SEMINAR

ON
ALTERED PULMONARY
CONDITIONS

SUBMITTED BY SUBMITTED TO

Mrs.M.Saranya, MRS.S.RUBANI,M.Sc.(N),

M.Sc.Nursing, - II Year, HOD Medical Surgical Nursing,

Sacred Heart College of Nursing, Sacred Heart College of Nursing ,

Kumbakonam. Kumbakonam.

SUBMITTED ON
 Altered pulmonary conditions

 Bronchitis
 Bronchial asthma
 Bronchiectasis
 Pneumonia
 Lung abscess, lung tumour
 Pulmonary tuberculosis,
 fibrosis,
 pneumoconiosis etc
 Pleuritis, effusion
 Pneumo, haemo and pyothorax
 Interstitial Lung Disease
 Cystic fibrosis
 Acute and Chronic obstructive pulmonary disease
 Cor pulmonale
 Acute respiratory failure
 Adult respiratory distress syndrome
 Pulmonary embolism
 Pulmonary Hypertension
 BRONCHITIS

 Introduction

 Definition

 Causes

 Pathophysiology

 Clinical features

 Diagnostic Evaluation

 Medical management

 Nursing management

 Prevention

 Complications

 Nursing Diagnosis

Introduction :

It is a condition where the lining of bronchial tubes becomes inflamed or infected .It have
reduced ability to breath in air and oxygen into the lungs.
DEFINITION :
It is an inflammation of the lower airways characterized by excessive secretion of
mucus, hypertrophy of mucous glands, and recurring infection, progressing to narrowing
and obstruction of airflow.

TYPES OF BRONCHITIS :
Acute bronchitis is a common condition that usually develops from a cold or other
respiratory infection and resolves within 7 to 10 days without lasting effects. Acute bronchitis
is often caused by viruses such as a cold or flu. Symptoms will resolve within 2-3 weeks.

Chronic bronchitis is characterized by constant inflammation of the bronchial tubes and is

often associated with chronic lung conditions such as emphysema, asthma, cystic fibrosis,
or COPD

CAUSES / RISK FACTORS :

 Cigarette smoking ( pipe, cigar, other types of tobacco smoking )
 Exposure to other chemical irritants
 Second hand smoke
 Air pollution
 People with weakened immune systems
 People with Gastroesophageal reflex disease ( GERD )
 Exposure to chemical fumes or dusts in occupational area
 Poor ventilation in work place and living environment.
 Low socio economic background
 a genetic condition called alpha-1 antitrypsin deficiency can play a role in causing
chronic bronchitis.
 Age above 45 years
PATHOPHYSIOLOGY :
Cigarette smoking RTI (Respiratory Tract Infection) Environmental pollutants

Inflammation

↑ capillary permeability

fluid/cellular exudation

edema of mucous membrane

hypersecretion of mucus

persistent cough

Signs and Symptoms :

Signs and symptoms of both acute and chronic bronchitis include:

 a persistent cough,

 Production of clear, white, yellow, grey, or green mucus (sputum)

 wheezing

 a low fever and chills

 Inflammation or swelling of the bronchi

 a feeling of tightness in the chest

 a sore throat

 Chest pain or discomfort

 body aches
  breathlessness

 headaches

 a blocked nose and sinus

A person with bronchitis may have a cough that lasts for several weeks or even a few months
if the bronchial tubes take a long time to heal fully.

DIAGNOSTIC EVALUATION :
 History collection
 Physical examination
 Nasal swab
 Chest X-ray
 Sputum test
 CT scan
 Pulmonary Function Test or Spirometer
 Blood investigations.
 Bronchoscopy

MEDICAL MANAGEMENT :
 Antiviral Medications ( Tamiflu , Relenza, Rapivab)
 Bronchodilators

These open the bronchial tubes and may help clear out mucus. Short and long-
acting β-Adrenergic receptor Agonists as well as Anticholinergic help by increasing the
airway lumen, increasing ciliary function and by increasing mucous hydration.

 Glucocorticoids

Reduce inflammation and mucus production. Inhaled corticosteroids reduce

exacerbation and improve quality of life. However, it is administered under medical
supervision and for short periods of time as long-term usage can induce osteoporosis,
diabetes, and hypertension.

 Anti-inflammatory medications ( Corticosteroids )

These can help reduce inflammation that can cause tissue damage.

 Cough suppressants ( Dexomethorphan , Benzonatate)

These loosen or thin mucus in the airways, making it easier to cough up

sputum.
  Oxygen therapy
In severe cases, a person may need supplemental oxygen to ease their
breathing.
 Antibiotics

These are effective for bacterial infections, but not for viral infections. They
may also prevent secondary infections.is not indicated in the treatment of chronic
bronchitis however macrolide therapy has been shown to have anti-inflammatory
property and hence may have a role in the treatment of chronic bronchitis.

 Phosphodiesterase-4 inhibitors

Decrease inflammation and promote airway smooth muscle relaxation by

preventing the hydrolysis of cyclic adenosine monophosphate a substance when
degraded leads to the release of inflammatory mediators.

NURSING MANAGEMENT :
Nursing management focuses on alleviating the symptoms and helping
patients clear pulmonary secretions.
 Encourage mobilization of secretion through ambulation, coughing, and deep breathing.
 Ensure adequate fluid intake to liquefy secretions and prevent dehydration caused by
fever and tachypnea.
 Encourage rest, avoidance of bronchial irritant, and a good diet to facilitate recovery.
 Instruct the patient to complete the full course of prescribed antibiotics and explain the
effect of meals on drug absorption.
 Caution the patient on using over-the-counter cough suppressants, antihistamines, and
decongestants, which may cause drying and retention of secretions. However, cough
preparations containing the mucolytic guaifenesin may be appropriate.
 Advise the patient that a dry cough may persist after bronchitis because of irritation of
airways. Suggest avoiding dry environments and using a humidifier at bedside.
Encourage smoking cessation.
 Teach the patient to recognize and immediately report early signs and symptoms of acute
bronchitis.
PREVENTION :
 Avoid tobacco smoke and exposure to second hand smoke
  Quitting smoking
 Avoiding people who are sick with colds or the flu Getting a yearly flu vaccine
 Getting a pneumonia vaccine (especially for those over 60 years of age)
 Washing hands regularly
 Avoiding cold, damp locations or areas with a lot of air pollution
 Wearing a mask around people who are coughing and sneezing

COMPLICATIONS :

 Chronic bronchitis
 Asthma
 Bronchiectasis
 Cystic fibrosis
 Tuberculosis
 Sinusitis
 Dyspnea, sometimes severe
 Respiratory failure
 Pneumonia
 Cor pulmonale
 Pneumothorax
 Polycythemia
 COPD
 Emphysema
 Chronic advancement of the disease and
 High mortality rate

NURSING DIAGNOSIS :
Ineffective Airway Clearance
Interventions Rationale
 Position head midline with flexion on  To gain or maintain open airway
appropriate for age/condition
 To decrease pressure on the
 Elevate HOB
diaphragm and enhancing drainage
 Observe Signs and Symptoms of
 infections  To identify infectious process
 Auscultate breath sounds & assess air  To ascertain status & note progress
movement
 Instruct the patient to increase fluid  To help to liquefy secretions.
intake
 Demonstrate effective coughing and  To maximize effort
deep-breathing techniques.
 Keep back dry  To prevent further complications

 Turn the patient q 2 hours  To prevent possible aspirations

 Demonstrate chest physiotherapy,

such as bronchial tapping when in  These techniques will prevent

cough, proper postural drainage. possible aspirations and prevent any

 Administer bronchodilators if untoward complications

prescribed.  More aggressive measures to

maintain airway patency.

Ineffective Breathing Pattern

Interventions Rationale
 Place patient in semi-fowlers position  To have a maximum lung expansion
 Increase fluid intake as applicable  To liquefy secretions
 Keep patient back dry  To avoid stasis of secretions and
avoid further complication
 Change position every 2 hours  To facilitate secretion movement and
drainage
 Perform CPT  To loosen secretion
 Place a pillow when the client is  To provide adequate lung expansion
sleeping while sleeping.
 Instruct how to splint the chest wall  To promote physiological ease of
with a pillow for comfort during maximal inspiration
coughing and elevation of head over
 body as appropriate
 Maintain a patent airway, suctioning  To remove secretions that obstructs
of secretions may be done as ordered the airway
 Provide respiratory support. Oxygen
inhalation is provided per doctor’s  To aid in relieving patient from
order dyspnea
 Administer prescribed cough
suppressants and analgesics and be  To promote deeper respirations and
cautious, however, because opioids cough
may depress respirations more than
desired.

Impaired Gas Exchange

Interventions Rationale
 Monitor level of consciousness or  Restlessness,anxiety, confusion,
mental status somnolence are common manifestation
of hypoxia and hypoxemia.
 Assist the client into the High-  The upright position allows full lung
Fowlers position excursion and enhances air exchange
 To help liquefy secretions
 Increase patient’s fluid intake
 Encourage expectoration  To eliminate thick, tenacious, copious
secretions which contribute for the
impairment of gas exchange.
 Encourage frequent position  To promote drainage of secretions
changes
 Encourage adequate rest & limit  Helps limit oxygen needs/consumption
activities to within client tolerance
 Promote calm/restful environments  To correct/improve existing
 Administer supplemental oxygen deficiencies
judiciously as indicated
 Administer meds as indicated such  May correct or prevent worsening of
as bronchodilators hypoxia.
  To treat the underlying condition

Sleep Pattern Disturbance

Interventions Rationale
 Monitor level of consciousness or  Restlessness, anxiety,confusion,
mental status somnolence are common
manifestation of hypoxia and
hypoxemia.
 Promote comfort measures such as  To provide non pharmacologic
back rub and change in position as management
necessary
 Observe provision of emotional  Lack of knowledge and problems,
support relationships may create tension.
Interfering with sleep routines
based on adult schedules may not
meet child’s needs

 Provide quiet environment.  To promote an environment

conducive to sleep.
 Increase patient’s fluid intake
 Encourage expectoration  To help liquefy secretions
 To eliminate thick, tenacious,
copious secretions which
 Limit the fluid intake in evening if contribute for the DOB
nocturia is a problem
 Obtain feedback from SO regarding  To reduce need for nighttime
usual bedtime, rituals/routines elimination
 Provide safety for patient sleep time
safety  To determine usual sleep patterns
 Recommend mid morning nap if one & provide comparative baseline
required
 To promote comfort/safety
  Administer pain medication as ordered.

 Napping esp. in the afternoon can

disrupt normal sleep pattern

 To relieve discomfort and take

maximum advantage of sedative
effect

Risk for Spread of Infection

Interventions Rationale
 Review importance of breathing  These activities promote mobilization
exercises, effective cough, frequent and expectoration of secretions to
position changes, and adequate fluid reduce the risk of developing
intake pulmonary infection.

 To facilitate secretion movement and

 Turn the patient q 2 hours
drainage

 Encourage increase fluid intake  To liquefy secretions

 Stress the importance of handwashing  Handwashing is the primary defense

to SO’s against the spread of infection

 Teach the SO’s how to care for and  Water in respiratory equipment is a
clean respiratory equipment common source of bacterial growth

 Teach the SO’s the manifestations of  Early recognition of manifestations

pulmonary infections (change in color can lead to a rapid diagnosis.
of sputum, fever, chills) , self-care
and when to call the physician
  Recommend rinsing mouth with
water
 Administer antimicrobial such as  To prevent risk of oral candidiasis.

cefuroxime as indicated.
 Given prophylactically to reduce any
possible complications

Deficient Knowledge
Interventions Rationale
 Provide accurate information about  Ensure the information provided is
the disease process, prognosis, and correct and delivered in easy-to-
treatment regimen. understand language. Provide
brochures and reading materials as
appropriate.
 Reinforce learning through the  Frequent and regular education
provision of repetitive and follow-up sessions can help improve medication
sessions. and self-care management outcomes
for those who have chronic conditions
like chronic bronchitis and COPD.
 Smoking triggers airway
inflammation.
 Do not smoke or inhale toxins.  Hand washing is the best way to
 Wash hands and wear a mask. prevent the introduction of viruses.
Those with chronic respiratory
conditions should consider wearing a
mask in public places.
 older adults diagnosed with bronchitis
can benefit from the support they get
from family members. Family
 Include family members in patient members play an essential role in
education sessions. patient care, including decision-
making, assisting in healthcare
 interventions, and improving
the patient’s safety and quality of life.

