of the lung parenchyma such as
bronchioles and alveoli
- Can be caused by infectious and non-infectious agents
- Infectious agents-bacteria, viruses, fungi, parasites,
protozoa
- Non-infectious agents- gastric secretions that aspirate
into the lungs, inhalation of irritating fumes
PNEUMONIA
RISK FACTORS
 Advanced age
 Immunocompromised
 Underlying lung disease
 Alcoholism
 Altered consciousness
 Smoking
 Endotracheal intubation
 Malnutrition
 Immobilization
PNEUMONIA
CLASSIFICATION
 Typical(bacterial) or atypical(viral/mycoplasma)
:
Several other methods available based on
 Causative agent:
-Virus
- Bacterium
-Fungus
 Anatomic location of the infection
- Bronchopneumonia- Diffuse and patchy throughout both
lungs
-Lobar Pneumonia(restricted to one lobe)
- Atypical Pneumonia-confined to alveolar septum and
interstitium of lungl
PNEUMONIA

Most recent classification

 Community Acquired Pneumonia
 Hospital Acquired/Nosocomial Pneumonia
 immunocompromised
PNEUMONIA CAUSES
COMMUNITY ACQUIRED
 Streptococcus pneumoniae/pneumococcus- most
common cause and has a high mortality rate in the
elderly
 Mycoplasma pneumoniae- most common in young
people living in group housing
 Hemophilus pneumoniae
 Influenza virus
 Legionella pneumophilia (Legionnaire’s Disease)
PNEUMONIA CAUSES(cont’d)
NOSOCOMIAL
 psuedomonas
 Staphylococcus
 Klebsiella
 Escherichia coli
PNEUMONIA CAUSES(cont’d)
IMMUNOCOMPROMISED INDIVIDUALS
 Pneumocystis carinii
 Mycobacterium tuberculosis
 Mycobacteria
 Fungi
 Respiratory viruses
 Protozoa
 Parasites
PATHOPHYSIOLOGY OF PNEUMONIA
N.B. Bacteria commonly enters the upper and lower
respiratory tract but do not normally cause pneumonia
in healthy individuals, because of extensive defense
mechanisms
Pneumonia occurs if the organism is extremely virulent
or present in large amounts or if the individual is
immunocompromised.
PATHOPHYSIOLOGY OF PNEUMONIA (CONT’D
ROUTES OF ENTRY
 Aspiration of oropharyngeal secretions which contain
colonized bacteria
 Inhalation from air that contains microorganisms which
were released when an infected person coughs, talks or
sneezes or from respiratory therapy equipment
 Directly from infected sites
 Bloodstream
PATHOPHYSIOLOGY OF PNEUMONIA (CONT’D
NORMAL DEFENSE MECHANISMS
 Nasopharyngeal defenses-sneeze(removes particles
inhaled from the air)
 Glottic and cough reflexes( prevent aspiration of
microorganisms into the tracheobronchial tree)
 Mucociliary blanket(removes microorganisms from
respiratory tract)
 Pulmonary macrophages (removes microorganisms from
the lungs)
PATHOPHYSIOLOGY OF PNEUMONIA (CONT’D
Large numbers of microorganisms entering the lower respiratory
tract will
 Overwhelm the alveolar macrophage
 Microorganisms will grow and multiply(become colonized) and
adhere to the walls of the respiratory tract
 Inflammatory response is activated
 Release of inflammatory mediators(phagocytes, macrophages,
immunoglobulins)
 Inflammatory mediators damage bronchial mucous membranes
 Acini and terminal bronchioles fill with infectious debris and
exudate
 Microorganisms also release toxins which cause further damage
to the lungs
 Accumulation of debris and exudate leads to dyspnea, V/Q
mismatch and hypoxia
MANIFESTATIONS
SIGNS OF VIRAL INFECTION
 Fever, chills, malaise, headache, productive cough,
muscle ache, pleural pain, dyspnea, hemoptysis
PHYSICAL EXAMINATION
 Dullness on percussion indicating pulmonary
consolidation
 Inspiratory crackles, increased tactile fremitus,
egophony,whisphered pectoriloquy
LABORATORY
 Elevated WBC
EVALUATION AND TREATMENT
 Chest X-Ray
 Sputum cultures
 Blood investigations

