• Pulmonary Pathophysiology

• Lung function tests

• Tidal volume (TV): it is the amount of gas inhaled

or exhaled with each resting breath.

• Residual volume (RV): it is the amount of gas

remaining in the lungs at the end of maximum

I
exhalation. dredies
• Vital capacity (VC): it is the total amount of gas
that can exhaled following maximum inhalation.

• Total lung capacity (TLC): it is the amount of gas

in the lung at the end of maximum inhalation.

TLC = RV+ VC
 Signs and Symptoms of Pulmonary
Disease
• Dyspnea: subjective sensation of uncomfortable

breathing, feeling “short of breath”

Causes of Dyspnea :

– Airway obstruction

–Greater force needed to provide adequate

ventilation
• Signs of dyspnea:

• Flaring nostrils

• Use of accessory muscles in breathing

• Retraction (pulling back) of intercostal spaces

• Cough:

• Attempt to clear the lower respiratory passages by

abrupt and forceful expulsion of air

• Cough may result from
• Inflammation of lung tissue
• Increased secretion in response to mucosal irritation
– Inhalation of irritants
– Intrinsic source of mucosal disruption – such as tumor
invasion of bronchial wall
• Excessive blood hydrostatic pressure in pulmonary
capillaries
– Pulmonary edema – excess fluid passes into airways
– Production of bloody sputum is called hemoptysis
–Tuberculosis, lung abscess, cancer, pulmonary
infarction.
most common TO
• Cyanosis
• When blood contains a large amount of
unoxygenated hemoglobin, it has a dark red-blue
color which gives skin a characteristic bluish
appearance.
• Pain
• Originates in pleurae, airways or chest wall
• Inflammation of the parietal pleura causes sharp or
stabbing pain when pleura stretches during
inspiration
• Clubbing
• The selective bulbous enlargement of the end of a
digit (finger or toe).
• Usually painless
• Commonly associated with diseases that cause
decreased oxygenation Croni hypoxia
– Lung cancer
– Cystic fibrosis
– Lung abscess
– Congenital heart disease
 Respiratory Failure

• The inability of the lungs to adequately

oxygenate the blood and to clear it of carbon
dioxide.
• Can be acute:
– ARDS or pulmonary embolism
– Direct injury to the lungs, airways or chest wall
– Indirect due to injury of another body system, such
as the brain or spinal cord.
• Chronic respiratory failure
– Due to progressive hypoventilation from airway
obstruction or restrictive disease
• Two principal patterns
100 105
1. Hypoxic Respiratory Failure: pressure
Lunt
Seen when pO2 falls to or below 60 mm Hg
Typically seen in chronic bronchititis and
emphysema, in lung consolidation due to
bacterial infection, or in lung collapse,
pulmonary hypertension, pulmonary embolism
and ARDS.
• 2. Hypoxic-Hypercapnic Respiratory Failure
• When arterial pCO2 (normally 40 mm Hg) exceeds
45 mm HG, condition is called hypercapnia
• Most often, obstructive conditions produce this form
of respiratory failure, as can hypoventilation from
CNS problem, thoracic cage or neuromuscular
abnormalities
CNS
• Attempts to compensate include increased heart rate
and vasodilation, which produces warm, moist skin.
Is
• CNS effects produce muscular tremors, drowsiness
and coma.
•aHypercapnia also produces acidosis
• COPD: Definition
• Chronic airflow obstruction due to chronic
• bronchitis and/or pulmonary emphysema
• Chronic Bronchitis
• Definition
• – persistent cough and sputum production for at
least three months in at least two consecutive years.
• Submucosal gland hyperplasia
• Airway edema
• Mucus plugging and airways fibrosis
• Pathophysiology
• Chronic inflammation
• Hypertrophy & hyperplasia of bronchial glands that
secrete mucus
0 5
but
• Increase number of goblet cells
• Cilia are destroyed
• Bronchospasm often occurs
• End result
– Hypoxemia
– Hypercapnea
– Polycythemia (increase RBCs)
– Cyanosis
– Cor pulmonale (enlargement of right side of heart)
• PFTs Pulmonary function tests
– FVC:  Forced vital capacity
– FEV1:  Forcible exhale in 1 second
– FEV1/FVC = <70%
• ABGs ArteriolebloodGas CBC cerculationblood clot
–  PaCO2 Increased Hct
–  PaO2
 Abnormal permanent
enlargement of the airspace
distal to the terminal
bronchioles, accompanied
by destruction of their
walls and without obvious
fibrosis.
alvioles II do I
• Major cause is cigarette smoking lifestyle
• Other causes are air pollution and childhood
respiratory infections
• Primary emphysema linked to an inherited
deficiency of the enzyme alpha 1- antitrypsin which
1
S