BRONCHIAL ASTHMA

INTRODUCTION:

Asthma, also called bronchial asthma, is a disease that affects the lungs. It’s a chronic
condition, meaning it doesn’t go away and needs medical management. Asthma affects more
than 25 million people. This total includes more than 5 million children. Asthma can be life-
threatening if don’t get treatment. Asthma occurs because of inflammation and mucus in the
lining of the airways. During an attack, this commonly causes a wheezing or whistling sound
when breathing but can cause other symptoms. To understand asthma, it’s necessary to
understand a little about what happens during breathe. Normally, with every breath we take
in, air goes through the nose or mouth, down into the throat, and into the airways, eventually
making it to the lungs.
DEFINITION :
Asthma is a chronic condition, which alters the airways (bronchial tubes).
The bronchial tubes function by permitting the entry and exit of air into the lungs. This
syndrome is characterized by inflammation in airways, causing difficulty in breathing.

ETIOLOGY:
Predisposing factors for asthma

Host risk factors:

 Genetics
 Studies of families show heritability of asthma.
 Multiple genes and environmental influence complicate genetic studies.
 Atopy
 Genetic predisposition to produce immunoglobulin E (IgE ) antibodies on allergen
exposure
 Strong risk factor for asthma
 Perinatal factors (increased asthma risk)
 Prematurity at birth
 Neonatal or early abnormality of lung function
 Sex
 Asthma is more common in boys before puberty
 1:1 ratio in adulthood, with women affected more by age 40
 Unclear if sex hormones are linked to development of asthma
 Obesity
 ↑ risk of asthma

Maternal factors

 Decreased risk of asthma:

 Increasing maternal age at delivery (> 30 years)
 Breastfeeding
 ↓ wheezing in the first 2 years of life
 Increased risk of asthma:
 Maternal diet: low in vitamin D and omega-3 polyunsaturated fatty acid
 Poorly controlled maternal asthma
 Prenatal exposure to maternal smoking

Environmental factors

 Respiratory infections early in life:

 40% have asthma/wheezing later in life.
 Commonly from respiratory syncytial virus, human rhinovirus
 Pollution: living close to a major road and ↑ nitrogen dioxide → ↑ asthma
 Smoking(including secondhand smoke)
 Occupational exposure (fires, pesticides, industrial agents)
 Allergens (fungi, dust mite, cockroach allergen)
 Early exposure to pet allergens:
 Varied results
 Protects by decreasing sensitization to pet allergens
 In some, asthma develops, possibly influenced by other exposures (tobacco, pollution).

TRIGGERING FACTORS:
In established asthma, different triggers may exacerbate the symptoms. These include the
following:

Environmental and drug-induced:

Allergens
Cold air
Paints and fumes
Irritant gasses
Air pollution
Drugs (beta blockers and aspirin)

Endocrine:

Premenstrual hormones
Thyrotoxicosis
Hypothyroidism
Behavioral and psychological:

Exercise
Hyperventilation
Stress

Other triggers:

Upper respiratory tract infections

Gastroesophageal reflux

PATHOPHYSIOLOGY :
SIGNS AND SYMPTOMS :

 Recurrent wheezing
 Dyspnea: chest tightness/heavy weight on the chest
 Cough:
 Can be dry or productive of sputum
 Worse at night and in the early morning hours
 Episodic, can resolve spontaneously or with treatment
 Symptoms occur with characteristic triggers (i.e., allergens, cold air).
 Asymptomatic when under control
 When symptomatic:
 Tachypnea, tachycardia
 Expiratory ± inspiratory wheezingand rhonchi
 Prolonged expiratory phase of respiration
 CLASSIFICATION OF ASTHMA BASED ON SEVERITY :

DIAGNOSIS :

Pulmonary function tests

Spirometry:

 Maximal inhalation followed by rapid forceful exhalation (at least 6 seconds)

 Measures:
1. FEV1 (forced expiratory volume in 1 second)
2. FVC (forced vital capacity or the maximal volume exhaled with maximally forced effort)
 ↓ FEV1 and FEV1/FVC ratio < 0.70 (suggests airway obstruction)

Bronchodilator response:

 Nebulized or 2–4 puffs of bronchodilator (e.g., albuterol) given, then spirometry rechecked
after 15 minutes
 Increase in FEV1 by > 12% and 200 mL (bronchodilator responsiveness)
Peak expiratory flow (PEF):

 Maximal inhalation, then fast forceful exhalation (< 2 seconds) into peak flowmeter
 A single peak flow is obtained during symptoms.
 Results compared with average normal values (based on height and age)
 Post-bronchodilator administration, improvement of > 20% suggests reversible airway
obstruction(favors diagnosis of asthma)
 Used more for monitoring than for diagnosis

Bronchoprovocation testing:

 A stimulus (methacholine, exercise, histamine, inhaled mannitol) is tried,

to trigger bronchoconstriction.
 ≥ 20% reduction in FEV1 with challenge/testing (airway hyperresponsiveness)

Impulse oscillometry (IOS):

 For children < 5 years old or those who cannot perform spirometry
 Passive measurement of lung mechanics
 Requires minimal patient cooperation, but not available to many clinicians

Chest X-ray

 Excludes other diagnosis (pneumothorax or pneumonia in exacerbations)

 Normal in mild asthma
 May show hyperinflation in severe asthma (flattened diaphragm, wide intercostal spaces)
 Indicated for atypical presentation of asthma (fever, crackles, hypoxemia)

Additional tests

 No blood test can confirm diagnosis of asthma.

 Complete blood count: may show eosinophilia(which suggests atopic asthma)
 IgE level:
1. Moderate-to-severe asthma
2. When anti-IgE monoclonal antibody treatment is considered
 Allergy tests: may determine allergic triggers and help provide allergen avoidance
measures
 Alpha-1 antitrypsin level: detects alpha-1 antitrypsin deficiency (for patients with
persistent airway obstruction)
 Biomarkers:
 Sputum eosinophils: can be used as biomarker for T2-high asthma
 Periostin: biomarker for eosinophilic inflammation despite use of corticosteroids

Sweat chloride test:

 In children with persistent respiratory symptoms, to rule out cystic fibrosis

 Low threshold in performing test due to lifelong implications of disease

Arterial blood gas(in severe asthma exacerbation):

1. Obtain when oxygen saturation of < 94%, no bronchodilator response, mental status
change(s)
2. Initial finding(s): hypoxia (reduced oxygen), hypocarbia (due to hyperventilation),
↑ pH4
3. Respiratory failure: hypoxia, hypercarbia, ↓ pH(respiratory acidosis)

MEDICAL MANAGEMENT :

There are two classes of medications—long- acting control and quick-relief medications— as
well as combination products.
Long-acting control medications
 Inhaled corticosteroid medications- Fluticasone
 Leuketrine modifiers- Montelukast
 Long term beta agonists- Salmeterol
 Methylxanthines-Theophylline
 Combination inhalers- Fluticasone & Salmeterol
 Cromolyn sodium- omalizumab
Quick Relief Medications :

 Short-acting beta2-adrenergic agonists- Albuterol

 Anticholinergics – Ipratropium bromide
 Oral & IV Corticosteroids: prednisolone
 Leukotriene modifiers inhibitors/antileukotrienes
 Methylxanthines

Non Pharmalogical Interventions :

 Oxygen therapy
 Postural drainage & chest physiotherapy
 Coughing & deep breathing exercises
 Relaxation techniques
 Acupuncture

NURSING MANAGEMENT :

Assessment of a patient with asthma includes the following:

 Assess the patient’s respiratory status by monitoring the severity of the symptoms.
 Assess for breath sounds.
 Assess the patient’s peak flow.
 Assess the level of oxygen saturation through the pulse oximeter.
 Monitor the patient’s vital signs.
 Maintenance of airway patency.
 Expectoration or clearance of secretions.
 Absence /reduction of congestion with breath sound clear, noiseless respirations, and
improved oxygen exchange.
 Verbalized understanding of causes and therapeutic management regimen.
 Demonstrated behaviors to improve or maintain clear airway.
 Identified potential complications and how to initiate appropriate preventive or
corrective actions.
NURSING DIAGNOSIS :

 Ineffective airway clearance related to increased production of mucus and

bronchospasm.
 Impaired gas exchange related to altered delivery of inspired O2.
 Anxiety related to perceived threat of death.

PREVENTION :

 Avoiding triggers. Steer clear of chemicals, smells, or products that have caused
breathing problems in the past.

 Reducing exposure to allergens. If have identified allergens, such as dust or mold,

that trigger an asthma attack, avoid them if possible.

 Getting allergy shots. Allergen immunotherapy is a type of treatment that may help
alter the immune system. With routine shots, The body may become less sensitive to
any triggers the encounter.

 Taking preventive medication. The doctor may prescribe medication for to take on
a daily basis. This medication may be used in addition to the use in case of an
emergency.

 Eating a healthier diet. Eating a healthy, balanced diet can help improve the overall
health.

 Maintaining a moderate weight. Asthma tends to be worse in people with

overweight and obesity. Losing weight is healthy for the heart, the joints, and the
lungs.

 Quitting smoking, if you smoke. Irritants such as cigarette smoke can trigger asthma
and increase the risk for COPD.

 Exercising regularly. Activity can trigger an asthma attack, but regular exercise may
actually help reduce the risk of breathing problems.

 Managing stress. Stress can be a trigger for asthma symptoms. Stress can also make
stopping an asthma attack more difficult.
COMPLICATIONS :

Complications for asthma include the following:

 Status asthmaticus. Airway obstruction in status asthmaticus often results

in hypoxemia.
 Respiratory failure. Asthma, if left untreated, progresses to respiratory failure.
 Pneumonia. Mucus that pools in the lungs and becomes infected can lead to the
development of pneumonia.
 BRONCHIECTASIS

INTRODUCTION :

The term bronchiectasis simply means damaged bronchial tubes (airways). Healthy
airways allow the air that you breathe in to reach your lungs. Sometimes they become
damaged in places, with enlargement and irregularity of the normally smooth tubes and filled
with extra mucus. . If the airway becomes blocked after accidentally inhaling material into
the lungs this can also cause permanent damage. There are a number of different causes of
bronchiectasis. In many people the damages results from serious chest infections, often many
years previously. Pneumonia, tuberculosis, whooping cough and severe measles can all result
in bronchiectasis. This results in irreversible damage to the lungs, which allows mucus to
pool in the damaged airways. Infection in these breathing tubes contributes to ongoing
inflammation in the airways. It may affect many areas of the lung, or it may appear in only
one or two areas.

DEFINITION :

 Bronchiectasis is a chronic, irreversible dilation of the bronchi and the bronchioles

which result in retention of secretions ,obstruction and eventual alveolar collapse. It is
usually localized in a lobe or segment of a lung.
CAUSES :

Bronchiectasis may be caused by a variety of conditions including

1. Airway obstruction

2. Diffuse airway injury

3. Pulmonary infections and obstruction of the bronchus or complications of long-term

pulmonary infections

4. Genetic disorders (eg, cystic fibrosis)

5. Abnormal host defense (eg, ciliary dyskinesia or humoral immunodeficiency)

6. Idiopathic causes

SIGNS AND SYMPTOMS :

 coughing with blood stains

 night sweats and chills
 fatigue
 weight loss
 chest pain
 wheezing or a whistling sound when you breathe
 frequent respiratory infections

DIAGNOSTIC EVALUATION :

 Prolonged history of productive cough with sputum

 Blood tests
 Sputum culture
 Bronchoscopy
 CT Scan
 Lung function test
 Chest X-ray
MEDICAL MANAGEMENT :

Expectorants:

These are medications that thin mucus and help to cough it out. These are available
over-the-counter or by prescription.

Antibiotics :

Antibiotics can treat infections caused by bacteria. physicians often prescribe inhaled
antibiotics for bronchiectasis.

Macrolides :

Macrolides are drugs that treat infections and inflammation at the same time.

Postural Drainage :

Postural draining and chest percussion therapy can help loosen and remove mucus.
Breathing exercises can help open up the airways.

Antimicrobial therapy:
Antimicrobial therapy based on the results of sensitivity studies on organism cultured
from sputum is used to control infection.
Bronchodilator:.
Bronchodilators, which may be prescribed for patients who have reactive airway
disease, may also assist with secretion management.

SURGICAL MANAGEMENT :
Surgical intervention may be indicates for patients who continue to expectorate large
amounts of sputum and have repeated bouts of pneumonia.

 Segmental resection. The diseased segment of a lobe is removed.

