NCM 112 OXYGENATION

Bsn 3-D 1st Sem Prelim (2024-2025)

OVERVIEW OF THE RESPIRATORY SYSTEM PHYSIOLOGY OF BREATHING (INHALATION)

● The respiratory system is crucial for gas (INSPIRATION)
exchange, allowing oxygen to enter the blood and ➢ Diaphragm Contraction: The diaphragm contracts
carbon dioxide to be expelled from the body. and moves downward, expanding the thoracic
● It involves various structures that work together to cavity.
ensure this process is efficient. ➢ Intercostal Muscles: These muscles between the
ribs contract, raising the rib cage further
ANATOMY OF THE RESPIRATORY SYSTEM expanding the thoracic cavity.
● Upper Respiratory Tract ➢ Negative Pressure: This expansion creates
○ Nose and Nasal Cavity: The entry point negative pressure inside the lungs, causing air to
for air. The nasal cavity is lined with flow in from the outside environment.
mucous membranes and tiny hairs (cilia)
that help filter, warm, and humidify the air. GAS EXCHANGE
○ Pharynx (Throat): A passageway for air ● External Respiration- Takes place in the alveoli
from the nose to the larynx and for food where oxygen from inhaled air diffuses through
from the mouth to the esophagus. the alveolar membrane into the blood in the
○ Larynx (Voice Box): Located just below capillaries. Carbon dioxide, which is higher in the
the pharynx, the larynx contains the vocal blood, diffuses from the blood into the alveoli to
cords and is responsible for sound be exhaled.
production. It also serves as a ● Internal Respiration- Occurs in the tissues where
passageway for air to the trachea. oxygen is delivered from the blood into cells, and
● Lower Respiratory Tract carbon dioxide produced by cellular metabolism
○ Trachea (Windpipe): A rigid tube that diffuses from the cells into the blood.
extends from the larynx to the bronchi, t
is lined with cilia and mucus to trap and REGULATION OF BREATHING
expel particles and pathogens. ➢ Medulla Oblongata and Pons- Located in the
○ Bronchi: The trachea divides into the right brainstem, these structures control the rate and
and left bronchi, which further divide into depth of breathing by responding to changes in
smaller bronchioles within the lungs. blood pH, CO: levels, and O levels.
○ Lungs: Main organs of respiration where ➢ Chemoreceptors- Located in the carotid arteries
gas exchange occurs. The right lung has and aorta, they detect changes in blood pH and
three lobes, and the left lung has two COz concentration and send signals to the
lobes to accommodate the heart. brainstem to adjust breathing accordingly.
○ Alveoli: Tiny air sacs at the end of ➢ Common Respiratory Conditions
bronchioles where gas exchange occurs. ○ Asthma: Characterized by inflamed and
They are surrounded by capillaries where narrowed airways, making breathing
oxygen diffuses into the blood and carbon difficult.
dioxide diffuses out.

- Merimel
- 1
NCM 112 OXYGENATION
Bsn 3-D 1st Sem Prelim (2024-2025)

○ Chronic Obstructive Pulmonary Disease ● Congestion. This stage occurs within the first 24
(COPD): Includes emphysema and chronic hours of contracting pneumonia. During
bronchitis, leading to long-term breathing congestion, the body will experience vascular
difficulties. engorgement, intra-alveolar fluid, and multiple
○ Pneumonia: Infection causing bacteria. The lungs will be very heavy and red.
inflammation of the alveoli, potentially ● Gray Hepatization- This stage is characterized by
filled with fluid or pus. progressive disintegration of red blood cells
○ Tuberculosis: A bacterial infection that and the persistence of a fibrin exudates. Jun 9,
primarily affects the lungs, causing cough, 2020
fever, and weight loss.

PNEUMONIA
● Is an infection in one or both lungs. Bacteria,
viruses, and fungi cause it. The infection causes
inflammation in the air sacs in your lungs, which
are called alveoli. The alveoli fill with fluid or pus,
making it difficult to breathe.

FOUR STAGES OF PNEUMONIA

● Congestion- This stage occurs within the first 24
RESOLUTION OF PNEUMONIA
hours of contracting pneumonia. (Active
● has to be considered as two different phases:
Hyperemia and Edema)
resolution of the acute illness and resolution of
● Red Hepatization- This stage occurs two to three
radiographic opacities.
days after congestion. (Neutrophils, Congestion,
● The chest radiograph usually clears within four
Fibrin)
weeks in patients younger than 50 years without
● Grey Hepatization- This stage will occur two to
underlying pulmonary disease. In contrast,
three days after red hepatization and is an
resolution may be delayed for 12 weeks or longer
avascular stage. (Degradation of red blood cells,
in older individuals and those with underlying lung
Fibrino suppurative exudate)
disease.
● Resolution- (healing)

COLONIAL INVASIONS
RED HEPATIZATION
● Mycobacterium Tuberculosis
● is when there are red blood cells, neutrophils, and
● Mycoplasma Pneumoniae
fibrin in the pulmonary alveolus/ alveoli; it
● Streptococcus Pneumoniae
precedes gray hepatization, where the red cells
● Legionella Pneumophila
have been broken down leaving a fibrino
suppurative exudate. The main cause is lobar
pneumonia.

