Ventilation (Airway) = air movement in and out of

the Lungs Infectious rhinitis - mostly causes by viral infections

like rhinovirus and influeza
Oxygenation (Breathing) = O2 in the bloodstream
Non-allergic rhinitis - environmental factors such as
Perfusion (Circulation) = O2 in tissue seasonal changes

Lobes of the Lungs Clinical manifestations

Sneezing
Right lung - 3 Itching
Left lung - 2 Nasal congestion
Postnatal drip
Note : The heart sits slightly to the left side of the Watery discharge
chest, causing the left lung to be smaller and shaped
with two lobes instead of three. Diagnostic tests
History and physical exams
Lung Volumes Allergy testing ( skin prick)

1. Tidal Volume (TV) : is the amount of air you Pharyngitis - inflammation of pharynx often
breathe in or out in a normal, relaxed breath. Also characterized by a sore throat
known as your quiet breathing
2. Inspiratory Reserve (IRV) : maximum inhalation Types :
after a normal breath in
3. Expiratory Resevre (ERV) : maximum exhalation 1. Viral Pharyngitis - caused by Rhinovirus, EBV,
after a normal breath out and influenza
4. Residal Volume (RV) : amount of air that remains 2. Bacterial Pharyngitis - caused by Group A
in the lungs exhalation Streptoccocus
3. Fungal Pharyngitis - cuased by Candida
Lung Capacities Species, often in immunocompromised individuals
4. Allergic Pharyngitis - caused by allergens like
1. IRV + TV + ERV = Vital Capacity (VC) pollen, dust, pet dander.
2. TV + IRV = Inspiratory Capacity (IC)
3. ERV + RV = Functional Residual Capacity (FC) Clinical Manifestations
4. VC + IC + FRC = Total Lung Capacity Sore throat
Odynophagia
Normal Values Fever
Red, Inflammed throat
IRV = 3000mL
TV = 500 mL Diagnostic Test
ERV = 1100 mL Throat culture
RV = 1200 Rapid Antigen Test
Monospot Test
VC = 4600 mL
IC = 3500 mL Medical Management
FRC = 2300 mL ViralPharyngitis - NO ANTIBIOTICS, supportive
therapy only
Total Lung Capacity = 5800mL
Bacterial Pharyngitis - 1st Line of treatment for Upper
Respiratory Tract infection
Upper Respiratory Tract Disorders in Oxygenation
1. Penicillin
1. Rhinitis - inflammation of mucus membranes 2. Ceftriaxone
inside the nose 3. Azithromycin

Types Fungal Pharyngitis - Nystatin andFluconazole

Allergic Rhinitis - Triggered by allergens Allergic Pharyngitis - hydration and humidification of

air
Examples :
Pollen Potential Complications
Dust Rheumatic Fever
Mites Peritonsillar Abscess
Pet danders Post - Streptococcal Glomerlonephritis
Chronic Obstructive Pulmonary Disease (COPD) respiratory infections, due to ruptured
Is a progressive lung disease characterized by pulmonary alveoli, and
persistent respiratory symptoms and airflow limitation hypertension, and cor respiratory failure in
due to chronic= inflammaton in the lungs. pulmonale. advanced cases.

Two types Confirmed by

Based on history,
pulmonary function
Chronic bronchitis - defined by chronic cough pulmonary function
Diagnosis tests, chest CT scan,
and sputum production for atleast 3 MONTHS in 2 tests, chest X-ray, and
and diffusion capacity
consecutive years. Also known as BLUE BLOATERS blood gas analysis.
testing.

Emphysema - a condition where the alveoli in the

lungs are damaged, reducing surface area for gas
Chronic Bronchitis Laboratory and diagnostic
exchange. Also known as PINK PUFFERS
Findings
Characteristic Chronic Bronchitis Emphysema
Laboratory Findings:
Inflammation of the Damage to the alveoli
 Arterial Blood Gas (ABG):
bronchial tubes, (air sacs), causing their
Definition o Hypoxemia: Decreased oxygen
leading to excessive walls to weaken and
mucus production. rupture. levels (PaO2) due to impaired gas
exchange.
o Hypercapnia: Elevated carbon
Mainly caused by long- Primarily caused by
dioxide levels (PaCO2) due to airflow
term smoking or smoking, genetic
Cause obstruction and impaired ventilation.
exposure to air factors (e.g., alpha-1
o Respiratory acidosis: Occurs due to
pollutants. antitrypsin deficiency).
increased CO2 retention, which
lowers the pH of the blood.
Bronchial tubes Alveoli lose
 Sputum Culture:
become inflamed, elasticity, reducing
narrow, and produce surface area for gas
Pathophysiolo o Often shows increased mucus
thick mucus, exchange and
gy production, and the sputum may be
obstructing airflow. causing trapped air.
Patients are usually Patients are usually purulent or thick.
overweight older and thin
· Complete Blood Count (CBC):
Persistent, productive
Shortness of breath,  Leukocytosis: Elevated white blood cell
cough (coughing up
Main especially during count during acute exacerbations due to
mucus), wheezing,
Symptoms exertion, and "barrel infection or inflammation.
crackles, ronchi, and
chest,"  May show polycythemia (elevated
shortness of breath.
hematocrit and hemoglobin ) as a
Chronic, productive Often minimal or compensatory mechanism due to impaired
Cough cough, often worse in absent cough; cough
gas exchange which stimulates the kidneys
the morning. usually dry if present.
to produce more erythropoietin