 Lobectomy. The diseased lobe is removed.
 Pneumonectomy. The entire diseased lung segment is removed, but this rarely
happens.
NURSING MANAGEMENT :
Nursing management of patients with bronchiectasis focuses on alleviating and helping
patients clear Pulmonary secretions.
 Patients teaching targeted mainly smoking cessation and breathing exercises
 Patients and family members should taught to perform the PD and avoid expose to
people with upper respiratory tract infections.
 The patient should taught early signs and symptoms of respiratory infections and
progression of the disorder, so that appropriate treatment can be implemented
promptly.
 The presence of large amount of mucus may decrease the patients appetite and
results in an inadequate dietary intake, therefore the patients nutritional status
assessed and strategies to important ensure to adequate nutrition.
 Maintaining the patient hydration status is major important encourage patient to take
fluid at least 3 liters per day unless contraindicated.
 Assist in PD and CPT
 Encourage patient to perform deep breathing and effective coughing techniques
 Provide adequate rest.
The focus of documentation for patients with bronchiectasis include:

 Respiratory rate, character of breath sounds, and presence of cyanosis.

 Frequency, amount, and appearance of secretions.
 Character of cough.
 Relevant history of the problem.
 Respiratory pattern.
 Use of respiratory aids.
 Level of activity.
 Vital signs before, during, and after the activity.
 Plan of care.
 Teaching plan.
 Client’s responses to treatment, teaching, and actions performed.
 Attainment or progress towards desired outcomes.
 Modifications to plan of care.
 Long term needs
NURSING DIAGNOSIS :

The major nursing diagnoses for a patient with bronchiectasis are:

 Impaired gas exchange related to ventilation-perfusion imbalance.

 Ineffective airway clearance related to increased mucus production.
 Ineffective breathing pattern related to mucus and airway irritants.
 Activity intolerance related to hypoxemia and ineffective breathing patterns.

COMPLICATIONS :

Damage caused by severe bronchiectasis can lead to life threatening complications

including :

 Respiratory Failure
 Severe Bleeding
 Antibiotic Resistance
 Atelectasis
 Empyema
 Pneumonia
 PNEUMONIA

INTRODUCTION :

Pneumonia is a lower respiratory lung infection that causes inflammation in one or

both lungs. Air sacs in your lungs called alveoli can then fill up with fluid or pus, causing flu-
like symptoms that can persist for weeks or cause rapid deterioration of breathing leading to
hospitalization. Pneumonia doesn’t respond to over-the-counter cold and sinus medicines.
Pneumonia comes in different forms and is caused primarily by bacteria or viruses, which are
contagious, and less commonly by fungi or parasites.
DEFINITION :

Pneumonia is one of the most common respiratory problems and it affects all stages
of life.

 Pneumonia is an inflammation of the lung parenchyma caused by various

microorganisms, including bacteria, mycobacteria, fungi, and viruses.
 Pneumonitis is a more general term that describes the inflammatory process in the
lung tissue that may predispose and place the patient at risk for microbial invasion.

CAUSES :
Each type of pneumonia is caused by different and several factors
Community-Acquired Pneumonia

 Streptococcus pneumoniae. This is the leading cause of CAP in people younger than
60 years of age without comorbidity and in those 60 years and older with
comorbidity.
 Haemophilus influenzae. This causes a type of CAP that frequently
affects elderly people and those with comorbid illnesses.
 Mycoplasma pneumoniae.
Hospital-Acquired Pneumonia

 Staphylococcus aureus.
Staphylococcus pneumonia occurs through inhalation of the organism.
 Impaired host defenses.
When the defenses of the body are down, several pathogens may invade the
body.
 Comorbid conditions.
There are several conditions that lower the immune system, causing bacteria to
pool in the lungs and eventually result in pneumonia.
 Supine positioning.
When the patient stays in a prolonged supine position, fluid in the lungs pools
down and stays stagnant, making it a breeding place for bacteria.
 Prolonged hospitalization.
 The risk for hospital infections or nosocomial infections increases the longer
the patient stays in the hospital.

CLASSIFICATION:
Pneumonia is classified into four: community-acquired pneumonia (CAP) and
hospital-acquired pneumonia (HAP), pneumonia in the immuno compromised host,
and aspiration pneumonia.
Community-Acquired Pneumonia

 CAP occurs either in the community setting or within the first 48 hours after
hospitalization.
 The causative agents for CAP that needs hospitalization
include streptococcus pneumoniae, H. influenza, Legionella, and Pseudomonas
aeruginosa.
 Only in 50% of the cases does the specific etiologic agent become identified.
 Pneumonia is the most common cause of CAP in people younger than 60 years of age.
 Viruses are the most common cause of pneumonia in infants and children.
Hospital-Acquired Pneumonia

 HAP is also called nosocomial pneumonia and is defined as the onset of pneumonia
symptoms more than 48 hours after admission in patients with no evidence of
infection at the time of admission.
 HAP is the most lethal nosocomial infection and the leading cause of death in
patients with such infections.
 Common microorganisms that are responsible for HAP include Enterobacter
species, Escherichia coli, influenza, Klebsiella species, Proteus, Serratia
marcescens, S. aureus, and S. pneumonia.
 The usual presentation of HAP is a new pulmonary infiltrate on chest x-
ray combined with evidence of infection.

Pneumonia in the Immunocompromised Host

 Pneumonia in immunocompromised hosts includes Pneumocystis pneumonia, fungal

pneumonias and Mycobacterium tuberculosis.
  Patients who are immunocompromised commonly develop pneumonia from
organisms of low virulence.
 Pneumonia in immunocompromised hosts may be caused by the organisms also
observe in HAP and CAP.
Aspiration Pneumonia

 Aspiration pneumonia refers to the pulmonary consequences resulting from entry of

endogenous or exogenous substances into the lower airway.
 The most common form of aspiration pneumonia is a bacterial infection from
aspiration of bacteria that normally reside in the upper airways.
 Aspiration pneumonia may occur in the community or hospital setting.
 Common pathogens are S. pneumonia, H.influenza, and S. aureus.
SIGNS AND SYMPTOMS :

Signs and symptoms of pneumonia can vary from mild to severe

 Cough
 Fever and chills
 Rapid, shallow breathing or shortness of breath
 Sharp or stabbing chest pain that worsens when you cough or breathe deeply
 Fatigue
 Loss of appetite
 Nausea and vomiting, especially in small children
 Blueness of the lips
 Confusion, particularly in older people
DIAGNOSTIC EVALUATION :

The following are assessments and diagnostic tests that could determine pneumonia.

 History taking. The diagnosis of pneumonia is made through history taking,

particularly a recent respiratory tract infection.
 Physical examination. Mainly, the number of breaths per minute and breath sounds
is assessed during physical examination.
 Chest x-ray. Identifies structural distribution (e.g., lobar, bronchial); may also reveal
multiple abscesses/infiltrates, empyema (staphylococcus); scattered or localized
infiltration (bacterial); or diffuse/extensive nodular infiltrates (more often viral). In
mycoplasmal pneumonia, chest x-ray may be clear.
 Fiberoptic bronchoscopy. May be both diagnostic (qualitative cultures) and
therapeutic (re-expansion of lung segment).
 ABGs/pulse oximetry. Abnormalities may be present, depending on extent of lung
involvement and underlying lung disease.
 Gram stain/cultures. Sputum collection; needle aspiration of empyema, pleural, and
transtracheal or transthoracic fluids; lung biopsies and blood cultures may be done to
recover causative organism. More than one type of organism may be present;
common bacteria include Diplococcus pneumoniae, Staphylococcus aureus, a-
hemolytic streptococcus, Haemophilus influenzae; cytomegalovirus (CMV). Note:
Sputum cultures may not identify all offending organisms. Blood cultures may show
transient bacteremia.
 CBC. Leukocytosis usually present, although a low white blood cell (WBC) count
may be present in viral infection, immunosuppressed conditions such as AIDS, and
overwhelming bacterial pneumonia. Erythrocyte sedimentation rate (ESR) is elevated.
 Serologic studies, e.g., viral or Legionella titers, cold agglutinins. Assist in
differential diagnosis of specific organism.
 Pulmonary function studies. Volumes may be decreased (congestion and alveolar
collapse); airway pressure may be increased and compliance decreased. Shunting is
present (hypoxemia).
 Electrolytes. Sodium and chloride levels may be low.
 Bilirubin. May be increased.
  Percutaneous aspiration/open biopsy of lung tissues. May reveal typical
intranuclear and cytoplasmic inclusions (CMV), characteristic giant cells (rubeola).

MEDICAL MANAGEMENT :

 Antibiotics. These medicines are used to treat bacterial pneumonia. It may take time
to identify the type of bacteria causing the pneumonia and to choose the best
antibiotic to treat it. They can’t treat a virus but a provider may prescribe them if you
have a bacterial infection at the same time as a virus.
 Antifungal : Antifungal can treat pneumonia caused by a fungal infection.
 Antiviral Medications : Viral pneumonia usually isn’t treated with medication and
can go away on its own. A provider may prescribe antivirals such
as oseltamivir (Tamiflu), zanamivir (Relenza) or peramivir (Rapivab) to reduce the
symptoms
 Cough medicine. This medicine may be used to calm the cough so that they can rest.
Because coughing helps loosen and move fluid from the lungs, it's a good idea not to

eliminate the cough completely.

 Oxygen Therapy
 IV Fluids - Fluids delivered directly to your vein (IV) treat or prevent dehydration.
 Breathing Exercises - These treatments to help loosen mucus and help to breathe.
 Fever reducers/pain relievers. These include drugs such as aspirin, ibuprofen
(Advil, Motrin IB, others) and acetaminophen (Tylenol, others).

NURSING MANAGEMENT :
 Maintain a patent airway and adequate oxygenation.
 Obtain sputum specimens as needed.
 Use suction if the patient can’t produce a specimen.
 Perform chest physiotherapy.
 Provide a high calorie, high protein diet of soft foods.
 To prevent aspiration during nasogastric tube feedings, check the position of tube, and
administer feedings slowly.
 Provide a quiet, calm environment, with frequent rest periods.
  Explain the importance of respiratory exercise such as spirometry, deep breathing,
effective coughing, and chest physical therapy etc.
 Monitor the patient’s ABG levels, especially if he’s hypoxic.
 Assess the patient’s respiratory status, auscultate breath sounds at least every 4 hours

NURSING DIAGNOSIS :
 Ineffective airway clearance related to copious tracheobronchial secretions
 Activity intolerance related to impaired respiratory function
 Risk for deficient fluid volume related to fever and dyspnea
 Imbalance Nutrition less than body requirements
 Deficient knowledge about the treatment regimen and preventive health measure

NURSING INTERVENTIONS :
1. Improve airway patency.
2. Rest to conserve energy.
3. Maintenance of proper fluid volume.
4. Maintenance of adequate nutrition.
5. Understanding of treatment protocol and preventive measures.
6. Absence of complications.

PREVENTION:

It is better to prevent the occurrence of pneumonia instead of treating the disease itself.
Here are several ways that can help prevent pneumonia.

COMPLICATIONS :

 Empyema
 Lung Abscess.
 Bronchiolitis Obliterans.
 Acute Respiratory Distress Syndrome (ARDS).
 Sepsis.
 Bacterimia.
 Hypotension and shock, especially in gram negative bacterial disease, particularly in
elderly patients.
 Atelectasis.
 Pleural effusion.
 Pericarditis.
 LUNG ABSCESS

A lung abscess is a localized necrotic lesion of the lung parenchyma containing purulent
material that collapses and forms a cavity. It is generally caused by aspiration of anaerobic
bacteria.
An acute or ongoing lung infection known as a lung abscess is characterized by a localized
pus collection, swelling, and tissue degeneration.

Cause of Lungs Abscess

 Aspiration
o Aspiration is the term used to describe the unintentional inhalation of material into the
airway and lungs from the mouth or throat.
Patients who are unconscious or only partially conscious as a result of seizures,
alcoholism, or drug abuse experience it.
 Bronchial Obstruction
o The two branches of the windpipe that enter the lungs are known as bronchi. if they
are obstructed by foreign objects, cancerous tumors, or swollen tissue.
 Spread of Infection
o The spread of other infections from open chest wounds in the liver abdominal cavity
can also result in lung abscesses.
o Lung abscesses in AIDS patients are extremely uncommon.
Pathophysiology

The lung abscess most usually develops as a side effect of aspiration pneumonia brought on
by oral anaerobes. Patients at risk for aspiration and frequently suffering from periodontal
disease are those who develop lung abscesses. Infection begins when a bacterial inoculum
from the gingival crevice enters the lower airways and is not eliminated by the patient's host
defense system. As a result, aspiration pneumonitis develops, and 7–14 days later, tissue
necrosis progresses to lung abscess formation.

Symptoms
 An adult will usually have the moderate fever, chills , chest pain and general
weakness.
 Children may or may not have chest pain but usually, suffer weight loss and high
fever.
 Patients will cough up foul or musty smelling sputum,
 A cough with blood.

Diagnosis
 History taking,
 Sputum test,
 Bronchoscopy,
 Chest x-ray,
 CT scan,
 MRI.