- Merimel
- 2
NCM 112 OXYGENATION
Bsn 3-D 1st Sem Prelim (2024-2025)

NURSING MANAGEMENT OF PNEUMONIA or cardiovascular diseases, cerebrovascular

● Administer antibiotics (prime treatment) Antibiotic disease, epilepsy, dementia, dysphagia, HIV, or
Type depend on organism chronic renal or liver disease were all at increased
● Primary nursing intervention: Maintain airway and risk of CAP.
O2 saturation above 93%
● Promote nutrition and hydration COMMUNITY ACQUIRED PNEUMONIA
● Provide small, frequent, high-carb, high-protein RISK FACTORS FOR PNEUMONIA
meals 1. age
2. alcoholism
NURSING ASSESSMENT 3. smoking
● Take a careful history to help establish etiologic 4. asthma
diagnosis. 5. Immunosuppression
● Assess the elderly patient for unusual behavior, 6. institutionalizations
altered mental status, dehydration, excessive 7. COPD
fatigue, and concomitant heart failure. 8. Dementia
● Observe anxious, flushed appearance, shallow
respirations, splinting of affected side, confusion, CAP RISK FACTORS
disorientation. ● Several factors put patients place at risk for
● Auscultate for crackles overlying affected region, community acquired pneumonia (CAP), including
and for bronchial breath sounds when comorbidities, lifestyle, and patient characteristics.
consolidation (filling of airspaces with exudate) is ● Comorbidities
present. 1. Altered mental state
2. Asthma
CAUSES OF NON RESOLVING PNEUMONIA 3. Bronchiectasis
● Inappropriate antimicrobial therapy. 4. Chronic obstructive pulmonary disease
● Super-infection. 5. Cystic fibrosis
● Complications of initial pneumonia. 6. Diabetes
● Host factors. 7. Heart disease
● Delayed radiological recovery ● Lifestyle factors
● Presence of resistant organisms a. Alcohol or substance misuse
● Presence of unusual organisms. b. Homelessness
● Defects in defense. c. Overcrowded living conditions
● Diseases mimicking pneumonia d. Smoking
● Patient’s Characteristics
MODIFIABLE AND NON MODIFIABLE a. Extremes of age
● Lifestyle factors included smoking, alcohol abuse, b. Immunocompromised status
being underweight and regular contact with
children, whereas patients with chronic respiratory

- Merimel
- 3
NCM 112 OXYGENATION
Bsn 3-D 1st Sem Prelim (2024-2025)

CLINICAL MANIFESTATIONS
➢ The signs and symptoms of pneumonia may
include:
BRONCHITIS
➢ Cough, which may produce greenish, yellow or
Lower respiratory tract infections
even bloody mucus.
➢ Infection of the trachea (trachealitis)
➢ Fever, sweating and shaking chills.
➢ Bronchial tree (bronchitis and bronchiolitis)
➢ Shortness of breath.
➢ Often associated with URTI infection (viruses)
➢ Rapid, shallow breathing.
➢ Caused by a wide range of viruses and bacteria:
➢ Sharp or stabbing chest pain that gets worse
o Viruses : rhinovirus, adenovirus, influenza,
when you breathe deeply or cough.
Parainfluenza, metapneumonia
➢ Loss of appetite, low energy, and fatigue.

BEST MEDICATIONS FOR PNEUMONIA

1. Cipro (ciprofloxacin)Antibiotic Oral, Injection
2. Levaquin (levofloxacin)- Antibiotic OralOracea
3. Doxycycline -AntibioticOral
4. Zanamivir-AntibioticOral inhaler

o Bacteria : S. pneumoniae, H. influenzae,

o Causes : inflammation of the airway
epithelium

CONSEQUENCES
➢ Cough
➢ Transparent Phlegm: No bacteria
➢ Green phlegm : Bacteria
- Merimel
- 4
NCM 112 OXYGENATION
Bsn 3-D 1st Sem Prelim (2024-2025)

THE COLOUR OF PHLEGM Bronchitis cause infective exacerbations

● White mucus Commonest cause of admission to hospital
○ Your mucus is thicker and cloudy. /Significant mortality
A virus may be present ● Viral or bacterial bronchitis in patients
● Green mucus with:
○ High concentration de white blood ● Chronic obstructive pulmonary disease
cells after fighting the infection (COPD)
● Clear mucus ● Asthma
○ Your body produces this even ● Bronchiectasis
when you're healthy Causes a deterioration in the underlying lung dses.
● Yellow mucus with increased airways obstruction
○ White blo0o cells are pushing to
the site of infection Chronic Acute
bronchitis bronchitis
INVESTIGATION
symptoms symptoms
● None usually
● May need CXR / C reactive protein to cough that Cough that
exclude pneumonia lasts for many lasts a few
weeks or even days or weeks
TREATMENT months
● None for most cases
● Antibiotics ( Amox, Clari, Doxy) If : Wheezing productive
● Severe / purulent phlegm cough
● Older patients / underlying disease produces
yellow or
SYMPTOMS green mucus
● Cough
Pressure or Fever
● Phlegm: purulent suggests bacterial
tightness in
infection
chest
● Fever + some systemic symptoms feel ill,
anorexic, no energy) Fatigue Chills