Excessive mucus Diagnostic Imaging:

Sputum Minimal to no sputum
production, often thick
Production production.  Chest X-ray:
and discolored.
o Enlarged heart (cor pulmonale) due
"Pink puffer" to right-sided heart failure.
"Blue bloater" o Increased bronchovascular
appearance; thin, with
Breathing appearance; cyanosis markings and prominent pulmonary
pursed-lip breathing
Pattern due to hypoxia, and arteries due to chronic inflammation.
to help exhale trapped
bloated due to edema. o May show signs of pulmonary
air.
hypertension.
Rare, oxygen levels
Common due to
are often more
Cyanosis reduced oxygen levels
preserved than in
(hypoxia). High-Resolution CT Scan:
chronic bronchitis.

Complications Higher risk of Risk of pneumothorax  Can show bronchial wall thickening, mucus
plugging, and air trapping
Pulmonary Function Tests (PFTs):  Spirometry shows decreased FEV1 and
increased residual volume due to loss of
 Spirometry shows decreased FEV1 (Forced elastic recoil and air trapping.
Expiratory Volume in 1 second) and  FEV1/FVC ratio is reduced, indicating airflow
increased residual volume (RV) due to limitation.
airway obstruction.  Increased Total Lung Capacity (TLC) and
 FEV1/FVC ratio (Forced Vital Capacity) is Functional Residual Capacity (FRC) due to
typically reduced (below 70%), indicating air trapping.
airflow limitation.  Decreased Diffusing Capacity for Carbon
 Increased Functional Residual Capacity Monoxide (DLCO), indicating impaired gas
(FRC): Due to trapped air in the lungs. exchange due to alveolar destruction.

Emphysema Laboratory and diagnostic Findings Chronic Bronchitis: Pathophysiology

Laboratory Findings: Initial Irritation and Inflammation

 Arterial Blood Gas (ABG):  Chronic exposure to irritants, such as

o Hypoxemia: Decreased oxygen cigarette smoke or pollutants, leads to
levels (PaO2) as the alveolar surface repeated inflammation of the bronchi (the
area for gas exchange is reduced. large airways).
o Hypercapnia: Elevated carbon  This chronic irritation causes hyperplasia and
dioxide levels (PaCO2) due to hypertrophy of the goblet cells and
impaired exhalation. submucosal glands, leading to excessive
o Respiratory acidosis in advanced mucus production in the airways
stages.
 Complete Blood Count (CBC): Mucus Hypersecretion and Impaired Ciliary
Function
o Leukocytosis may be seen during
acute exacerbations.  Increased mucus production thickens airway
secretions, making it harder to clear mucus
 Alpha-1 Antitrypsin Levels: and other particles from the airways.
 The cilia (hair-like structures) in the bronchi
are damaged by inflammation and smoke,
o Low levels of alpha-1 antitrypsin in
impairing their ability to move mucus out of
some individuals (especially younger the lungs.
adults) may contribute to the  Stagnant mucus in the airways creates a
development of emphysema. breeding ground for bacteria, increasing the
risk of infections.
Diagnostic Imaging:
Airway Obstruction
 Chest X-ray:
o Hyperinflation of the lungs:  As the bronchi become increasingly inflamed
Increased lung volume with a and mucus-filled, the airway lumen narrows,
flattened diaphragm. causing airway obstruction.
o Increased retrosternal air space.  This obstruction limits airflow, especially
o Barrel chest appearance due to the during expiration, leading to air trapping and
expansion of the chest. decreased oxygen exchange.
 High-Resolution CT Scan:
Hypoxemia and Hypercapnia
o Bullae (large air-filled spaces) and
blebs (small bubbles) in the lung  Due to impaired gas exchange, patients often
parenchyma. experience hypoxemia (low blood oxygen
o Emphysematous changes in the levels) and hypercapnia (elevated CO₂
alveolar walls. levels).
 Hypoxemia stimulates increased red blood
cell production (polycythemia), which
thickens the blood and further complicates
circulation.