Treatment
 Antibiotic,
 Oxygen therapy,
 Surgery.

PHARMACOLOGIC THERAPY

 Intravenous antimicrobial therapy depends on the results of the sputum culture and
sensitivity and is administered for an ex-tended period. Penicillin G or clindamycin (
Cleocin ) is the medication of choice, followed by penicillin with metronidazole. Large
 intravenous doses are generally required because the anti-biotic must penetrate the
necrotic tissue and the fluid in the abscess. The intravenous dose is continued until
there is evidence of symptom improvement.
 Long-term therapy with oral antibiotics replaces intravenous therapy after the patient
shows signs of improvement (usually 3 to 5 days). Improvement is demonstrated by
normal temperature, decreased white blood cell count, and improvement on the chest
x-ray (resolution of surrounding infiltrate, reduction in cavity size, absence of fluid).
Oral administration of antibiotic therapy is continued for an additional 4 to 8 weeks. If
treatment stops too soon, a relapse may occur.

Nursing Management
 Ensure peace and enough sleep.
 Antibiotic administration,
 Proper dietary support,
 Offer emotional assistance,
 Good drainage posture,
 Encourage the patient to drink more fluids to help the lung secretions loosen up.
 Encourage the patient to have a high-calorie, high-protein diet.
 Encourage the patient to finish the entire course of antibiotics.
 When recommended, get the patient ready for surgery if necessary.
 PULMONARY TUBERCULOSIS

DEFINITION :
Tuberculosis (TB) or known as the White Plague during the 19thcentury, has inflicted
the human race ever since. It is described as a chronic infectious disease caused by an
organism called Mycobacterium tuberculosis through droplet transmission, like coughing,
sneezing, or if the person inhales the infected droplet.It can be considered as primary or
secondary infection depending on recovery of the client from the communicable infection. It
is a reportable communicable disease and a repeated exposure to it causes a person to acquire
it.
STAGES :
According to a study conducted by Knechel, the progression of tuberculosis has several
stages.

1. Latent Tuberculosis – It is the stage of infection when the person who had been
exposed to the M. tuberculosis nuclei does not manifest signs and symptoms of the
disease and do not have the capacity to infect other people. The nuclei just persist in the
system in its necrotic form which could stay for a long time, not until that
immunosuppression or a certain factor triggers it to become its virulent form.
2. Primary Pulmonary Tuberculosis – Since the most immediate location of
pathogenesis of the organism is in the lungs, primary activation of disease in the
pulmonary cavity is considered. It is usually asymptomatic and only identified through
significant diagnostic examinations. Only the presence of lymphadenopathy is
something that is indicative for its infection.
3. Primary Progressive Tuberculosis – It is the stage of the disease process when it is
already considered as active. Clinical manifestations are evident and the client may
reveal positive in sputum examination for presence of the organism. Sometimes, he or
she may manifest cough with purulent sputum and some pleuritic chest pains because of
inflammation in the parenchymal walls.
4. Extra pulmonary Tuberculosis – It is when tuberculosis extends its infection to other
parts of the aside from the pulmonary cavity. The most fatal location is the central
nervous system and its infection to the bloodstream. Other locations may include the
lymphatic system, the bones and joints and at times the genitourinary system.
Tuberculosis(TB) Pathophysiology
CAUSES

Pulmonary TB is caused by the bacterium Mycobacterium tuberculosis (M tuberculosis). TB

is contagious. This means the bacteria may spread from an infected person to someone else.
You can get TB by breathing in air droplets from a cough or sneeze of an infected person.
The resulting lung infection is called primary TB.
Most people recover from primary TB infection without further evidence of the disease. The
infection may stay inactive (dormant) for years. In some people, it becomes active again
(reactivates).
Most people who develop symptoms of a TB infection first became infected in the past. In
some cases, the disease becomes active within weeks after the primary infection.

The following people are at higher risk of active TB or reactivation of TB:

 Older adults

 Infants

 People with weakened immune systems, for example due

to HIV/AIDS, chemotherapy, diabetes, or medicines that weaken the immune system
risk for catching TB increases

 Are around people who have TB

 Live in crowded or unclean living conditions

 Have poor nutrition

The following factors can increase the rate of TB infection in a population:

 Increase in HIV infections

 Increase in number of homeless people (poor environment and nutrition)

 Presence of drug-resistant strains of TB

PATHOPHYSIOLOGY
CLINICAL MANIFESTATIONS OF TUBERCULOSIS

 Easy fatigability
 Anorexia or loss of appetite
 Weight loss and body wasting
 Persistent, long term low- grade fever
 Chills and night sweats
 Persistent, progressive cough which may be non-productive at first but may produce
purulent sputum in the long term (2 weeks or more)
 Non-resolving bronchopneumonia
 Dull or pleuritic chest pains
 Dyspnea
 Hemoptysis
 Anemia

DIAGNOSTIC EVALUATION :

To diagnose tuberculosis, the following tests could be performed:

 Sputum culture: Positive for Mycobacterium tuberculosis in the active stage of the
disease.
 Ziehl-Neelsen (acid-fast stain applied to a smear of body fluid): Positive for acid-
fast bacilli (AFB).
 Skin tests (purified protein derivative [PPD] or Old tuberculin [OT]
administered by intradermal injection [Mantoux]): A positive reaction (area of
induration 10 mm or greater, occurring 48–72 hr after interdermal injection of the
antigen) indicates past infection and the presence of antibodies but is not necessarily
indicative of active disease. Factors associated with a decreased response to tuberculin
include underlying viral or bacterial infection, malnutrition, lymphadenopathy,
overwhelming TB infection, insufficient antigen injection, and conscious or
unconscious bias. A significant reaction in a patient who is clinically ill means that
active TB cannot be dismissed as a diagnostic possibility. A significant reaction in
healthy persons usually signifies dormant TB or an infection caused by a different
mycobacterium.
  Enzyme-linked immunosorbent assay (ELISA)/Western blot: May reveal presence
of HIV.
 Chest x-ray: May show small, patchy infiltrations of early lesions in the upper-lung
field, calcium deposits of healed primary lesions, or fluid of an effusion. Changes
indicating more advanced TB may include cavitation, scar tissue/fibrotic areas.
 CT or MRI scan: Determines degree of lung damage and may confirm a difficult
diagnosis.
 Bronchoscopy: Shows inflammation and altered lung tissue. May also be performed
to obtain sputum if patient is unable to produce an adequate specimen.
 Histologic or tissue cultures (including gastric washings; urine and cerebrospinal
fluid [CSF]; skin biopsy): Positive for Mycobacterium tuberculosis and may indicate
extrapulmonary involvement.
 Needle biopsy of lung tissue: Positive for granulomas of TB; presence of giant cells
indicating necrosis.
 Electrolytes: May be abnormal depending on the location and severity of infection;
e.g., hyponatremia caused by abnormal water retention may be found in extensive
chronic pulmonary TB.
 ABGs: May be abnormal depending on location, severity, and residual damage to the
lungs.
 Pulmonary function studies: Decreased vital capacity, increased dead space,
increased ratio of residual air to total lung capacity, and decreased oxygen saturation
are secondary to parenchymal infiltration/fibrosis, loss of lung tissue, and pleural
disease (extensive chronic pulmonary TB).

MEDICAL MANAGEMENT :
Pulmonary tuberculosis is treated primarily with antituberculosis agents for 6 to 12 months.

 First line treatment. First-line agents for the treatment of tuberculosis are isoniazid
(INH), rifampin (RIF), ethambutol (EMB), and pyrazinamide.
 Active TB. For most adults with active TB, the recommended dosing includes the
administration of all four drugs daily for 2 months, followed by 4 months of INH and
RIF.
 Latent TB. Latent TB is usually treated daily for 9 months.
  Treatment guidelines. Recommended treatment guidelines for newly diagnosed
cases of pulmonary TB have two parts: an initial treatment phase and a continuation
phase.
 Initial phase. The initial phase consists of a multiple-medication regimen of INH,
rifampin, pyrazinamide, and ethambutol and lasts for 8 weeks.
 Continuation phase. The continuation phase of treatment include INH and rifampin
or INH and rifapentine, and lasts for an additional 4 or 7 months.
 Prophylactic isoniazid. Prophylactic INH treatment involves taking daily doses for 6
to 12 months.
 DOT. Directly observed therapy may be selected, wherein an
assigned caregiver directly observes the administration of the drug.

PHARMACOLOGIC THERAPY

The first line antituberculosis medications include:

 Isoniazid (INH). INH is a bactericidal agent that is used as prophylaxis for neuritis,
and has side effects of peripheral neuritis, hepatic enzyme elevation, hepatitis, and
hypersensitivity.
 Rifampin (Rifadin). Rifampin is a bactericidal agent that turns the urine and other
body secretions into orange or red, and has common side effects of hepatitis, febrile
reaction, purpura, nausea, and vomiting.
 Pyrazinamide. Pyrazinamide is a bactericidal agent which increases the uric acid in
the blood and has common side effects of hyperuricemia, hepatotoxicity, skin rash,
arthralgias, and GI distress.
 Ethambutol (Myambutol). Ethambutol is a bacteriostatic agent that should be used
with caution with renal disease, and has common side effects of optic neuritis and
skin rash.
NURSING MANAGEMENT

Nursing management includes the following:

NURSING ASSESSMENT

The nurse may assess the following:

 Complete history. Past and present medical history is assessed as well as both of the
parents’ histories.
 Physical examination. A TB patient loses weight dramatically and may show the loss
in physical appearance.
Nursing interventions for the patient include:

 Promoting airway clearance. The nurse instructs the patient

about correct positioning to facilitate drainage and to increase fluid intake to
promote systemic hydration.
 Adherence to the treatment regimen. The nurse should teach the patient that TB is a
communicable disease and taking medications is the most effective means of
preventing transmission.
 Promoting activity and adequate nutrition. The nurse plans a progressive activity
schedule that focuses on increasing activity tolerance and muscle strength and a
nutritional plan that allows for small, frequent meals.
 Preventing spreading of tuberculosis infection. The nurse carefully instructs the
patient about important hygienic measures including mouth care, covering the mouth
and nose when coughing and sneezing, proper disposal of tissues, and handwashing.
 Acid-fast bacillus isolation. Initiate AFB isolation immediately, including the use of
a private room with negative pressure in relation to surrounding areas and a minimum
of six air changes per hour.
 Disposal. Place a covered trash can nearby or tape a lined bag to the side of the bed to
dispose of used tissues.
 Monitor adverse effects. Be alert for adverse effects of medications.
NURSING CARE ALGORITHM :

Documentation

The focus of documentation should include:

 Recent or current antibiotic therapy.

 Signs and symptoms of infectious process.
 Breath sounds, presence and character of secretions, and use of accessory muscles for
breathing.
 Character of cough and sputum.
 Respiratory rate, pulse oximetry, oxygen saturation, and vital sign.
 Level of activity.
 Causative or precipitating factors.
 Client reports of difficulty or change.
 Caloric intake.
 Individual cultural or religious restrictions and personal preferences.
  Plan of care.
 Teaching plan.
 Responses to interventions, teaching, and actions performed.
 Attainment or progress toward desired outcomes.
 Modifications to plan of care.
 Discharge needs.

PREVENTION
a) TB is preventable, even in those who have been exposed to an infected person. Skin
testing for TB is used in high risk populations or in people who may have been exposed
to TB, such as health care workers.

b) People who have been exposed to TB should have a skin test as soon as possible and have
a follow-up test at a later date, if the first test is negative.

c) A positive skin test means have come into contact with the TB bacteria. It does not mean
that they have active TB or are contagious.

d) Prompt treatment is very important in preventing the spread of TB from those who have
active TB to those who have never been infected with TB.

e) Some countries with a high incidence of TB give people a vaccine called BCG to prevent
TB. But, the effectiveness of this vaccine is limited and it is not used in the United States
for the prevention of TB.

f) People who have had BCG may still be skin tested for TB. Discuss the test results (if
positive).

COMPLICATIONS :

 Respiratory failure. Respiratory failure is one of the most common complication of

pulmonary tuberculosis.
 Pneumothorax. Pneumothorax becomes a complication when tuberculosis is not
treated properly.
  Pneumonia. One of the most fatal complications of tuberculosis is pneumonia as it
could cause infection all over the lungs.