SIGNS
● Pyrexia and maybe a mild tachycardia
DIAGNOSTIC PROCEDURES
● No lung signs unusual unless there is an
● Sputum Studies
underlying lung disease
○ Methods- standard, saline
inhalation, gastric washing

- Merimel
- 5
NCM 112 OXYGENATION
Bsn 3-D 1st Sem Prelim (2024-2025)

● Arterial Blood Gases BRONCHITIS MEDICATION

○ measurements of blood pH , ● Antimicrobials.
arterial 02 & CO2 tensions, acid- ● Antitussives/expectorants.
base balance ● Bronchodilators.
● Pulse Oximetry ● Corticosteroids, Systemic.
● Chest X-ray ● Corticosteroids, Inhaled.
● Bronchoscopy ● Antiviral Agents.
● Thoracentesis ● Analgesics/antipyretics.
● Laryngoscopy
ANTIBIOTICS
CHRONIC BRONCHITIS: ● First line agents
Diagnostic Tests ○ Doxycycline
● PFTs ○ Amoxicillin
○ FVC: 4 Forced vital capacity ● 2nd line agents
○ FEV: Forcible exhale in 1 second ○ Coamoxicalv
● FEV1/FVC • <70% ○ Clarithromycin
● ABGs ○ Cefixime
○ PaCO2
○ PaO2 NURSING MANAGEMENT
● CBC 1. Assess The Condition Of Patient.
○ Hct 2. Assess The Vital Signs
3. Provide Comfortable Position.
COMMON CAUSES OF ATELECTASIS 4. Change The Position Periodically.
➢ Hypoventilation 5. Maintain Personal Hygiene.
➢ Airway Obstruction 6. Use pulse oximetry & Suction.
➢ Compression 7. Deep Breathing Exercise Learn To Patient.
➢ Adhesions 8. Refer To Physiotherapist(if Need).
9. Provide Oxygen According To Physician Order.
BRONCHITIS CAUSE INFECTIVE EXACERBATIONS 10. Provide Psychological Support To Patient.
Commonest cause of admission to hospital / Significant 11. Provide Knowledge About Chronic Bronchitis.
mortality 12. Administer medication according to physician
order
➢ Can precipitate cause of admission to hospital, 13. Bronchodilators,antibiotics, mucolytics.
respiratory failure, and death
➢ Treat the infection with antibiotics/neuraminidase ASTHMA
inhibitors ➢ A chronic inflammatory disorder of the airways
➢ Plus treat the underlying lung disease (corti and ➢ Chronic inflammation is associated with airway
bronchodi) hyper responsiveness that leads to recurrent

- Merimel
- 6
NCM 112 OXYGENATION
Bsn 3-D 1st Sem Prelim (2024-2025)

episodes of wheezing, breathlessness, chest ➢ Eosinophils (type of white blood cell)

tightness, and coughing ➢ Neutrophils (type of white blood cell)
➢ Widespread, variable, and often reversible airflow ➢ Airway smooth muscle hypertrophy
limitation
ASTHMA FLARE
CAUSES OF ASTHMA ➢ Quick-relief medicine
• Allergies (dust, pollen, mold) ➢ Emergency care
• Triggers (air pollution, tobacco smoke) ➢ Controller medicine
• Infections
TYPES OF ASTHMA MEDICINE:
SYMPTOMS OF ASTHMA ➢ Long-term medicines
• Coughing o This can result from infections by bacteria
• Wheezing such as mycobacterium pneumoniae,
• Chest tightness chlamydia, bordetella.
• Shortness of breath
PREVALENCE
• 10-12% - adults
• 15%- children
• Childhood- Males > Females
• Adult- Equal sex ratio
• Mortality
o poorly controlled disease
o frequent use of bronchodilators
o lack of ICS use {Inhaled
corticosteroids}intercostal space
• near fatal asthma