 Antibiotics for bacterial pneumonia

 Supportive care for viral pneumonia
 Adequate hydration
 Deep breathing and coughing exercises
 Chest physio
LOWER RESPIRATORY TRACT INFECTIONS (cont’d)
Bronchitis—inflammation of the bronchi
 Acute/Chronic
 Acute- follows a viral illness, presents with a non-
productive cough that occurs in paroxysms(sudden
and uncontrollable), agrravated by cold, dry or dusty
air, chest pain on coughing
 Treatment- rest, cough suppressant ,ASA, humidity
 Chronic- COPD
LOWER RESPIRATORY TRACT INFECTIONS (cont’d)
BRONCHIOLITIS- inflammation of the bronchioles
 Viral infection
 Most common in infants 3mths -2 yrs
 Inflammatory obstruction of bronchioles and necrosis of
cells lining the lower airways
 Air is trapped in the lungs
 Child presents with wheezing, increased respiratory rate
and effort, distressing cough, sternal recession, low grade
fever
 TREATMENT- supportive, humidified oxygenation and
adequate hydration, postural drainage, deep breathing
LOWER RESPIRATORY TRACT INFECTIONS (cont’d)
TUBERCULOSIS
 Infectious disease caused by mycobacterium
tuberculosis an acid fast bacillus that invades lungs
and other organs
 2 forms pose a threat to humans- M. tuberculosis
hominis and M. tuberculosis bovine
 Human TB is airborne while bovine TB is spread by
drinking milk from infected cows and initially affects
the GI tract
TUBERCULOSIS
CLASSIFICATION
 PRIMARY/SECONDARY
PRIMARY
Occurs in persons who never had previous contact
with the tubercle bacillus
SECONDARY
Represents either reinfection from inhaled droplet or
reactivation of previously healed primary lesion
TUBERCULOSIS
RISK FACTORS
 Immunocompromised eg.AIDS
 Living in crowded, poorly ventilated ,unsanitary settings
such as homeless shelters, prisons, slum areas
 Substance abuse eg. Alcoholics, IV drug abusers
 Elderly
 Emigration of infected individuals from high prevalence
areas also increases the risk of spread
TUBERCULOSIS (cont’d)
PATHOPHYSIOLOGY
 TB results from airborne infection, spread by minute
invisible particles (droplet nuclei) which are harbored in
respiratory secretions of persons with active TB
 Infected person coughs, sneezes, talks, releasing the
droplets into the atmosphere
 The droplets evaporate, leaving the organism suspended in
the air
 The droplets circulate via air currents and is inhaled by
other individuals
 The inhaled droplet nuclei pass down the bronchial tree
and lodges in the lower part of the upper lobe, upper
part of the lower lobe , bronchioles or alveoli
TUBERCULOSIS (cont’d)
 Once in the lungs , the bacillus is engulfed by
macrophages
 It grows slowly and multiplies for 2-12 weeks
causing the lungs to become inflammed
 Cell mediated immune response is activated
 Neutrophils, leucocytes and macrophages form a
granulomatous lesion(called a tubercle/Ghon’s
focus) around the bacilli to prevent spread
 Within 2-3 weeks, the infected cells within the
tubercle die, forming a cheeselike material called
caseation necrosis
TUBERCULOSIS (cont’d)
 Scar tissue grows around the tubercle, encapsulating
and isolating the bacilli
 During this time, some of the bacilli die, but some
escape and travel through the lymphatics to the
tracheobronchial lymph nodes of the affected lung
 There they encounter lymphocytes and immune
response is initiated resulting in the formation of
caseous granulomas (Ghon’s complex)
TUBERCULOSIS (cont’d)
 If the tubercles and inflammed nodes rupture, the
infection contaminates surrounding tissues and may
spread through the blood and lymphatic circulation to
distant sites (hematogenesis dissemination)
 In most persons , the M. tuberculosis is contained by
the cell mediated response by the host and the
infection remains latent/dormant for life.
 However latent TB can develop into active TB at any
time
 Can become active if the immune system is impaired
TUBERCULOSIS (cont’d)
CLINICAL MANIFESTATIONS
 Asymptomatic
 Fatigue
 Weight loss
 Lethargy
 Anorexia
 Low grade fever in the pm
 Productive cough
 Night sweats
 Dyspnea, chest pain and hemoptysis
DIAGNOSIS/TREATMENT
 Positive tuberculin skin test
 Serial sputum cultures
 Chest X ray