NURSING DIAGNOSIS :
The major nursing diagnoses for the patient include:

 Risk for infection related to inadequate primary defenses and lowered resistance.
 Ineffective airway clearance related to thick, viscous, or bloody secretions.
 Risk for impaired gas exchange related to decrease in effective lung surface.
 Activity intolerance related to imbalance between oxygen supply and demand.
 Imbalanced nutrition: less than body requirements related to inability to ingest
adequate nutrients.
 PULMONARY FIBROSIS
DEFINITION :

Pulmonary fibrosis is a rare chronic lung condition that causes lung tissue to become
scarred and stiff. This thickened, stiff tissue makes it more difficult for the lungs to work
properly. As pulmonary fibrosis worsens, it might become progressively more short of
breath.

CAUSES :

There are generally four different causes of pulmonary fibrosis. These are:

Idiopathic Pulmonary Fibrosis (IPF)

Idiopathic pulmonary fibrosis means that the cause of the pulmonary fibrosis is not known,
and is the most common diagnosis patients receive.

Pulmonary Fibrosis From Diseases

Conditions such as rheumatoid arthritis, scleroderma, viral infections and GERD can lead to
pulmonary fibrosis.
Pulmonary Fibrosis From Environmental or Chemical Exposure

Patient may develop pulmonary fibrosis as the result of breathing in toxins such as asbestos.
and can also develop pulmonary fibrosis from exposure to bird and other animal droppings
and certain medications or treatments, such as radiation treatment for cancer.

Familial Pulmonary Fibrosis

When certain types of interstitial lung diseases occur in two or more people in the family, it’s
called familial pulmonary fibrosis. This form of pulmonary fibrosis is rare and not well
understood, but researchers suspect genetics play a role.

RISK FACTORS

Factors that make you more susceptible to pulmonary fibrosis include:

Age. Although pulmonary fibrosis has been diagnosed in children and infants, the disorder is
much more likely to affect middle-aged and older adults.

Sex. Idiopathic pulmonary fibrosis is more likely to affect men than women.

Smoking. Far more smokers and former smokers develop pulmonary fibrosis than do people
who have never smoked. Pulmonary fibrosis can occur in patients with emphysema.

Certain occupations. have an increased risk of developing pulmonary fibrosis if you work
in mining, farming or construction or if you're exposed to pollutants known to damage the
lungs.

Cancer treatments. Having radiation treatments to the chest or using certain chemotherapy
drugs can increase the risk of pulmonary fibrosis.

Genetic factors. Some types of pulmonary fibrosis run in families, and genetic factors may
be a component.

SIGNS AND SYMPTOMS :

Signs and symptoms of pulmonary fibrosis may include:

 Shortness of breath (dyspnea)

 A dry cough
  Fatigue
 Unexplained weight loss
 Aching muscles and joints
 Widening and rounding of the tips of the fingers or toes (clubbing)

The course of pulmonary fibrosis — and the severity of symptoms — can vary considerably
from person to person. Some people become ill very quickly with severe disease. Others have
moderate symptoms that worsen more slowly, over months or years.

Some people may experience a rapid worsening of their symptoms (acute exacerbation), such
as severe shortness of breath, that may last for several days to weeks. People who have acute
exacerbations may be placed on a mechanical ventilator. Doctors may also prescribe
antibiotics, corticosteroid medications or other medications to treat an acute exacerbation.

DIAGNOSIS

Pulmonary fibrosis can be difficult to distinguish from other lung diseases. That’s why the
diagnosis of pulmonary fibrosis is based on a number of factors. The lung specialist will talk
about the medical history, symptoms, and any family history that may have of lung disease.
The number of tests that may include:

 Biopsy or sample of the lung tissue

 Blood tests to see how liver and kidneys are functioning

 Chest X-ray and other imaging exams

 Lung function tests, including spirometry

Patient may also have tests to rule out other conditions, such as tuberculosis.

TREATMENT :

Medication: Two medications — pirfenidone (Esbriet®) and nintedanib (OFEV®) —may

slow down lung scarring. These medications can help preserve lung function.
Oxygen therapy: Giving body extra oxygen helps to breathe more easily. It may also
increase the energy and strength.

Pulmonary rehabilitation: Staying active in this special exercise program may improve how
much (or how easily) patient can do everyday tasks or activities.

Lung transplant: A lung transplant replaces one or both diseased lungs with a healthy lung
(or lungs) from a donor. It offers the potential to improve the health and quality of life. A
lung transplant is major surgery, and not everyone is a candidate. Ask whether a provider
may be eligible for a lung transplant.

COMPLICATIONS :

Complications of pulmonary fibrosis may include:

 High blood pressure in the lungs (pulmonary hypertension). Unlike systemic high
blood pressure, this condition affects only the arteries in the lungs. It begins when the
smallest arteries and capillaries are compressed by scar tissue, causing increased
resistance to blood flow in the lungs.

This in turn raises pressure within the pulmonary arteries and the lower right heart
chamber (right ventricle). Some forms of pulmonary hypertension are serious illnesses
that become progressively worse and are sometimes fatal.

 Right-sided heart failure (cor pulmonale). This serious condition occurs when the
heart's lower right chamber (ventricle) has to pump harder than usual to move blood
through partially blocked pulmonary arteries.

 Respiratory failure. This is often the last stage of chronic lung disease. It occurs when
blood oxygen levels fall dangerously low.

 Lung cancer. Long-standing pulmonary fibrosis also increases the risk of developing
lung cancer.

 Lung complications. As pulmonary fibrosis progresses, it may lead to complications

such as blood clots in the lungs, a collapsed lung or lung infections.
 PNEUMOCONIOSIS

Pneumoconiosis is the general term for a class of interstitial lung diseases where
inhalation of dust has caused interstitial fibrosis. Pneumoconiosis often causes restrictive
impairment, although diagnosable pneumoconiosis can occur without measurable impairment
of lung function. Depending on extent and severity ,it may cause death within months or
years, or it may never produce symptoms usually an occupational lung disease, typically from
years of dust exposure during work in mining; textile milling; shipbuilding, ship repairing,
and/or ship breaking; sandblasting; industrial tasks; rock drilling (subways or building
pilings);or agriculture.

Pneumoconiosis is a lung disease that affects miners, builders, and other workers
who breathe in certain kinds of dust on the job

Pneumoconiosis is also known as "black lung disease" or "popcorn lung." There's no

cure, but treatments can make it easier to breathe and go for regular activities.

TYPES:

Depending upon the type of dust, the disease is given different names:

 Coal worker's pneumoconiosis (also known as miner's lung, black lung or

anthracosis ) – coal, carbon
 Aluminosis – Aluminium
 Asbestosis – asbestos
 Silicosis (also known as "grinder's disease" or Potter's rot, or when related to
silica inhaled from the ash of anerupting volcano, pneumono ultramicroscopic
silico volcano coniosis) – crystalline silica dust
  Bauxite fibrosis – bauxite
 Berylliosis – beryllium
 Siderosis – iron
 Byssinosis – cotton
 Silicosiderosis – mixed dust containing silica and iron Labrador lung (found in
miners in Labrador, Canada) – mixed dust containing iron, silica and
anthophyllite,a type of asbestos
 Stannosis – tin oxide
 Talcosis- talc

DIAGNOSIS

 Positive indications on patient assessment:

 Shortness of breath
 Chest X-ray may show a characteristic patchy, sub pleural, bibasilar interstitial
infiltrates or small cystic radiolucencies called honeycombing.

TREATMENT

Pneumoconiosis can’t be cured. Once the disease has been diagnosed, treatment is aimed at
keeping it from getting worse and controlling the symptoms. A treatment plan may include:

 Not smoking
 Avoiding all dust exposure
 Using oxygen
 Taking medications called bronchodilators that open lung passages

COMPLICATIONS

The main complication is when simple pneumoconiosis progresses to PMF. These are other
possible complications:

 Progressive respiratory failure

 Lung cancer
 Tuberculosis (but this is now rare)
 Heart failure caused by pressure inside the lungs
PREVENTION

Prevention is important because the disease cannot be treated or reversed. The Occupational
Safety and Health Administration sets standard prevention rules for workers at risk for
pneumoconiosis. These are common prevention measures:

 Wearing a mask
 Washing areas of skin that come in contact with dust
 Safe removal of dust from clothing
 Washing the face and hands thoroughly before eating, drinking, or taking any
medications
 Not smoking
 Letting health care personnel know about any symptoms of pneumoconiosis
 Getting regular chest X-rays and physical exams
 PLEURITIS

Definition:

Pleuritis, also known as pleurisy, is an inflammation of the visceral and parietal layers
of the pleural membranes of the lungs. The condition can be primary or secondary and results
in sudden, sharp, and intense chest pain on inhalation and exhalation.

CAUSES :

A variety of conditions can cause pleuritis. Causes include:

 Viral infection, such as the flu (influenza).

 Bacterial infection, such as pneumonia.
 Fungal infection.
 Autoimmune disorder, such as rheumatoid arthritis or lupus.
 Lung cancer near the pleural surface.
 Pulmonary embolism.
 Tuberculosis (TB).
 Rib fracture or trauma.
 Certain inherited diseases, such as sickle cell disease.
 Certain medications and recreational drugs.
 PATHOPHYSIOLOGY :

Infection/ inflammation/trauma ( causative factors)

Inflammation of pleura

Irritate the sensory fibers of the parietal pleura

During respiration ( intensified on inspiration), the pleural membrane rub together and the
result is severe, sharp pain.

CLINICAL MANIFESTATIONS :

 Chest pain becomes severe, sharp, and stabbing on inspiration (pleuritic pain)
 It may become minimal or absent when breath is held
 May be localized or radiate to shoulder or abdomen
 Intercostal tenderness on palpation.
 Pleural friction rub grating or leathery sounds heard in both phases of
respiration; heard low in the axilla or over the lung base posteriorly; may be heard for
only a day or so)
 Evidence of infection : fever, malaise , increased white cell count.

DIAGNOSTIC EVALUATION :

Blood tests

o Test for presence of infection via elevated WBC on CBC with differential
o Antibodiescan be tested to determine/rule out autoimmune conditions:
 Rheumatoid arthritis
 Systemic lupus erythematosus
o D-dimer elevation can suggest pulmonary embolism.
o Cardiac troponin is suggestive of myocardial infarction.
 Physical examination

o Pleural friction rub upon auscultation

o May also reveal other abnormal sounds if concomitant lung disease is present, such as
crackles and decreased breath sounds in pneumonia

Imaging

o Chest X-ray: may show air or fluid in the pleural space, and suggest a cause (e.g., fractured
rib, malignancy)
 Consolidation can represent pneumonia.
 Pneumothorax
 A widened mediastinum is indicative of aortic dissection.
 Cardiomegaly can represent pericarditis.
 Lymphadenopathy or cavitation may suggest tuberculosis.
o CT scan: may show signs of pneumonia or the presence of a causative abscess ,tumor, or
blood clot within the lung with angiography
o Ultrasound: can be used to confirm pleural effusion at bedside
 Electrocardiogram: used to help diagnose cardiac causes including myocardial infarction,
and pericarditis.

Diagnostic procedures

 Sputum testing: test for infectious causes, especially tuberculosis

 Thoracentesis: Fluid is aspirated for laboratory analysis.
o Exudative pleural fluid shows elevated pleural fluid protein, elevated lactate dehydrogenase,
or leukocytosis.
o Use Light’s criteria (see table below) to determine etiology.
 Thoracoscopy: direct visualization of the lungs and pleural cavity to visualize abnormalities
and obtain a tissue sample forpathologic examination and possible microbiologic culture

MANAGEMENT

 Relief of symptoms:
o NSAIDs are used to reduce pain and inflammation
o Opiate analgesics
o Corticosteroids
 Removal of the fluid, air, or blood from the pleural space:
o Thoracentesiscan be diagnostic as well as therapeutic
o The insertion of a chest tube may be required in the case of large amounts of fluid
accumulation.

COMPLICATIONS :

 Severe pleural effusion

 Atelectasis
 Pneumonia
 Pneumothorax / hemothorax
 PLEURAL EFFUSION

DEFINITION :

A pleural effusion describes an excess fluid in the pleural cavity. Sometimes referred
as ― water on the lungs‖. This condition usually results from an imbalance in normal rate of
pleural production or absorption or both.

TYPES :

 Transudative effusion
 Exudative effusion

Transudative effusion :

 Also refrred as watery fluid

 Caused by fluid leaking into pleural space.