RISK FACTORS
SIGNS OF SEVERE ASTHMA
• Atopy
➢ Visiting the ER or hospital
o Strongest risk factor: family history of
➢ Using quick-relief medicine more than 2 times per
atopic disease ( 3x-4x)
week
- House dust mites
➢ Needing a new quick-relief inhaler more than 2
- cat and dog fur
times per year
- cockroaches
➢ Needing steroid pills more than 2 times per year
- grass and tree pollens
➢ Difficulty with everyday activities
o Production of specific IgE antibodies
• Infections
TYPES OF SEVERE ASTHMA
o Common triggers of exacerbations
➢ Allergic asthma
- Merimel
- 7
NCM 112 OXYGENATION
Bsn 3-D 1st Sem Prelim (2024-2025)

o (?) role in etiology INFLAMMATION: MAST CELLS

o RSV- development of asthma • Initiates the acute bronchoconstriction responses
o Mycoplasma/Chlamydia to allergens
- severe asthma • Activated by allergens thru IgE dependent
- (?) etiology mechanisms
• Environmental Factors • Histamine, prostaglandins and
o Increasing incidence of asthma in cysteinylleukotrienes
developing countries
• Viral respiratory infection (Hygiene hypothesis) INFLAMMATION: MACROPHAGES AND DENDRITIC
o Exposure to infections early in life CELLS
influences the development of a child’s • Initiate inflammatory response thru activation of
immune system along a non-allergic certain cytokines
pathway leading to a reduced risk of
asthma and other allergic diseases. INFLAMMATION: EOSINOPHILS
• Diet • Characteristic of asthmatic airways
o Increased incidence: • Associated with airway hyper responsiveness
- Vitamins A and C, magnesium,
selenium and omega 3 INFLAMMATION: EOSINOPHILS
- Vitamin D deficiency • Characteristic of asthmatic airways
o Obesity: Independent risk factor • Associated with airway hyper responsiveness
• Air pollution
• Occupational exposure INFLAMMATION: T LYMPHOCYTES
• TH 2 predominant immune response
PATHOLOGY
• IL-5
• Increase numbers of activated eosinophils, T o eosinophilic inflammation
Lymphocytes and mast cells • IL-4/IL-13
• Thickening of the BM o increased IgE formation
o sub epithelial collagen deposition
EFFECTS OF INFLAMMATION
INFLAMMATION
• Epithelial Shedding
• Trachea to the terminal bronchioles • Fibrosis
• Predominance in the cartilaginous bronchi • Hypertrophy and hyperplasia of airway smooth
• Inflammation leads to airway hyper muscle
responsiveness→ variable airflow obstruction • Increase mucosal blood flow
• Increased number of different cells • Mucus hyper secretion

ASTHMATIC TRIGGERS
➢ Allergens:
- Merimel
- 8
NCM 112 OXYGENATION
Bsn 3-D 1st Sem Prelim (2024-2025)

o Activate mast cells ❖ Worse at night and typically awake in the wee
o Release of mediators hours of the morning
➢ Viral Infections ❖ Increased mucus production
o Rhinovirus, RSV and Coronavirus ❖ Inspiratory and expiratory rhonchi
o common triggers of exacerbations ❖ Hyperinflation
➢ Pharmacologic agents ❖ Some patients present with nonproductive cough
o beta blockers ❖ Absence of physical findings in controlled asthma
o aspirin
➢ Exercise DIAGNOSIS: PFT
o Typically begins after exercise has ended ❖ Spirometry
o resolves spontaneously after 30 minutes o reduced FEV1, FEV1/FVC ration and PEF
o worse in cold dry climates ❖ Reversibility
o prevented by regular treatment with ICS o >12% and 200 ml increase in FEV1 post
➢ Food bronchodilator
➢ Air pollution ❖ Measurement of PEF
➢ Occupational factors o diurnal variation of asthma
➢ Hormonal factors ❖ Increased airway resistance, TLC and RV
o fall in progesterone ❖ DLCO is usually normal
o premenstrual worsening
➢ GERD DIAGNOSIS: METHACHOLINE/HISTAMINE CHALLENGE
TEST
PATHOPHYSIOLOGY ❖ Increased AHR
➢ Airflow limitation ❖ Provocation with either metacholine or histamine
o mainly due to bronchoconstriction ❖ Provocative concentration that lead to a 20%
➢ Reduction in: decrease in FEV1
o FEV1
o FEV1/FVC Ratio DIAGNOSIS: IMAGING
o Peak Expiratory Flow rate ❖ Chest radiograph:
➢ Early closure of peripheral airways o usually normal
o hyperinflation o Hyper inflated lungs
o air trapping o rule out co- existing conditions
o increased residual volume
TREATMENT
CLINICAL FEATURES ➢ Relievers (Bronchodilators)
❖ Wheezing, dyspnea and coughing o rapid relief of symptoms
❖ Variable o relaxation of smooth muscles
❖ Resolves spontaneously or with treatment ➢ Controllers
o inhibit underlying inflammatory response

- Merimel
- 9
NCM 112 OXYGENATION
Bsn 3-D 1st Sem Prelim (2024-2025)