 TREATMENT
 Isolation during the active phase
 Antibiotics- rifampin, isoniazid,
pyrazinamide,ethambutol, streptomycin
 Must be taken for 6-9mths
 2-4 weeks the disease is no longer infectious and client
can resume normal activity
OBSTRUCTIVE AIRWAY DISEASES
BRONCHIAL ASTHMA
 is a chronic disease of the airways that involves
periodic episodes of severe but reversible bronchial
obstruction in persons with hypersensitive or
hyperresponsive airways
• Obstruction results from bronchospasms, increased
mucus secretions and mucosal edema
 Repeated attacks of acute asthma may lead to
irreversible damage to the lungs
 Acute attacks may be superimposed on a chronic
condition
ASTHMA
CAUSES
 EXTRINSIC FACTORS (atopic asthma)
Genetics-family history of allergies
Childhood/adolescent onset
Exposure to external airborne allergens- pollen,
animal dander, house dust, cockroach allergens
Persons with atopic asthma often have other allergic
disorders such as eczema, hay fever/ allergic rhinitis
ASTHMA (cont’d)
CAUSES (cont’d)
• INTRINSIC FACTORS (non-atopic asthma)
 Respiratory tract infections
 Exercise
 Inhaled irritants
 Emotional stress
 Fatigue
 Hormonal changes
 Temperature and humidity changes
 Gastroesophageal reflux
ASTHMA-PATHOPHYSIOLOGY
 Involves a genetic predisposition coupled with
environmental factors (viruses, allergens and
occupational exposure)
 In susceptible persons, an asthma attack can be
triggered by a variety of stimuli that do not necessarily
cause symptons
 These triggers can be bronchospastic/inflammatory
 Bronchoplastic triggers cause bronchspasms
 Inflammatory triggers produce inflammation
ASTHMA-PATHOPHYSIOLOGY (cont’d)
 Individual is exposed to the allergen (via inhalation)
 Early/acute phase response occurs (develops within 10-20
minutes)
 Antigen binds to sensitized mast cells on mucosal surface
of airways
 Mast cells in the lungs are stimulated to release chemical
inflammatory mediators---histamine, immunoglobulins,
prostaglandins ,leucotrienes, interleukins and nitrous
oxide
 These cause vasodilation and increased capillary
permeability and
 Bronchial infiltration with neutrophils, eosinophils and
lymphocytes
ASTHMA-PATHOPHYSIOLOGY (cont’d)
Histamine
 attaches to receptor sites in larger bronchi, causing swelling
of the smooth muscles
 Stimulates mucous membranes to secrete excessive
mucous
 Resulting in narrowed bronchial lumen

Leukotrienes
• Attach to receptor sites in smaller bronchi, causing swelling
of smooth muscle there
• Cause prostaglandins to travel through the bloodstream to
the lungs, enhancing the effect of histamine
ASTHMA-PATHOPHYSIOLOGY (cont’d)
 Parasympathetic receptors are also stimulated
resulting in
 Bronchoconstriction causing bronchospasms
 Increased vascular permeability which causes vascular
congestion and mucosal edema
 Increased bronchial hyperresponsiveness resulting in
 Increased mucous production by goblet cells
resulting in production of tenacious mucus which fill
the bases of the lungs .
 Impaired mucociliary function. This results in
airway edema and plugging, leading to
 Thickening and narrowing of bronchial lumen
ASTHMA-PATHOPHYSIOLOGY (cont’d)
 Airway becomes obstructed increasing resistance to airflow
 On inhalation, the narrowed bronchial lumen expands slightly
 Air is thus able to enter and reach the alveoli
 However, on exhalation, increased intrathoracic pressure forces
the bronchial lumen to close completely
 Air becomes trapped
 Expiration is difficult and breathing becomes laboured/work of
breathing increases
 ACUTE RESPONSE CAN BE INHIBITED OR REVERSED BY
BRONCHODILATORS BUT NOT BY THE
ANTIINFLAMMATORY ACTIONS OF CORTICOSTEROIDS
ASTHMA-PATHOPHYSIOLOGY (cont’d)
 Late phase response- develops 4-8 hours after exposure to
allergen/trigger
 Exacerbation of reaction
 Involves release of inflammatory mediators from mast
cells, macrophages, and epithelial cells, basophils,
eosinophils and neutrophils
 Results in epithelial injury and edema, decreased
mucociliary function, accumulation of mucus and
increased mucus responsiveness
 CHRONIC INFLAMMATION CAN LEAD TO AIRWAY
REMODELLING IN WHICH CASE AIRFLOW LIMITATIONS
MAY ONLY BE PARTIALLY REVERSIBLE
ASTHMA MANIFESTATIONS (cont’d)
 Hyperventilation (2o increased lung volume from air trapping and
obstruction)
 Intrapleural and alveolar gas pressures rise resulting in
 Decreased perfusion of alveoli
 Ventilation-perfusion mismatch
 Early- hypoxia, with decrease pCO2 and increased pH (respiratory
alkalosis)
 Late- CO2 retention and respiratory acidosis
 Respiratory failure
 NB. If bronchospasm is not reversed by normal
measures the individual is now considered to have
severe bronchospasm known as Status Asthmaticus
which is life threatening and may result in Respiratory
Failure
Asthma Attack
ASTHMA- MANIFESTATIONS
MILD ATTACK
 Chest tightness (bronchial constriction)
 Increased respiratory rate with prolonged expiration
(airway obstruction)
 Mild wheezing on expiration
 Non-productive cough
 Tachycardia
ASTHMA- MANIFESTATIONS
SEVERE ATTACK
 Use of accessory muscles
 Loud wheezing on inspiration
 Dyspnea
 Fatigue
 Moist skin
 Anxiety
 Apprehension
ASTHMA- CLASSIFICATION BASED ON SEVERITY
 See handout
 Mild intermittent
 Mild persistent
 Moderate persistent
 Severe persistent
ASTHMA TREATMENT
Best treatment is prevention by
 Identifying and avoiding precipitating factors
Other treatment includes
 Relaxation techniques
 Breathing exercises
 Oxygenation-low humidified
 Medication-bronchodilators, antiinflammatory agents namely
corticosteroids
 Quick relief meds-short acting B2-adrenergic agonists which
relax smooth muscles e.g albuterol/salbutamol/ventolin
 Anticholinergic drugs eg atrovent –block the vagal pathway that
cause broncho-constriction
 corticosteroids
ASTHMA TREATMENT (CONT’D)
Long term medications
 Taken on a daily basis
 Include
 anti-inflammatory agents eg sodium cromolyn, low
dose inhaled corticosteroid eg beclometasome/
becotide inhaler
 Long acting B2-agonists eg salmeterol
DIAGNOSTIC TESTING
 Pulmonary function tests-will reveal signs of
obstructive airway disease
 Serum immunoglobulins- increase from allergic
reactions
 CBC-reveals increased eosinophil count
 Chest X-ray-detect areas of hyperinflation or
atelectasis
 ABGs- detects hypoxemia
 Skin testing- identifies specific allergens
 Pulse oximetry-detects reduced O2 Saturation
CHRONIC OBSTRUCTIVE PULMONARY DISEASES
Chronic bronchitis
 Inflammation of major and small airways resulting in
airway obstruction caused by mucus.
 Changes are non reversible