Exudative effusion:

 It is a protein rich fluid

 It is caused by infection, inflammation, lung injury or tumors .
CAUSES :

Transudative :

 Heart failure

 Pulmonary embolism
 Cirrhosis
 Post open heart surgery

Exudative :

 Pneumonia
 Cancer
 Pulmonary embolism
 Kidney disease
 Inflammatory diseases

Other causes

 Tuberculosis
 Autoimmune disease
 Bleeding (due to chest trauma)
 Rare chest and abdominal infections
 Asbestos pleural effusion (due to exposure to asbestos)
 Certain medications, abdominal surgery radiation therapy occur with several types of
cancer including lung cancer, breast cancer and lymphoma
PATHOPHYSIOLOGY :

Transudative :

Increased hydrostatic pressure

Decrease in plasma oncotic pressure

Unable to remain the fluid within the intra vascular space

Fluid shifts to interstitial space

Effusion

Exudative :

Invasion of microbes

Initiation of inflammatory reaction

Vasodilation

Increase in capillary permeability

Leak in plasma protein

 Decrease in oncotic pressure

Fluid shift into interstitial space

Effusion

Clinical features :

 Pleuretic chest pain

 Dyspnea
 Wheeze
 Dry or non- productive cough
 Orthopnea
 Fever
 Weight loss
 Respiratory distress
 Haemoptysis
 Clammy skin
 Chills
 Fatigue

Diagnostic Evaluation :

History collection :

 History of pneumonia
 Chest tumor
 Cardiac, renal, or liver impairement
 Cancer related treatment.

Physical examination :

 Decreased breathe sound

 Dullness in percussion
 Decreased fremitus
Imaging studies :

 Chest radiography
 Ultrasonography thorax
 CT scan thorax

Others :

 Biopsy
 Blood pH
 BUN
 Serum electrolytes
 Serum creatinine
 Platelets count

 BLOOD pH = 7.35 - 7.45

 BUN ( Bile Urea Nitrogen ) = 7-30mg /dl
 Serum Electrolytes
 Sodium – 135-145 m eq / l
 Potassium - 3.5 – 5 m eq / l
 Calcium – 9-11 meq / l
 Bicarbonate - 24 – 30meq / l
 Creatinine – 0.7-1.2 meq /l
 Platelets count – 150,000-450,000/ mc
Management :

Medical management :

 Pencillin
 Amoxicillin
 Ampicillin
 Cephalosporin
 Ceftriaxone
 Cefuroxime
 Macrolides
 Azithromycin
 Clarithromycin
 Fluroquinolones
 Levofloxacin
 Moxifloxacin
 Diuretics
 Frusemide
 Spironolactone
 Hydrochlorothiazide
 NSAIDS
 Aspirin
 Ibuprofen
 Naproxen
 Corticosteroids
 Prednisone
 Methylprednisolone
 Chemotherapy
 Opiods
 Morphine
 Acetaminophen
 Oxycodone
Surgical management

Thoracentesis

VATS – Video Assisted Thoracoscopic Surgery

Thoracotomy : ( open thoracic surgery )

 Anterolateral thoracotomy
 Axillary thoracotomy
 Postero lateral Thoracotomy

Nursing management :

 It involves a comprehensive evaluation of the patient `s symptoms, medical history

and physical examination.
 The nurse will gather information about patient`s past medical history, including
previous episodes of pleural effusion or other lung conditions.
 Patient`s current symptoms including pain, dyspnea, cough, its onset and duration
 Must perform proper physical examinationwhich includes abnormal breath sounds,
signs of distress
 Monitor the patient`s oxygen saturation level
 Monitoring vital signs to look for any signs of infection
 Assessment of pain and its management
 Proper positioning ( semi- fowlers )
 Reassurance / relaxation / distraction
 Education of controlled breathing techniques
 Advice about wearing loose clothing
 Proper oral care
 Minimize sodium intake Cessation of smoking and alcohol
 Administering supplemental oxygen
 Encouraging deep breathing and coughing exercises
 Monitor fluid balance to prevent overload
 Follow sterile techniques
 Use of PPE during invasive procedures
  Encouraging energy conservation techniques
 Ensure proper chest tube drain and dressing
 Proper wound care
 Monitoring electrolyte levels
 Preventive measures of pressure ulcers
 Self care measures
 Follow up care to adjust treatment plans

Complications :

 Iatrogenic pneumothorax ( injury to pleura )

 Infection spread that turns into abscess
 Recurrent effusion
 Respiratory distress
 Pulmonary edema
 Hemothorax
 Tension pneumothorax
 Empyema
 Bloody tap
 Collapse of lung
 Respiratory failure
 Pleural thickening ( scarring of lining of the lung)

Prevention :

 Treat the cause

 Early seek to medical aid
 Administration of prompt medications ( diuretics ,antibiotics , albumin , anti
inflammatory agents, bronchodilators, corticosteroids,etc.)
 Recognition of clinical features
 Regular exercises
 Avoidance of alcohol
Nursing diagnosis :

1. Impaired gas exchange related to decreased lung expansion and ventilation perfusion
imbalance.
2. Ineffective airway clearance related to pleural fluid accumulation and lung
compression.
3. Acute pain related to inflammation and irritation of pleural membrane .
4. Anxiety related to difficulty breathing and fear of unknown.
5. Activity intolerance related to decrease lung function and dyspnea.
6. Ineffective coping related to chronic illness and multiple treatment modalities.
7. Disturbed sleep pattern related to coughpain, and shortness of breath.

8. Imbalanced nutrition less than body requirement related to increased metabolic demand
and difficulty eating due to pain and dyspnea.

9. Impaired skin integrity related to drainage tube placement and adhesive dressings.

10. Risk for infection related to invasive diagnostic and therapeutic procedures.

11. Risk for fluid volume excess related to decrease urine output and fluid overload.

12. Risk for impaired liver function related to medication side effects and congestion.

13. Risk for acute kidney injury related to decreased renal blood flow and medication side
effects.
 PNEUMOTHORAX

Pneumothorax is the accumulation of atmospheric air in the pleural space, which

results in a rise in intrathoracic pressure and reduced vital capacity. The loss of negative
intrapleural pressure results in collapse of the lung. A spontaneous pneumothorax occurs with
the rupture of a bleb. An open pneumothorax occurs when an opening through the chest wall
allows the entrance of positive atmospheric pressure into the pleural space.Diagnosis of
pneumothorax is made by chest x-ray film.
 Causes

The cause of a closed or primary spontaneous penumothorax is the rupture of a bleb

(vesicle) on the surface of the visceral pleura. Secondary spontaneous pneumothorax can
result from chronic obstructive pulmonary disease (COPD), which is related to hyperinflation
or air trapping, or from the effects of cancer, which can result in the weakening of lung tissue
or erosion into the pleural space by the tumor. Blunt chest trauma and penetrating chest
trauma are the primary causes of traumatic and tension pneumothorax. Other possible causes
include therapeutic procedures such as thoracotomy, thoracentesis, and insertion of a central
line.

CLASSIFICATION

 Traumatic:
o Open: a connection through the chest wall
o Closed: no connection to the outside air
 Spontaneous:
o Primary: No underlying disease can be identified.
o Secondary: known pre-existing lung conditions

PATHOPHYSIOLOGY:

Normal physiology

 Pleural spacehas a negative pressure.

 Chest wall expands → surface tension between parietal and visceral pleura expands the lung
 Lung tissue has an elasticrecoil→ innate tendency to collapse inwardTraumatic
pneumothorax

 Closed pneumothorax: blunt trauma → lung damage → air flows from the lung into
the pleural space
 Open pneumothorax: penetrating trauma to the chest wall → pathway for air directly into
pleural space.
 Spontaneous pneumothorax

 Ruptured bleb → air flows from the lung into the pleural space→ positive pleural pressure →
compressed lung
 Lung collapses until an equilibrium is achieved or the rupture seals.
 ↓ Vital capacityand ↓ partial pressureof oxygen

Tension pneumothorax

 Life threatening and can develop from any type of a pneumothorax

 Air enters the pleural space through a 1-way valve mechanism → air cannot escape
 Air accumulates in the pleural spacewith each inspiratory phase → ↑ pleural space pressure
→shifting of the mediastinum → compression of the contralateral lung → hypoxia
 Eventual compression of the vena cava and atria → ↓ venous return to the heart and ↓ cardiac
function
 Leads to rapid cardiopulmonary collapse
 CLINICAL MANIFESTATIONS:

Chest pain (sharp and sudden and worst on inspiration), Cyanosis

Overt tachycardia and tachypnea

Low blood pressure

Low SpO2

Absent lung sounds on affected side

Pushing of trachea to unaffected side (tension pneumo.)

Subcutaneous emphysema (escaping carbon dioxide collecting in the skin…crunchy bulges

on the skin), Sucking sound with open pneumothorax

Expansion of chest rise and fall unequal

Dyspnea

DIAGNOSTIC EVALUATION :

Imaging

The diagnosis is suspected based on the clinical presentation, and confirmed by imaging.
Tension pneumothorax is a clinical diagnosis, and management should not wait for imaging
confirmation.

 Chest radiograph:

 The easiest available imaging

 Should be performed in the upright position (when possible)

o General findings:

 White visceral pleural line defining the lung and pleural air
 Bronchovascular markings are not visible beyond the pleural edge.
 Deep sulcus sign (gas outlines the costophrenic sulcus)
 Ipsilateral hemidiaphragm elevation
 Trauma patients may have a concurrent hemothorax.

o Tension pneumothorax findings:

  Potential mediastinal shift to the contralateral side
 Tracheal deviation to the contralateral side
 Ipsilateral hemidiaphragm flattening
 Ribs are spread apart.
 Small pneumothoraces will typically not show on an X-ray.

 Ultrasound:

 More sensitive than X-ray, but is technician dependent

 Can be done rapidly at the bedside

o Findings:

 Presence of a lung point (the boundary between the lung and pneumothorax)
 Lung sliding will be absent at the location of a pneumothorax.

 Computed tomography (CT):

 The most sensitive

 Used if the diagnosis remains uncertain after radiographs
 Can provide additional information about associated causes

o Findings:

 Air in the pleural space

 Can evaluate for loculations, pleural pathology, and lung disease

MANAGEMENT :

The management of a pneumothorax depends on the amount of air collected in the pleural
cavity and the stability of the patient.

Tension pneumothorax and unstable patients

 Supplemental oxygen
 Immediate chest tube thoracotomy:
 A catheter is inserted into the chest wall.
 Placed in the 4th to 5th intercostal space at the midaxillary line
  Needle decompression if chest tube placement needs to be delayed (e.g., pre hospital
care):
 14- or 16-gauge needle is inserted through the chest wall.
 2nd or 3rd intercostal space in the mid clavicular line
 5th intercostal space in the anterior or mid axillary line is another option.
 Should be followed by chest tube placement .

COMPLICATIONS :

 Respiratory failure
 Cardiac arrest
 Pneumomediastinum(air is present in the mediastinum)
 Pneumoperitoneum(air is in the peritoneal cavity)
 Re-expansion pulmonary edema:

 Occurs with rapid expansion of the lung

 Higher risk if the lung has been collapsed for several days

 Procedure complications:

 Infection
  Fistula formation and air leaks
 Intercostal nerve damage
 Bleeding

 Recurrence
 PYOTHORAX

Pyothorax is the presence of septic inflammatory fluid or pus in the pleural cavity.
The pleural cavity is the space that lies between the pleura, the two thin membranes that line
and surround the lungs.

CAUSES:

It is typically caused by microorganisms that infect the oral cavity or upper

respiratory tract. In humans, bacterial pneumonia which spreads from the lungs into the
pleural space is generally the cause, but the condition can also result from lung abscesses and
tuberculosis. The bronchial tree distributes air to the lungs and when it is infected, a
pneumothorax may also develop from air entering the pleural cavity.

STAGES :

There are three stages:

 Exudative: when there is an increase in pleural fluid with or without the presence of pus
 Fibrinopurulent: when fibrous septa form localized pus pockets
 Organizing stage: when there is scarring of the pleura membranes with possible inability of
the lung to expand

CLINICAL MANIFESTATIONS :

Symptoms of pyothorax include:

 Trouble breathing
 Cough
 Fever
 Chest pains
 Decreased appetite
 Weight loss
 Confusion
 Headaches

DIAGNOSTIC EVALUTAION:

Diagnosis of pyothorax begins with a complete medical history and physical

examination. Blood tests, such as:

 Blood cultures (to identify what bacterium or organism is causing the infection)
 C-reactive protein (CRP) (elevated levels are seen in inflammatory conditions)
 White blood cell count (WBC) (elevated levels in inflammatory and infectious
conditions)

 X-ray (to diagnose pneumonia, lung abscess document fluid accumulation)

 Thoracentesis (aspiration of pleural fluid for microscopic examination and testing)
 Thoracic ultrasound (use of sound waves to tell if loculations are present)
 CAT scan of the chest (use of computerized X-ray analysis to evaluate the lungs and
pleural space)
TREATMENT :

 Pyothorax is treated with intravenous antibiotics, such as cephalosporins, metronidazole,

and penicillins with beta-lactamase (ampicillin/sulbactam). Clindamycin can be used for
patients who are allergic to penicillin

 Fluids lost, due to lack of appetite and fever, are replaced, and medications such as
acetaminophen

 Pleural fluid drainage: a chest tube is used to drain pus from the pleural space and allow
the lungs to expand normally
 HEMOTHORAX

DEFINITION :

A hemothorax is defined as a collection of fluid with a Haematocrit of at least 50%

accumulated in the potential space between the parietal and visceral pleura of the lungs.