TREATMENT: BRONCHODILATORS ➢ Low doses→ anti-inflammatory effects

➢ Reverses bronchoconstriction ➢ Slow release preparation: OD/BID
➢ Little or no effect on inflammation ➢ Add- on medication in poorly controlled asthma
➢ B2 agonists, anticholinergics and theophylline ➢ Nausea, vomiting and headaches
➢ Arrhythmias and seizures
TREATMENT: B2 AGONISTS
➢ Stimulates adenyl cyclase TREATMENT: CONTROLLERS
o increased intracellular CAMP ➢ ICS
o relaxes smooth muscles o most effective controller
o inhibits certain inflammatory cells particularly o reduces inflammatory numbers and their
mast cells activation
➢ SABA o reduction of AHR
o 3 to 6 hours
o rapid onset TREATMENT: ICS
o increased use→ uncontrolled asthma ➢ Inhibition of NF- KB
o nebulizer/MDI ➢ Recruitment of histone deacetylase 2
➢ LABA ➢ Increase expression of B2 receptors
o 12 hours duration ➢ Given BID
o should not be used as a monotherapy (without ➢ Rapidly improve symptoms and lung function
ICS) ➢ Prevents exacerbations, EIA, AHR
o improve control and reduce exacerbations ➢ Maximal improvement may take several months
when added to ICS ➢ Prevents irreversible changes in airway function
o muscles tremors and palpitations ➢ 1st line therapy for persistent asthma
➢ Added to a LABA if still uncontrolled with ICS
TREATMENT: ANTICHOLINERGICS alone
➢ Anticholinergics ➢ Hoarseness and Oral candidiasis
o prevents cholinergic nerve induced o reduced by a large volume spacer device
bronchoconstriction and mucus secretion ➢ Minimal systemic side effects
o less effective than b2 agonists
o only used as an additional medication in
uncontrolled asthma
o dry mouth and urinary retention

TREATMENT: THEOPHYLLINE
➢ Oral bronchodilator
➢ Inhibition of phosphodiesterase’s→ increases
CAMP
➢ Narrow Therapeutic range

- Merimel
- 10
NCM 112 OXYGENATION
Bsn 3-D 1st Sem Prelim (2024-2025)

TREATMENT: CONTROLLER
➢ OCS
o used for treatment of acute severe asthma
o Prednisone/Prednisole 30-45 mg/day once
daily for 5-10 days and no tapering
needed

TREATMENT: OCS
➢ 1% of asthmatics may require maintenance
treatment with OCS
➢ Systemic side effects: Trucal obesity, bruising,
osteoporosis, diabetes, hypertension, gastric
ulceration, depression and cataract

TREATMENT: ANTILEUKOTRIENES
➢ Cysteinyl Leukotrienes
o potenet bronchoconstrictors
➢ Montelukast/Zafirlukas
o LT 1 receptor blockers
➢ Less effective than ICS
➢ Add on therapy
➢ Less effective than LABA as add on
➢ OD/BID

TREATMENT: CROMONES
➢ Cromolyn Na/Nedocromil Na
➢ Inhibit mast cell degranulation
➢ Effective in EIA/Allergen induced asthma

TREATMENT: OMALUZIMAB
➢ Anti IgE
➢ Reduces number of exacerbations
➢ Subcutaneous injection every 2-4 weeks
➢ Side Effect: Anaphylaxis

MANAGEMENT: CHRONIC ASTHMA

➢ Stepwise Approach

- Merimel
- 11
NCM 112 OXYGENATION
Bsn 3-D 1st Sem Prelim (2024-2025)

ACUTE SEVERE ASTHMA o Anti leukotrienes

➢ High o2 ➢ Cigarette Smoking
➢ SABA via nebulizer/MDI with spacer o interferes with anti-inflammatory actions
➢ SAMA of corticosteroids
➢ IV Steroids o higher doses of steroids
➢ IV Aminophylline o Cessation improves lung function and
➢ Magnesium Sulfate reduces steroid resistance
➢ Impending Respiratory Failure ➢ Surgery
➢ Avoid sedation o Well controlled: No contraindication to GA
➢ Antibiotics- Pneumonia and intubations
o FEV1 < 80%: Should be given a boost of
REFRACTORY ASTHMA OCS prior to surgery
➢ Difficult to control despite maximal medications o High doses of steroids: Contraindicated
➢ 5% of asthmatics
➢ Require maintenance OCS INTRODUCTION TO URIs NCM112 OXYGENATION
➢ Non compliance with medications Upper respiratory infections affect the structures of the
➢ Allergic rhinitis upper respiratory tract, including the nose, nasal cavity,
➢ GERD sinuses, pharynx, and larynx. Common types of URIs
➢ Drugs include the common cold, influenza, sinusitis, and
pharyngitis.
STEROID RESISTANT ASTHMA
➢ Failure to respond to a high dose of oral 2. PATHOPHYSIOLOGY BY INFECTION TYPE
prednisone/prednisolone (40md OD over 2 weeks) A. COMMON COLD (ACUTE VIRAL RHINOPHARYNGITIS)
➢ Reduction in response of circulating Etiology: Primarily caused by viruses, such as
monocytes/lymphocytes rhinoviruses, coronaviruses, and adenoviruses.
• Mechanism:
SPECIAL CONSIDERATIONS o Virus Entry: The virus enters through the nose or mouth
➢ Pregnancy and attaches to the epithelial cells of the upper respiratory
o 1/3 rule tract.
o same treatment as non pregnant o Viral Replication: Once inside the cells, the virus
o OCS: Prednisone better than prednisolone replicates, leading to cell damage and death.
➢ Breastfeeding: Same treatment as non pregnant o Immune Response: The host’s immune system detects
➢ Aspirin-Sensitive Asthma the viral infection and mounts an inflammatory response.
o preceded by rhinitis and nasal polyps This response includes the release of cytokines, which
o provokes rhinorrhea, conjunctival attract immune cells and increase
irritation, facial flushing and wheezing blood flow to the affected area.
o Non selective COX should be avoided o Symptoms: Inflammation and increased mucus
o Respond to ICS production lead to symptoms such as nasal congestion,