inhibits action of many proteolytic enzymes which

can affect lung tissue. scar tissue I
• With this deficiency, smokers are even more
susceptible.
 Pathophysiology of Emphysema
• Begins with the destruction of the alveolar
septa, which eliminates portions of the
capillary bed, and increases the volume of air
in the alveolus.
• Inhaled oxidants inhibit the activity of
endogenous antiproteases, and stimulate
inflammation with increased activity of
proteases.
 N
E
alveoli

I 6H
 Bronchi I

k.sn Ebt
feet
• Bronchial Asthma
• Is a chronic inflammatory disease of the airways
that causes an episodic "attacks" of coughing,
wheezing and shortness of breath.
• Etiopathogenesis:
lid bid
• It occurs at all ages but nearly 50% of cases develop
it before the age of 10 years (in children the ratio is
2 male: 1 female, in adult the same ratio 1:1)
• Classification:
• Two broad etiologic types
• 1. Extrinsic (Allergic) Type I hypersensitivity
• 2. Intrinsic (None allergic)
15 W N b
Pathogenesis of Type I hypersensitivity immune system
(Extrinsic asthma)
• The classic asthmatic attack lasts up to several
hours and is followed by prolonged coughing
• In its most severe form, status asthmaticus, the
severe acute paroxysm persists for days and even
weeks, and under these circumstances, ventilatory
function might be so impaired as to cause severe
cyanosis and even death.
• The clinical diagnosis is aided by the demonstration
of an elevated eosinophil count in the peripheral
blood and the finding of eosinophils, Curschmann
spirals, and Charcot-Leyden crystals in the sputum
• ACUTE RESPIRATORY DISTRESS SYNDROME (DIFFUSE
ALVEOLAR DAMAGE)
• is a clinical syndrome caused by diffuse alveolar
capillary damage. It is characterized clinically by the
rapid onset of severe life-threatening respiratory
insufficiency, cyanosis, and severe arterial
hypoxemia that is refractory to oxygen therapy and
that may progress to extra-pulmonary multisystem
organ failure.
• Conditions Associated with Development of Acute
Respiratory Distress Syndrome
• Infection--- Diffuse pulmonary infections ,Viral,
Mycoplasma, and miliary tuberculosis.
• Physical/Injury--- Fractures with fat embolism Burns
• Chemical injury --- Oxygen toxicity Smoke Irritant
gases and chemicals
• Multiple transfusions
• Pancreatitis
• Uremia
• Drugs
• In the acute stage (first), the lungs are heavy, firm,
red, and boggy. They exhibit congestion, interstitial
and intra-alveolar edema, inflammation, and fibrin

fists
deposition. The alveolar walls become lined with
waxy hyaline membranes
• In the organizing stage (second), type Il epithelial
cells undergo proliferation in an attempt to
regenerate the alveolar lining. Resolution is
unusual; more commonly, there is organization of
the fibrin exudates, with resultant intra-alveolar
fibrosis.
• Marked thickening of the alveolar septa caused by
proliferation of interstitial cells and deposition of
collagen.
NO
• PULMONARY EMBOLISM and INFARCTION
• A pulmonary embolism occurs when a blood clot
(thrombus), becomes dislodged from elsewhere in
the body and moves (embolizes) into the pulmonary
arterial circulation. ded vein thrombus
• If the embolism significantly disrupts pulmonary
blood flow pulmonary infarction develops and
causes alveolar atelectasis, consolidation and tissue
necrosis. I Mists but
i
it
• A pulmonary embolism is the most common cause
of maternal death after a live birth
• The diagnosis of pulmonary embolism is missed in
about 70% of cases overall.
30 35
• The classic tried of symptoms
SY.be and pleuritic chest pain.
• dyspnea, hemoptysis
Occurs in fewer than 20% of cases.
• Although there are many possible sources of
pulmonary emboli (e.g., fat, air, amniotic fluid),
blood clots from venous thrombosis are by far the
most common.
• Most pulmonary emboli caused by blood clots originate
from deep veins in the lower part of the body (i.e., the leg
and pelvic veins).
• A deep vein blood clot is commonly called a deep vein
thrombus (DVT). When a thrombus break loose in a deep
vein the clot is carried through the venous system to the
right atrium and ventricle of the heart and ultimately lodges
in the pulmonary arteries.
• Risk factors:
• The following are some of the factors predisposing to
pulmonary embolism
• I. Venous stasis To
• 1. Prolonged sitting (car), bed rest and/or immobilization
• 2. Congestive heart failure
• 3. Varicose veins
31
• II. Trauma
• 1. Bone fractures
• 2. Extensive injury to soft tissue
He t ist d d
• 3. Postoperative or postpartum states
• 4. Extensive hip or abdominal operation. I e it
• III. Hypercoagulation disorders
• 1. Oral contraceptives
• 2. Polycythemia
• 3. Multiple myeloma
• IV. Others
• Obesity. Pregnancy. Burns. Malignant neoplasm.
 DEFENSES OF THE RESPIRATORY SYSTEM