Pulmonary Function Tests (PFTs): Compensatory Responses and "Blue Bloater"

Appearance
  The body attempts to compensate for low with a genetic deficiency, allowing unchecked
oxygen by increasing cardiac output, leading elastin destruction.
to a bluish skin tone (cyanosis) and bloating
from fluid retention. Loss of Alveolar Wall Integrity and Elasticity
 This results in the characteristic “blue
bloater” appearance: cyanotic skin tone and  The destruction of elastin weakens the
signs of right-sided heart failure. alveolar walls, causing them to rupture and
form larger, irregular air spaces (bullae).
Progressive Airway Remodeling and Chronic  The alveoli lose their natural elasticity, making
Obstruction it difficult for the airways to remain open
during expiration, leading to air trapping and
 Over time, airway walls thicken and fibrosis hyperinflation of the lungs.
develops, making airway obstruction
irreversible. Impaired Gas Exchange
 Chronic inflammation eventually leads to
structural changes in the bronchi, further  With fewer intact alveoli, the surface area for
limiting airflow and causing persistent gas exchange is significantly reduced,
symptoms of chronic bronchitis. impairing oxygen intake and carbon dioxide
elimination.
Complications  This reduction in surface area leads to
hypoxemia (reduced blood oxygen) and, in
 Pulmonary hypertension develops as blood advanced cases, hypercapnia (elevated
vessels in the lungs constrict in response to blood CO₂).
chronic hypoxemia.
 This can lead to cor pulmonale (right-sided Dynamic Hyperinflation and Air Trapping
heart failure), as the right side of the heart
struggles to pump blood through the lungs  Air becomes trapped in the damaged alveoli
against increased resistance. With overuse of during expiration, leading to overinflation of
heart muscle, it looses its function to pump the lungs.
out blood through the lungs so instead, blood  This causes the characteristic "barrel chest"
back flows to other systems causing appearance as the chest adapts to the
peripheral edema, Hepatomegaly, etc. increased lung volume.
 Polycythemia occurs particularly as a result  Over time, patients adopt pursed-lip
of prolonged hypoxemia (low blood oxygen breathing to create back pressure, helping
levels). It is characterized by an increase in keep airways open and facilitating expiration.
the number of red blood cells (RBCs), leading
to thickened blood and an increased risk of
Increased Work of Breathing and "Pink Puffer"
clotting and other circulatory complications.
Appearance
 Bacterial infections are common in chronic
bronchitis, and the thick mucus can provide
an environment for bacteria to grow, leading  Patients with emphysema tend to be thin and
to pneumonia use accessory muscles (like neck and
 Hypoxemia (low oxygen levels) and shoulder muscles) to assist with breathing.
hypercapnia (high carbon dioxide levels) may  The increased effort to breathe, combined
develop over time, causing respiratory with relatively maintained blood oxygenation,
failure. leads to the "pink puffer" appearance:
flushed or pink skin tone, thin build, and
labored breathing.
Emphysema: Pathophysiology
Progression of Disease and Irreversible Lung
Damage
Elastase Release and Alveolar Damage
 As emphysema progresses, more alveoli are
 The primary cause of emphysema is
destroyed, leading to further reductions in
smoking or, in rare cases, genetic factors
lung function and worsening hypoxemia.
(such as alpha-1 antitrypsin deficiency).
 Emphysematous lung tissue loses its
 Chronic irritants activate macrophages and
structure permanently, making the condition
neutrophils in the alveoli, which release
irreversible and progressively debilitating.
enzymes like elastase that break down
elastin in the alveolar walls.
 Alpha-1 antitrypsin, a protective enzyme Complications
that inhibits elastase, is decreased or
overwhelmed in smokers and in individuals
  The formation of bullae (large air spaces) Chest Physiotherapy:
increases the risk of pneumothorax, as
weakened alveoli can rupture, causing air to  Refer to respiratory therapy for chest
leak into the pleural space. physiotherapy (e.g., postural drainage,
 Advanced emphysema can lead to percussion) to help loosen mucus and
respiratory failure and cor pulmonale due facilitate airway clearance.
to increased pressure in the pulmonary
circulation from extensive lung damage. Use of Medications, Nebulizers and Inhalers:
 The destruction of alveolar walls makes the
lungs more vulnerable to infection by bacteria
 Administer prescribed bronchodilators (e.g.,
or viruses, which can lead to pneumonia
beta-agonists, anticholinergics) and
 Acute exacerbations of emphysema, often
corticosteroids via nebulizer or metered-
triggered by infections, can precipitate acute
dose inhaler to reduce bronchoconstriction
respiratory failure
and inflammation.
 Monitor for side effects of medications such
Nursing Management for Chronic Bronchitis as bronchodilators (e.g., tachycardia,
jitteriness), corticosteroids (e.g., oral thrush,
1. Assessment and Monitoring hyperglycemia), or antibiotics (in cases of
infection).
Monitor Respiratory Status:  Use mucolytics like acetylcysteine or
hypertonic saline to thin secretions and make
o Regularly assess vital signs, them easier to clear
particularly respiratory rate, pulse
oximetry (typically 88–93%) and Dietary Recommendations:
blood pressure.
o Monitor for signs of hypoxia (e.g.,  Recommend small, frequent meals if the
cyanosis, irritability, confusion, patient experiences shortness of breath
and restlessness) and hypercapnia during meals (dyspnea-related anorexia).
(elevated carbon dioxide levels).  Encourage weight management to reduce the
o Assess breath sounds for wheezing, strain on the respiratory system, especially if
crackles, ronchi, or decreased air the patient is obese.
entry.
o Evaluate sputum characteristics (e.g., Vaccinations:
color, consistency, amount) to detect
signs of infection or exacerbation.  Encourage annual flu vaccination and
pneumococcal vaccination every 5 years
Airway Management for those at higher risk.