- Merimel
- 12
NCM 112 OXYGENATION
Bsn 3-D 1st Sem Prelim (2024-2025)

sneezing, and sore throat. The body's attempt to expel the • Etiology: Can be viral (e.g., adenovirus, influenza) or
virus results in coughing and increased mucus production. bacterial (e.g., Group A Streptococcus).
• Mechanism:
B. INFLUENZA (FLU) o Viral Pharyngitis: Viral infection leads to inflammation of
the pharyngeal mucosa. The infection often spreads from
• Etiology: Caused by influenza viruses (types A, B,
the nasopharynx and can cause symptoms similar to those
and C).
of a cold or flu.
• Mechanism: o Bacterial Pharyngitis: Bacterial infection, particularly from
o Virus Entry: Influenza viruses enter through the Group A Streptococcus, causes direct invasion and
respiratory tract and bind to sialic acid receptors on destruction of pharyngeal epithelial cells. The bacteria
respiratory epithelial cells. release toxins that further exacerbate inflammation.
o Viral Replication: The virus hijacks the host cell’s o Symptoms: Sore throat, difficulty swallowing, and often
machinery to replicate, causing cell death and damage. fever and swollen lymph nodes. The inflammation can also
cause redness and swelling of the pharyngeal tissues.
o Immune Response: The infection triggers a strong
immune response, including the release of pro- 3. HOST RESPONSE
inflammatory cytokines and interferons. This response
A. Immune Response:
contributes to systemic symptoms such as fever, muscle
• Innate Immunity: The body’s initial defense includes
aches, and fatigue.
physical barriers (e.g., mucus, cilia), and immune cells (e.g.,
o Symptoms: Acute onset of high fever, chills, body aches,
macrophages, neutrophils) that respond to the infection.
and fatigue, in addition to respiratory symptoms like cough
• Adaptive Immunity: The immune system produces
and sore throat.
specific antibodies and activated T-cells to target and
eliminate the pathogen. This response is slower but
C. SINUSITIS
provides long-term protection.
• Etiology: Can be viral (often following a cold),
bacterial, or fungal. B. Inflammation:
• Mechanism: • Cytokine Release: Inflammatory cytokines (e.g.,
o Viral Sinusitis: Similar to the common cold, viral infection interleukins, tumor necrosis factor) are released in
leads to inflammation and swelling of the sinus lining. This response to infection, leading to symptoms like fever,
swelling obstructs sinus drainage and leads to mucus redness, and swelling.
accumulation. • Mucosal Changes: Inflammation increases mucus
production and leads to swelling of mucosal tissues, which
o Bacterial Sinusitis: Bacteria can invade the inflamed sinus
can obstruct airflow and sinus drainage.
cavities, exacerbating inflammation and leading to more
severe symptoms.
4. COMPLICATIONS
o Symptoms: Nasal congestion, facial pain or pressure, and • Secondary Infections: Infections can lead to complications
purulent nasal discharge. The obstruction and infection such as bacterial sinusitis, otitis media, or lower respiratory
create an environment conducive to further microbial tract infections (e.g., pneumonia) due to compromised
growth and inflammation. mucosal defenses.
• Chronic Conditions: Persistent inflammation or recurrent
infections can lead to chronic conditions like chronic
sinusitis or allergic rhinitis.
D. PHARYNGITIS (SORE THROAT)

- Merimel
- 13
NCM 112 OXYGENATION
Bsn 3-D 1st Sem Prelim (2024-2025)