Emphysema
 Characterized by loss of lung elasticity and an abnormal
permanent enlargement of the acinii (gas exchange airways)
resulting in destruction of alveolar walls and capillary beds
 Obstruction results from tissue changes rather than
mucus production
 Changes are non reversible
CHRONIC BRONCHITIS PATHOPHYSIOLOGY
 Irritants are inhaled over a prolonged period of time
 Airways become inflammed and neutrophils, macrophages
and lymphocytes infiltrate the bronchial wall
 Bronchial edema and hyperplasia of mucus glands and
goblet cells resulting in
 Excess mucus excretion into the bronchial tree
 Thick tenacious mucus is produced
 Ciliary function becomes impaired and is unable to clear
mucus resulting in
 Chronic productive cough of more than 3 months
duration for at least 2 consecutive years
CHRONIC BRONCHITIS PATHOPHYSIOLOIGY (Cont’d)
 Bronchial secretions and airway obstruction cause
mismatching of ventilation and perfusion which decreases
arterial oxygenation resulting in hypoxemia
 Respiratory drive is diminished
 Individuals are unable to compensate by increasing their
ventilation instead they hypoventilate
 Chronic hypoxia causes the kidneys to produce
erythropoietin to stimulate RBC production
 Excessive RBC result in polycythemia
 Hb levels are high, but amt of hemoglobin coming into
contact with O2 is low
 Client will therefore presents with cyanosis
 Clients are known as BLUE BLOATERS or NON
Fighters
DIAGNOSIS OF CHRONIC BRONCHITIS
 Physical examination
 Chest X-ray-hyperinflation
 Pulmonary function tests- indicate residual volume
and vital capacity, normal compliance
 Blood gas analysis
 Sputum culture
 ECG-reveal arrythmias, hypertrophy
 Pulse oximetry
TREATMENT OF CHRONIC BRONCHITIS
 Avoid air pollutants
 Quit smoking
 Bronchodilators- to relieve bronchospasms and facilitate mucus
clearance
 Expectorants
 Antibiotics
 Nebulizers
 Corticosteroids
 Chest physio
 Adequate hydration
 Diuretics
 Oxygen- 1-2L/min –to maintain arterial pO2 levels between 55 -
65 mmHg, and O2 saturation of @least 90%
 Education –nutrition, respiratory hygiene, pursed lip breathing
EMPHYSEMA- PATHOPHYSIOLOGY
 Inhaled irritant eg tobacco smoke or deficiency of alpha 1
antitrypsin (an antiprotease enzyme that protects the lung
from injury)
 Stimulation of movement of inflammatory cells into the
lungs resulting in
 Increased release of elastase and proteases (from
leucocytes, macrophages and other inflammatory cells)
 Antiprotease production and release may be inadequate to
excess protease production
 Alveolar destruction occurs and loss of normal elastic recoil
of the bronchi
 Bronchioles may collapse
EMPHYSEMA- PATHOPHYSIOLOGY (cont’d)
 Loss of elastic recoil and collapse of bronchioles leads to
difficulty getting air out i.e. expiration becomes difficult
 Volume of expired air is thus reduced leading to
 Hyperinflation of alveoli and air trapping which causes
 Destruction of alveolar membranes
 This destruction is progressive and leads to
 Enlargement of distal airspaces
 Hyperinflation of alveoli produces large air spaces called
bullae
 Hyperinflation of airspaces adjacent to the pleurae are
called blebs
EMPHYSEMA- PATHOPHYSIOLOGY (cont’d)
 Alveoli are unable to recoil after expanding on inhalation
causing the bronchioles to collapse on expiration ,
because pressure in surrounding lung tissues exceeds
airway pressure. This causes obstruction of the airways
and air becomes trapped in the lungs.
 This produces in an increase in the anteroposterior
dimensions of the chest resulting in –barrel chest