Encourage Effective Breathing Exercises Nursing Management for Emphysema

and Coughing Techniques:
1. Assessment and Monitoring
o Huff coughing to expel mucus
effectively  Assess the patient's respiratory rate, depth,
o Diaphragmatic Breathing and effort, including the use of accessory
(Abdominal Breathing) to help muscles. Evaluate oxygen saturation levels,
strengthen the diaphragm lung sounds, and signs of hypoxia (e.g.,
o Pursed-Lip Breathing to slow the cyanosis, irritability, restlessness and
breathing rate, keeps the airways confusion).
open longer, and improves airflow,  Observe for tachypnea, dyspnea, and a
especially during exhalation. prolonged expiratory phase. Look for
barrel chest, clubbing, and cyanosis.
 Track lung function regularly to evaluate
disease progression

Promote Hydration:
Oxygen Therapy
 Encourage adequate fluid intake (if not
contraindicated) to help thin mucus, making  Provide supplemental oxygen if the patient
it easier to expel. has low oxygen saturation (SpO2 below
88%). Use nasal cannula or mask as
 prescribed.Keep the flow rate at around 2  Pain management: Manage discomfort from
L/min chronic coughing or respiratory effort with
 Monitor oxygen flow rates and adjust as appropriate analgesics (if necessary).
necessary to avoid oxygen toxicity or CO2
retention (especially in hypercapnic Vaccinations:
patients).
 In COPD, the primary drive to breathe is often  Encourage annual flu vaccination and
hypoxia (low oxygen levels) rather than the pneumococcal vaccination every 5 years
buildup of CO2. If too much oxygen is for those at higher risk.
administered, it may suppress this hypoxic
drive, leading to reduced ventilation and CO2
retention.

Breathing Exercises

 Teach pursed-lip breathing: Instruct the

patient to breathe in slowly through the nose
and exhale through pursed lips to help reduce
air trapping and improve exhalation.
 Diaphragmatic breathing: Teach the patient
to use the diaphragm to breathe, encouraging
deeper and more efficient breaths.
 Incentive spirometry: Use an incentive
spirometer to help expand the lungs and
improve ventilation.

Use of Medications, Nebulizers and Inhalers:

 Administer prescribed bronchodilators (e.g.,

beta-agonists, anticholinergics) and
corticosteroids via nebulizer or metered-
dose inhaler to reduce bronchoconstriction
and inflammation.
 Monitor for side effects of medications such
as bronchodilators (e.g., tachycardia,
jitteriness), corticosteroids (e.g., oral thrush,
hyperglycemia), or antibiotics (in cases of
infection).

Nutritional Support

 Provide high-calorie, high-protein diet:

Emphysema patients often experience weight
loss due to increased energy demands from
breathing. A high-calorie, nutrient-dense diet
helps support strength and immune function.
 Small, frequent meals: Encourage small
meals to reduce fatigue and improve
digestion.
 Monitor for malnutrition: Keep track of the
patient's weight, and assess for signs of
malnutrition (e.g., muscle wasting)

Promote Comfort and Prevent Fatigue

 Positioning: Encourage the patient to sit

upright or lean forward with their arms on a
table (tripod position) to ease breathing and
reduce fatigue.
 Limit activity: Assist with planning rest
periods between activities to prevent fatigue
and reduce oxygen demand.