• Decongestants: Over-the-counter decongestants (e.g.,

5.CONCLUSION pseudoephedrine) can reduce nasal congestion. However,
The pathophysiology of upper respiratory infections they should be used with caution in patients with
involves the interplay between infectious agents and the hypertension or other contraindications.
host’s immune and inflammatory responses. Understanding • Antihistamines: These can help alleviate sneezing and
these mechanisms helps in diagnosing and treating URIs runny nose, especially in cases of allergic rhinitis.
effectively and highlights the importance of managing • Cough Suppressants/Expectorants: Cough suppressants
symptoms and preventing complications. If you have (e.g., dextromethorphan) can help with a dry cough, while
specific questions or need further details on any aspect of expectorants (e.g., guaifenesin) can help loosen mucus in
URI pathophysiology, feel free to ask! cases of productive cough.
Get smarter responses, upload files and images, and more.
C. Non-Pharmacological Interventions:
Managing upper respiratory infections (URIs) involves a • Saline Nasal Irrigation: Helps clear nasal passages and
combination of symptom relief, supportive care, and, when reduce congestion.
necessary, specific treatments. URIs can be caused by • Humidification: Using a humidifier can add moisture to
various pathogens, including viruses (like rhinoviruses and the air, which may soothe irritated nasal passages and
influenza) and bacteria (like Streptococcus pneumoniae and throat.
Haemophilus influenzae). Here’s a comprehensive approach • Throat Lozenges and Gargles: Gargling with warm salt
to managing URIs: water or using throat lozenges can soothe a sore throat.

1. ASSESSMENT AND DIAGNOSIS 3. SPECIFIC MANAGEMENT FOR COMMON TYPES OF

A. Clinical Evaluation: URIs
• History: Gather information about symptom onset, A. Common Cold (Acute Viral Rhinopharyngitis):
duration, and severity. Ask about fever, cough, sore throat, • Treatment: Mainly symptomatic; rest, hydration, and over-
nasal congestion, and any associated symptoms like fatigue the-counter medications. Antibiotics are not effective
or headache. against viral infections.
• Physical Examination: Check for nasal discharge, throat
redness, swollen lymph nodes, and any signs of respiratory B. Influenza (Flu):
distress. Auscultate the lungs for abnormal sounds. • Antiviral Medications: If started within 48 hours of
• Diagnostic Tests: In some cases, rapid tests for influenza symptom onset, antiviral drugs like oseltamivir (Tamiflu) or
or streptococcal throat infections, or cultures of nasal or zanamivir (Relenza) can reduce the duration and severity of
throat swabs, may be warranted. symptoms.
• Supportive Care: Similar to the common cold; rest,
2. GENERAL MANAGEMENT STRATEGIES hydration, and analgesics.
A. Symptom Management:
• Rest: Encourage adequate rest to help the body recover. C. Pharyngitis (Sore Throat):
• Hydration: Advise increased fluid intake to help thin • Viral Pharyngitis: Managed with symptomatic treatments.
mucus and prevent dehydration. • Bacterial Pharyngitis (Strep Throat): Requires antibiotics,
• Nutrition: Encourage a balanced diet rich in vitamins and usually penicillin or amoxicillin, as prescribed by a
minerals to support immune function. healthcare provider. A throat culture or rapid strep test
confirms the diagnosis.
B. Medications:
• Analgesics/Antipyretics: Use acetaminophen or ibuprofen D. Sinusitis:
to manage fever, headache, and sore throat.
- Merimel
- 14
NCM 112 OXYGENATION
Bsn 3-D 1st Sem Prelim (2024-2025)

• Acute Sinusitis: Often viral, so supportive care is usually and preventive measures to support recovery and overall
sufficient. Decongestants and nasal saline sprays can help. respiratory health.
• Chronic Sinusitis: May require nasal corticosteroids and,
if bacterial, antibiotics based on culture results. A nursing care plan for respiratory system issues focuses
on addressing the patient's respiratory needs and managing
any related conditions. The plan typically involves
4. PREVENTIVE MEASURES assessment, diagnosis, planning, implementation, and
• Hand Hygiene: Encourage frequent hand washing and use evaluation. Here’s a structured example of a nursing care
of hand sanitizers to prevent the spread of infections. plan for a patient with respiratory issues, such as chronic
• Avoiding Close Contact: Stay away from individuals who obstructive pulmonary disease (COPD) or pneumonia.
are sick and avoid sharing utensils or personal items.
• Vaccination: Recommend annual influenza vaccinations to NURSING CARE PLAN: RESRPIRATORY SYSTEM
reduce the risk of flu.
• Healthy Lifestyle: Promote a healthy diet, regular 1. ASSESSMENT
exercise, and adequate sleep to strengthen the immune A. Subjective Data:
system. • Patient reports shortness of breath, chest pain, or
increased sputum production.
5. FOLLOW-UP AND MONITORING • Patient describes changes in breathing patterns or
• Monitor Symptoms: Regularly assess for any worsening difficulty performing activities of daily living.
symptoms or new signs that might indicate complications.
• Educate the Patient: Provide information on when to seek B. Objective Data:
medical attention (e.g., persistent high fever, difficulty • Vital signs: Increased respiratory rate, oxygen saturation
breathing, or worsening symptoms). levels, and temperature.
• Physical examination: Use of accessory muscles,
6. WHEN TO SEEK MEDICAL ATTENTION abnormal lung sounds (e.g., wheezing, crackles), cyanosis,
Severe Symptoms: High fever, difficulty breathing, chest and signs of respiratory distress.
pain, or confusion. • Diagnostic tests: Abnormal findings on chest X-ray,
• Persistent Symptoms: Symptoms that do not improve arterial blood gases (ABGs), or pulmonary function tests.
with typical treatments or last longer than expected.
• Complications: Signs of complications such as sinus 2. NURSING DIAGNOSES
infections, ear infections, or pneumonia. 1. Impaired Gas Exchange
Related to: Reduced alveolar-capillary membrane surface
7. SPECIAL CONSIDERATIONS area (e.g., pneumonia, COPD).
• Children: Be cautious with medications and dosages. As evidenced by: Decreased oxygen saturation, abnormal
Seek medical advice for young children, especially for ABG results, and patient reports of shortness of breath.
symptoms that are severe or persistent.
• Elderly: Older adults may experience more severe 2. Ineffective Airway Clearance
symptoms and require closer monitoring. Ensure that any Related to: Excessive mucus production,
underlying conditions are managed properly. bronchoconstriction, or inflammation.
As evidenced by: Productive cough, adventitious lung
This management approach ensures a comprehensive sounds, and difficulty clearing secretions.
strategy for addressing upper respiratory infections,
focusing on symptomatic relief, appropriate medication use, 3. Activity Intolerance