ETIOLOGY

The source of blood may be the chest wall, lung parenchyma, heart, or great vessels
from either traumatic or non-traumatic causes.

Traumatic causes:

Lung parenchymal injury:

o Most common cause

o More commonly small (< 10%)
o Often self-limited

Arterial injury:

o Intercostal artery injury (most common)

o Internal mammary artery injury
o Great large vessels (rare, but life threatening)

Iatrogenic:

o Central venous catheter placement

o Thoracostomy tube placement

Non-traumatic causes:

 Malignancy
 Anticoagulant medications
 Coagulopathies
 Aortic dissection or aneurysm
 Tuberculosis and necrotizing infections

CLINICAL MANIFESTATIONS :

 Shortness of breath
 Chest pain
 Ipsilateral absent or ↓ breath sounds
 Tracheal deviation
 Dullness on percussion
 Crepitus
 Signs of hemorrhagic shock in large hemothoraces:
 Hypotension
 Tachycardia
 Tachypnea
 ↓ Jugular venous pressure

DIAGNOSTIC EVALUATION :

Imaging

Chest X-ray: best initial diagnostic study

 Upright imaging shows layering of blood.

 Supine imaging shows haziness or opacity (whiteout).
  May also show free air if a pneumothorax is present

Ultrasound of the lungs (thorax sonography):

 Part of the Extended Focused Assessment with Sonography for Trauma (eFAST)
exam
 Able to be obtained quickly
 Can show complex fluid in the pleural cavity
 More sensitive than a chest X-ray in detecting a hemothorax, but is technician
dependent

Chest computed tomography(CT)—definitive imaging choice:

 Should only be obtained if the patient is stable

 CT can show other associated pathology.
 CT angiogram can show the source of bleeding.

MANAGEMENT:
 ATLS: Advanced Trauma Life Support
CXR: chest X-ray
Hb: hemoglobin
HCT: hematocrit
INR: international normalized ratio
PTT: prothrombin time
VATS: video-assisted thoracoscopic surgery

 Airway, breathing, and circulation (ABC) assessment → administer 100% oxygen→

establish intravenous (IV) access
 Stabilize the patient (fluid resuscitationand blood transfusion as necessary).
 Reverse anticoagulants, if necessary.
 Provide analgesia appropriate to the level of the patient's pain.
 Insert a chest tube (thoracostomy) for large hemothoraces or in an unstable patient:
o Chest tube inserted on the midaxillary lineat the 5th intercostal space
o Used to drain the hemothorax
o Monitor output of the hemothorax.
 Surgical intervention (thoracotomy) is indicated when:
o Evacuating > 1,500 mL of blood directly after inserting a chest tube
o Continued high output → collecting of > 1 L (1,000 mL) of blood over 4 hours or > 200
mL/hour for 3 consecutive hours
COMPLICATIONS

Impaired ventilation on the affected side:

 Leads to respiratory distress

 May require intubation

Empyema:

 Retained blood collection develops a bacterial infection.

 5% of cases

Fibrothorax:

 Formation of scar tissues within the lungs due to blood irritation

 1% of cases.
 INTERSTITIAL LUNG DISEASE

DEFINITION

Interstitial lung disease (ILD) is a group of lung disorders in which the lung tissues
become inflamed and then damaged.

CAUSES :

ILD can occur without a known cause. This is called idiopathic ILD. Idiopathic pulmonary
fibrosis (IPF) is the most common disease of this type.

There are also dozens of known causes of ILD, including:

 Autoimmune diseases (in which the immune system attacks the body) such as lupus,
rheumatoid arthritis, sarcoidosis, and scleroderma.
 Lung inflammation due to breathing in a foreign substance such as certain types of
dust, fungus, or mold (hypersensitivity pneumonitis).
 Medicines (such as nitrofurantoin, sulfonamides, bleomycin, amiodarone,
methotrexate, gold, infliximab, etanercept, and other chemotherapy medicines).
 Radiation treatment to the chest.
 Working with or around asbestos, coal dust, cotton dust, and silica dust (called
occupational lung disease).
  Infection and partial recovery from diseases like COVID-19.
 Cigarette smoking may increase the risk of developing some forms of ILD and may
cause the disease to be more severe.

CLINICAL MANIESTATIONS :

 Shortness of breath is a main symptom of ILD. You may breathe faster or need to take
deep breaths:
 At first, shortness of breath may not be severe and is only noticed with exercise,
climbing stairs, and other activities.
 Over time, it can occur with less strenuous activity such as bathing or dressing, and as
the disease worsens, even with eating or talking.
 Most people with this condition also have a dry cough. A dry cough means you do not
cough up any mucus or sputum.
 Over time, weight loss, fatigue, and muscle and joint pain are also present.
 People with more advanced ILD may have:
 Abnormal enlargement and curving of the base of the fingernails (clubbing).
 Blue color of the lips, skin, or fingernails due to low blood oxygen levels (cyanosis).
 Symptoms of the other diseases such as arthritis or trouble swallowing (scleroderma),
associated with ILD.

DIAGNOSTIC EVALUATION :

Laboratory tests

Blood tests. Certain bloodwork can detect proteins, antibodies and other markers of
autoimmune diseases or inflammatory responses to environmental exposures, such as those
caused by molds or bird protein.

Imaging tests

Computerized tomography (CT) scan. This imaging test is key to, and sometimes the first
step in, the diagnosis of interstitial lung disease. CT scanners use a computer to combine X-
ray images taken from many different angles to produce cross-sectional images of internal
structures. A high-resolution CT scan can be particularly helpful in determining the extent of
lung damage caused by interstitial lung disease. It can show details of the fibrosis, which can
be helpful in narrowing down the diagnosis and in guiding treatment decisions.

Echocardiogram. A sonogram for the heart, an echocardiogram uses sound waves to

visualize the heart. It can produce still images of the heart's structures, as well as videos that
show how the heart is functioning. This test can evaluate the amount of pressure occurring in
the right side of the heart.

Spirometry and diffusion capacity. This test requires you to exhale quickly and forcefully
through a tube connected to a machine that measures how much air the lungs can hold, and
how quickly you can move air out of the lungs. It also measures how easily oxygen can move
from the lungs into the bloodstream.

Oximetry. This simple test uses a small device placed on one of the fingers to measure the
oxygen saturation in the blood. It may be done at rest or with activity to monitor the course
and severity of lung disease.

Lung tissue analysis

Often, pulmonary fibrosis can be definitively diagnosed only by examining a small amount of
lung tissue (biopsy) in a laboratory.

The tissue sample may be obtained in one of these ways:

Bronchoscopy. In this procedure, the doctor removes very small tissue samples — generally
no larger than the head of a pin — using a small, flexible tube (bronchoscope) that's passed
through the mouth or nose into the lungs. The risks of bronchoscopy are generally minor —
most often a temporary sore throat and hoarseness from the bronchoscope — but the tissue
samples are sometimes too small for an accurate diagnosis.

Bronchoalveolar lavage. In this procedure, the doctor injects about a tablespoon of salt
water through a bronchoscope into a section of the lung, and then immediately suctions it out.
The solution that's withdrawn contains cells from the air sacs. Although bronchoalveolar
lavage samples a larger area of the lung than other procedures do, it may not provide enough
information to diagnose pulmonary fibrosis.

Surgical biopsy. Although this is a more invasive procedure with potential complications, it's
often the only way to obtain a large enough tissue sample to make an accurate diagnosis.
While you are under general anesthesia, surgical instruments and a small camera are inserted
through two or three small incisions between the ribs. The camera allows the surgeon to view
the lungs on a video monitor while removing tissue samples from the lungs.

TREATMENT :

The lung scarring that occurs in interstitial lung disease can't be reversed, and treatment will
not always be effective in stopping the ultimate progression of the disease. Some treatments
may improve symptoms temporarily or slow the disease's progress. Others help improve
quality of life.

Because many of the different types of scarring disorders have no approved or proven
therapies, clinical studies may be an option to receive an experimental treatment.

Medications

Intense research to identify treatment options for specific types of interstitial lung
disease is ongoing. Based on currently available, scientific evidence, however, the doctor
may recommend:

Corticosteroid medications. Many people diagnosed with interstitial lung diseases are
initially treated with a corticosteroid (prednisone), sometimes in combination with other
drugs that suppress the immune system. Depending on the cause of the interstitial lung
disease, this combination may slow or even stabilize disease progression.

Medications that slow the progression of idiopathic pulmonary fibrosis. The medications
pirfenidone (Esbriet) and nintedanib (Ofev) may slow the rate of disease progression.
Treatment-related side effects may be significant. Talk through the pros and cons of these
medications with the doctor.

Medications that reduce stomach acid. Gastroesophageal reflux disease (GERD) affects the
majority of people with idiopathic pulmonary fibrosis and is associated with worsening lung
damage. If you have symptoms of acid reflux, the doctor may prescribe GERD therapies that
reduce stomach acid, including H-2-receptor antagonists or proton pump inhibitors such as
lansoprazole (Prevacid 24HR), omeprazole (Prilosec OTC) and pantoprazole (protonix).

Oxygen therapy

 Using oxygen can't stop lung damage, but it can:

  Make breathing and exercise easier
 Prevent or lessen complications from low blood oxygen levels
 Reduce blood pressure in the right side of the heart
 Improve the sleep and sense of well-being
 You're most likely to receive oxygen when you sleep or exercise, although some
people may use it round-the-clock.

Pulmonary rehabilitation

The aim of pulmonary rehabilitation is not only to improve daily functioning but also
to help people with intersitial lung disease live full, satisfying lives. To that end, pulmonary
rehabilitation programs focus on:

 Physical exercise, to improve the endurance

 Breathing techniques that improve lung efficiency
 Emotional support
 Nutritional counseling

Surgery

Lung transplantation may be an option of last resort for some people with severe
interstitial lung disease who haven't benefited from other treatment options.

COMPLICATIONS :

 Corpulmonale
 Pulmonary hypertension
 Respiratory failure
 CYSTIC FIBROSIS

Cystic fibrosis is a disease that causes thick, sticky mucus to build up in the lungs,
digestive tract, and other areas of the body. It is one of the most common chronic lung
diseases in children and young adults. It is a life-threatening disorder.

Cystic fibrosis (CF) is a disease that is passed down through families. It is caused by a
defective gene that makes the body produce abnormally thick and sticky fluid, called mucus.
This mucus builds up in the breathing passages of the lungs and in the pancreas.

The buildup of mucus results in life-threatening lung infections and serious digestion
problems. The disease may also affect the sweat glands and a man's reproductive system.

Many people carry a CF gene, but do not have symptoms. This is because a person with CF
must inherit 2 defective genes, 1 from each parent.