3rd Wall sitense

Folie
• INFECTIONS OF THE RESPIRATORY SYSTEM
• Can be divided into groups depending on the infections they
cause
1
– Otitis media, sinusitis, and mastoiditis.
– Pharyngitis aid I
– Typical and atypical community-acquired pneumonia
– Hospital-acquired (nosocomial) pneumonia
– BACTERIAL INFECTIONS OF THE UPPER
RESPIRATORY TRACT (URT)
• Laryngitis & Epiglottitis
• Otitis media, mastoiditis, and sinusitis
• Pharyngitis
• Scarlet fever
• Diphtheria
• Laryngitis is swelling and irritation (inflammation)
of the voice box (larynx) that is usually associated
with hoarseness or loss of voice- Haemophilus
influenzae & Streptococcus pneumoniae, could be
fungal and viral.
• Epiglottitis- Inflammation of the cartilage that
covers the trachea (windpipe)-Haemophilus
influenzae, Streptococcus pneumoniae or
Streptococcus pyogenes.
• Otitis media- general term for infection or
inflammation of the ear-fluid/exudates/pus/in the
middle ear due to Haemophilus influenzae,
Streptococcus pneumoniae or Streptococcus
pyogenes.
• PHARYNGITIS
 A variety of bacteria can cause infection in the pharynx.
 A classic infection is strep throat.
 Caused by Streptococcus pyogenes
 Contains M proteins which inhibits phagocytosis.
 Group A streptococci can cause abscesses on the tonsils.
• BACTERIAL PNEUMONIA
• One of the most serious lower respiratory tract infections.
• Bacterial pnemonia can be divided into two types:
– Nosocomial
– Community-acquired

• Each type can be caused by a variety of organisms.

 Nosocomial pneumonia
 Occurs approximately 48 hours after admission to
hospital
 Usually associated with Staphylococcus aureus
 Also caused by Gram-negative bacteria
 Particularly difficult to deal with if pathogen is resistant
to antibiotics
 Community-acquired pneumonia
 Usually presents as a lobar pneumonia
 Accompanied by fever,ifs chest pain, and production of purulent
sputum
9
 BACTERIAL PNEUMONIA
4
Pathogenesis
 Classical lobar pneumonia has four stages:
 Acute congestion
 Local capillaries become engorged with neutrophils.
 Red hepatization
1409
 Red blood cells from the capillaries flow into the alveolar
spaces.
 Grey hepatization
 Large numbers of dead neutrophils (are the first cells that reach
the site of infection through a process known as chemotaxis)
 Resolution
 Adaptive immune response begins to produce antibodies.
Which control the infection.
• Typical or Classic Pneumonia
• Typical bacterial pneumonia is a respiratory
condition with inflammation of the lung.
• Often characterized as inflammation of the
parenchyma of the lung (the alveoli) and abnormal
alveolar filling with fluid.
• Typical symptoms associated with pneumonia
include cough, chest pain, fever, and difficulty in
breathing.
• Bacterial pneumonia is treated with antibiotics
• Classification of Pneumonia
• Lobar Pneumonia:
g a
say
 Streptococcus pneumonia that affects a part of a
semester
lobe in the lung or it may affect more than one
lobes.
riemannian
• Bronchial Pneumonia:
 pneumonia spreads to several patches in one or_at
both
threesome ynesfe
lungs
three
 is most prevalant in infants, young children and
aged adults
 cough (with or without mucus), chest pain, rapid
breathing, and shortness of breath
 Complications of pneumonia
n

• Organisation (fibrous scarring)

dsesteeeesom .is
• Abscess
• Bronchiectasis
• Empyema (pus in the pleural cavity)

X Ray It
G YOU
5W 4
1