- Merimel
- 15
NCM 112 OXYGENATION
Bsn 3-D 1st Sem Prelim (2024-2025)

Related to: Decreased oxygenation and increased work of o Administer oxygen therapy: As prescribed, to maintain
breathing. optimal oxygen saturation levels.
As evidenced by: Fatigue, dyspnea on exertion, and inability o Positioning: Assist the patient in positioning (e.g.,
to complete activities of daily living. Fowler’s position) to maximize lung expansion.

4. Risk for Infection 2. For Ineffective Airway Clearance:

Related to: Impaired mucociliary function, presence of o Encourage deep breathing and coughing exercises: To
secretions, or use of corticosteroids. help clear secretions.
As evidenced by: History of frequent respiratory infections o Assist with chest physiotherapy: Such as postural
or changes in sputum color and consistency. drainage and percussion if indicated.
o Provide medications: Administer bronchodilators,
3. PLANNING mucolytics, and expectorants as prescribed.
A. Goals:
1. Impaired Gas Exchange: 3. For Activity Intolerance:
o The patient will maintain oxygen saturation levels within o Plan and schedule activities: Incorporate rest periods
normal range (e.g., > 92% on room air) by the end of the and gradual increases in activity levels.
shift. o Educate on energy conservation techniques: Teach the
o The patient will demonstrate improved respiratory patient how to balance activity and rest.
function, as evidenced by stable ABG results. o Encourage participation in a pulmonary rehabilitation
program: If available.
2. Ineffective Airway Clearance:
o The patient will exhibit effective airway clearance, as 4. For Risk for Infection:
evidenced by reduced sputum production and clear lung o Implement infection control measures: Follow standard
sounds by the end of the shift. precautions and hand hygiene.
o The patient will demonstrate effective coughing o Monitor for signs of infection: Check for changes in
techniques and use of prescribed medications to manage temperature, sputum, and overall condition.
mucus. o Educate on preventive measures: Teach the patient about
proper hygiene and the importance of vaccinations.
3. Activity Intolerance:
o The patient will report increased tolerance for activities of 5. EVALUATION
daily living with minimal shortness of breath by discharge. A. Evaluate the effectiveness of interventions:
o The patient will engage in and complete a prescribed o Impaired Gas Exchange: Assess if oxygen saturation and
activity program with appropriate rest periods. ABG levels have improved.
overall comfort.
4. Risk for Infection: o Ineffective Airway Clearance: Evaluate the patient's ability
o The patient will remain free from signs of new infections, to clear secretions and improvement in lung sounds. Check
as evidenced by normal temperature and no increase in for a reduction in coughing and sputum production.
sputum production or changes in color. o Activity Intolerance: Monitor the patient's tolerance to
activities and assess if they can perform daily tasks with
4. IMPLEMENTATION less fatigue.
A. Interventions: o Risk for Infection: Review the absence of new infection
1. For Impaired Gas Exchange: signs and overall clinical condition.
o Monitor vital signs: Regularly check respiratory rate,
oxygen saturation, and ABGs.
- Merimel
- 16
NCM 112 OXYGENATION
Bsn 3-D 1st Sem Prelim (2024-2025)

B. Adjust the care plan based on the patient’s progress and

any new symptoms or issues that arise. Continuous
assessment and modification are key to effective
management of respiratory conditions.

By following this structured care plan, nurses can help

manage and improve the respiratory health of their patients,
addressing both acute and chronic conditions effectively.

- Merimel
- 17