 Types of Emphysema
 Centriacinar emphysema-septal destruction in
respiratory bronchioles and alveolar ducts leading to
inflammation in bronchioles
 Panacinar Emphysema- involves the entire acinus
EMPHYSEMA- MANIFESTATIONS
 Dyspnea on exertion
 Prolonged expiratory wheeze
 Use of accessory muscles to exhale
 Barrel shaped chest
 See handout

 NB: Clients are referred to as pink puffers /fighters

because they are able to overventilate and
maintain relatively normal blood gas values until
late in the disease.
EMPHYSEMA- DIAGNOSTIC TESTS and
TREATMENT
 Pulmonary function tests
 Chest Xrays
 ABG analysis
 ECG
 CBC
 Pulse oximetry

 Treatment –as for bronchitis

 NB- Severe cases of Emphysema may be treated with
lung reduction surgery or lung transplant
PNUEMOTHORAX
 Accumulation of air or gas in the pleural cavity
resulting in
 Increased tension in the pleural cavity
 Leads to partial/complete lung collapse
 Is a life threatening condition since
 Air is trapped in the intrapleural space and venous
return may be impeded resulting in a TENSION
PNEUMOTHORAX
TYPES OF PNEUMOTHORAX
 Open/communicating
 Closed
 Tension

 Spontaneous
 Secondary/traumatic
CAUSES OF PNEUMOTHORAX
OPEN
 Penetrating chest injury
 Insertion of a central venous catheter
 Chest surgery
 Transbronchial biopsy
CAUSES OF PNEUMOTHORAX
CLOSED
 Blunt chest trauma
 Air leakage from ruptured blebs
 Interstitial lung disease
CAUSES OF PNEUMOTHORAX
TENSION
 Penetrating chest wound
 Fractured ribs
 Mechanical ventilation
PATHOPHYSIOLOGY
Spontaneous pneumothorax
 Rupture in visceral or parietal pleura
 Air accumulates and separates the visceral and parietal
pleurae
 Negative pressure is destroyed
 Lung recoils and collapses towards the hilus
PATHOPHYSIOLOGY
OPEN PNUEMOTHORAX
 Atmospheric air flows directly into pleural cavity
 Negative pressure is destroyed(air pressure in the
cavity becomes positive)
 Air pressure in the pleural space equals barometric
pressure
 Lung collapses on affected side towards the hilus
PATHOPHYSIOLOGY
CLOSED PNEUMOTHORAX
 Air enters the pleural space from within the lung
 Pleural pressure increases
 Lungs are unable to expand during inspiration
PATHOPHYSIOLOGY
TENSION PNEUMOTHORAX
 Air enters the pleural cavity on expiration but becomes
trapped as the rupture site acts as a one way valve
 Pressure in the pleural cavity exceeds barometric
pressure
 Air compresses and pushes against the already recoiled
lung
 Heart and great vessels are displaced
 Accumulating pressure causes lung to collapse
(compression atelectasis)
CLINICAL MANIFESTATIONS and
TREATMENT
 See handout