SYMPTOMS :

Symptoms in newborns may include:

1. Delayed growth
2. Failure to gain weight normally during childhood
3. No bowel movements in first 24 to 48 hours of life
4. Salty-tasting skin
Symptoms related to bowel function may include:

 Belly pain from severe constipation

 Increased gas, bloating, or a belly that appears swollen (distended)
 Nausea and loss of appetite
 Stools that are pale or clay-colored, foul smelling, have mucus, or that float
 Weight loss

Symptoms related to the lungs and sinuses may include:

 Coughing or increased mucus in the sinuses or lungs

 Fatigue
 Nasal congestion caused by nasal polyps
 Repeated episodes of pneumonia (symptoms of pneumonia in someone with cystic
fibrosis include fever, increased coughing and shortness of breath, increased mucus,
and loss of appetite)
 Sinus pain or pressure caused by infection or polyps

Symptoms that may be noticed later in life:

 Infertility (in men)

 Repeated inflammation of the pancreas (pancreatitis)
 Respiratory symptoms
 Clubbed fingers
DIAGNOSTIC EVALUATION :

 A blood test is done to help detect CF. The test looks for changes in the CF gene.
Other tests used to diagnose CF include:
 Immunoreactive trypsinogen (IRT) test is a standard newborn screening test for CF. A
high level of IRT suggests possible CF and requires further testing.
 Sweat chloride test is the standard diagnostic test for CF. A high salt level in the
person's sweat is a sign of the disease.
 Other tests that identify problems that can be related to CF include:
 Chest x-ray or CT scan
 Fecal fat test
 Lung function tests
 Measurement of pancreatic function (stool pancreatic elastase)
 Secretin stimulation test
 Trypsin and chymotrypsin in stool
 Upper GI and small bowel series
 Lung cultures (obtained by sputum, bronchoscopy or throat swab)

MANAGEMENT :

Treatment for lung problems includes:

 Antibiotics to prevent and treat lung and sinus infections. They may be taken by mouth,
or given in the veins or by breathing treatments. People with cystic fibrosis may take
antibiotics only when needed, or all the time. Doses are usually higher than normal.
 Inhaled medicines to help open the airways
 DNAse enzyme replacement therapy to thin mucus and make it easier to cough up
 Flu vaccine and pneumococcal polysaccharide vaccine (PPV) yearly (ask the health care
provider)
 Lung transplant is an option in some cases
 Oxygen therapy may be needed as lung disease gets worse
Treatment for bowel and nutritional problems may include:
 A special diet high in protein and calories for older children and adults (see: Cystic
fibrosis nutrional considerations)
 Pancreatic enzymes to help absorb fats and protein
 Vitamin supplements, especially vitamins A, D, E, and K
 The doctor can suggest other treatments if you have very hard stools

Pharmacologic Intervention

1. Antimicrobial therapy as indicated for pulmonary infection.

 Oral or I.V. antibiotics as required.
 Inhaled antibiotics, such as gentamicin or tobramycin, may be used for severe lung
disease or colonization of organisms.
2. Bronchodilators to increase airway size and assist in mucus clearance.
3. Pulmozyme recombinant human DNase (an enzyme) administered via nebulization to
decrease viscosity of secretions.
4. Pancreatic enzyme supplements with each feeding.
 Favored preparation is pancrelipase.
 Occasionally, antacid is helpful to improve tolerance of enzymes.
 Favorable response to enzymes is based on tolerance of fatty foods, decreased stool
frequency, absence of steatorrhea, improved appetite, and lack of abdominal pain.
5. Gene therapy, in which recombinant DNA containing a corrected gene sequence is
introduced into the diseased lung tissue by nebulization, is in clinical trials.

Nursing Intervention

 Monitor weight at least weekly to assess effectiveness of nutritional interventions.

 Monitor respiratory status and sputum production, to evaluate response to respiratory
care measures.
 To promote airway clearance, employ intermittent aerosol therapy three to four times per
day when the child is symptomatic.
 Perform chest physical therapy three to four times per day after aerosol therapy.
 Help the child to relax to cough more easily after postural drainage.
 Suction the infant or young child when necessary, if not able to cough.
 Teach the child breathing exercises using pursed lips to increase duration of exhalation.
 Provide good skin care and position changes to prevent skin breakdown in malnourished
child.
 Provide frequent mouth care to reduce chances of infection because mucus is present.
 Restrict contact with people with respiratory infection.
 Encourage diet composed of foods high in calories and protein and moderate to high in
fat because absorption of food is incomplete.
 Administer fat-soluble vitamins, as prescribed, to counteract malabsorption.
 Increase salt intake during hot weather, fever, or excessive exercise to prevent sodium
depletion and cardiovascular compromise.
 To prevent vomiting, allow ample time for feeding because of irritability if not feeling
well and coughing.
 Encourage regular exercise and activity to foster sense of accomplishments and
independence and improve pulmonary function.
 Provide opportunities for parents to learn all aspects of care for the child.
 Teach the parents about dietary regimen and special need for calories, fat, and vitamins.
 Discuss need for salt replacement, especially on hot summer days or when fever,
vomiting, and diarrhea occur.

COMPLICATIONS :
 complications include:
 Bowel problems, such as gallstones, intestinal blockage, and rectal prolapse
 Coughing up blood
 Chronic respiratory failure
 Diabetes
 Infertility
 Liver disease or liver failure, pancreatitis, biliary cirrhosis
 Malnutrition
 Nasal polyps and sinusitis
 Osteoporosis and arthritis
 Pneumonia that keeps coming back
 Pneumothorax
 Right-sided heart failure (cor pulmonale)
 Colorectal cancer
 CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory lung

disease that causes obstructed airflow from the lungs.

COPD is a progressive, obstructive airway disease that is not fully reversible. It results
from disease of the airways and parenchyma in the form of chronic bronchitis and
emphysema.

 Chronic bronchitis: clinical term relating to a chronic productive cough for at

least 3 months over two consecutive years. Alternative explanation for cough
should be excluded (e.g. bronchiectasis).
 Emphysema: pathological term due to structural lung changes. Typically refers to
abnormal airspace enlargement distal to terminal bronchioles with evidence of
alveoli destruction and no obvious fibrosis. These characteristic changes can be
detected on imaging (e.g. computed tomography).

CAUSES :

The cause of COPD is usually long-term exposure to irritants that damage the lungs
and airways. In the United States, cigarette smoke is the main cause. Pipe, cigar, and other
types of tobacco smoke can also cause COPD, especially if you inhale them.
Exposure to other inhaled irritants can contribute to COPD. These include secondhand
smoke, air pollution, and chemical fumes or dusts from the environment or workplace.
Rarely, a genetic condition called alpha-1 antitrypsin deficiency can play a role in causing
COPD.

RISK FACTORS :

The risk factors for COPD include:

 Smoking. This the main risk factor. Up to 75% of people who have COPD smoke or used to
smoke.
 Long-term exposure to other lung irritants, such as secondhand smoke, air pollution, and
chemical fumes and dusts from the environment or workplace
 Age. Most people who have COPD are at least 40 years old when their symptoms begin.
 Genetics. This includes alpha-1 antitrypsin deficiency, which is a genetic condition. Also,
smokers who get COPD are more likely to get it if they have a family history of COPD.
 Asthma. People who have asthma have more risk of developing COPD than people who
don't have asthma. But most people with asthma will not get COPD.

CLINICAL MANIFESTATIONS :

Chronic productive cough and dyspnea are the hallmarks of COPD.

Symptoms

 Chronic cough: usually productive

 Sputum production
 Breathlessness: usually on exertion in early stages
 Frequent episodes of 'bronchitis': usually in the winter
 Wheeze

Signs

 Dyspnoea
 Pursed lip breathing: (prevents alveolar collapse by increasing the positive end
expiratory pressure)
 Wheeze
 Coarse crackles
 Loss of cardiac dullness: due to hyperexpansion of lungs from emphysema
 Downward displacement of liver: due to hyperexpansion of lungs from emphysema
 Signs of C02 retention
 Drowsy
 Asterixis
 Confusion
 Signs of cor pulmonale
 Peripheral oedema
 Left parasternal heave: caused by right ventricular hypertrophy
  Raised JVP
 Hepatomegaly


Concerning features

There may be clinical features in the history and on examination, which are suggestive of an
alternative diagnosis such as lung cancer or pulmonary embolism. These require urgent
investigation.

 Weight loss
 Haemoptysis
 Anorexia
 Chest pain
 Lymphadenopathy
 Finger clubbing
 Unexplained fatigue
 Acute exacerbation

An acute exacerbation of COPD usually presents with similar features to chronic 'stable'
COPD, which are listed above. The key is that an exacerbation refers to an acute, sustained
worsening in the patients symptoms beyond the normal, expected, day-to-day variation.

An acute exacerbation may be mild, or life-threatening requiring hospital admission and

respiratory support. Commonly, an exacerbation is driven by an underlying infection, but
they can also be non-infective.

MRC dyspnoea scale

The Medical Research Council (MRC) dyspnoea scale is used to grade the severity of
breathlessness.

The MRC dyspnoea scale is divided from 1 to 5.

1. Breathlessness on strenuous exercise.

2. Breathlessness on hurrying or slight hill.
3. Walks slower than contemporaries on ground level due to breathlessness OR have to
stop to catch breath when walking at own pace.
4. Stops to catch breath after 100 metres OR a few minutes of walking
5. Breathlessness on minimal activity (dressing) or unable to leave the house due to
breathlessness

DIAGNOSTIC EVALUATION :

 A medical history, which includes asking about the symptoms

 A family history

 Various tests, such as lung function tests, a chest x-ray or CT scan, and blood tests
 Imaging

 Chest x-ray (CXR):

 Hyperexpanded
  Flattened hemidiaphragms
 Hypodense
 Saber-sheath trachea
 CT scan: consider performing if
 Symptoms disproportionate to spirometric assessment
 Alternative diagnosis suspected (e.g. bronchiectasis, fibrosis)
 Lung cancer suspected or to investigate abnormalities on chest x-ray
 Echocardiogram: if cor pulmonale suspected.

TREATMENT :

Pharmacological treatment of COPD

Long-term treatment:

 Bronchodilators
o Promote smooth muscle relaxation and prevent bronchoconstriction
o LABAs, LAMAs, methylxanthines
 Inhaled corticosteroids
o Decrease inflammation
o Combine with LABA or LAMA
o Beclomethasone
o Budesonide
o Fluticasone
o Methylxanthines
 Phosphodiesterase-4 inhibitors
o Used in severe cases
o Reduce inflammation by preventing breakdown of intracellular cyclic AMP
o Roflumilast

Acute treatment:

 Short-acting bronchodilators (SABAs)

 Oral corticosteroids
  Antibiotics if concern for bacterial infection
 Oxygen therapy, ranging from nasal cannula to mechanical ventilation based on
severity

Inhaler types

 Short-acting beta-agonists (SABA): Salbutamol

 Long-acting beta-agonists (LABA): Salmeterol
 Short-acting muscarinic antagonists (SAMA): Ipratropium
 Long-acting muscarinic antagonists (LAMA): Umeclidinium / tiotropium
 Inhaled corticosteroid (ICS): Beclomethasone
 LABA-ICS: Seretide (salmeterol/fluticasone)
 LABA-LAMA: Ultibro (indacaterol/glycopyrronium)
 LABA-LAMA-ICS: Trimbow (formoterol/glycopyrronium/beclometasone)

Delivery devices

Inhalers may deliver drugs by different mechanisms

 Metered dose inhalers (MDI): delivers a specific amount of medication to the

lungs by a short burst of aerosolised medicine. Patient dependent, requires good
breath and coordinating activation with breath. Many patients have poor technique.
 Dry powder inhaler (DPI): usually requires 'loading' or 'activation' of the device
for the powder to be administered. Requires good force of patient inhalation and
need to hold breath for certain period.
 Soft mist inhaler (SMI): contain liquid formulations of the drug. More drug
delivery to lungs and less coordination needed compared to MDI inhalers.
 Spacers: typically used with a MDI inhaler to enhance drug delivery and reduce
need for good coordination. Contains a chamber that the drug is delivered into and
the patient then completes normal tidal breathing to inhale the drug.
 Nebuliser: drug in liquid form is converted into a mist using a nebuliser machine
with compressed air. Typically reserved for patients with an acute exacerbation in
hospital or disabling symptoms despite maximal inhaler therapy.
SURGICAL INTERVENTION

Rarely, surgical intervention may be offered to some patients. Surgical options include:

 Lung reduction surgery

 Bullectomy
 Lung transplantation

NURSING MANAGEMENT :

 Medication management: educating clients on how to properly use prescribed

medications/inhalers, such as bronchodilators, corticosteroids, or antibiotics
 Patient education on medication adherence, how to recognize and manage
exacerbations, and lifestyle modifications such as smoking cessation, exercise, and a
healthy diet
 Breathing techniques and exercise: teaching strategies to manage shortness of
breath, encouraging physical activity
 Managing oxygen therapy and teaching clients and families how to safely use and
maintain oxygen equipment at home
 Monitoring vital signs, lung function, and overall symptoms
 Care coordination with respiratory therapists, physiotherapists, dietitians, and social
workers
 Emotional support for client and family
 End-of-life care: discussions about advance directives, palliative care options, and
hospice care in advanced cases

COMPLICATIONS :

Common complications associated with COPD include:

 Respiratory failure
 Pneumonia: often recurrent
 Pneumothorax: rupture of bullous disease
 Polycythaemia or anaemia
 Depression.
 CORPULMONALE

DEFINITION :

Cor pulmonale is a condition that causes the right side of the heart to fail. Long-term
high blood pressure in the arteries of the lung and right ventricle of the heart can lead to cor
pulmonale. ( Right-sided heart failure; Pulmonary heart disease )

CAUSES

 High blood pressure in the arteries of the lungs is called pulmonary hypertension. It is
the most common cause of cor pulmonale.
 In people who have pulmonary hypertension, changes in the small blood vessels
inside the lungs can lead to increased blood pressure in the right side of the heart. This
makes it harder for the heart to pump blood to the lungs. If this high pressure
continues, it puts a strain on the right side of the heart. That strain can cause cor
pulmonale.
 Lung conditions that cause a low blood oxygen level in the blood over a long time can
also lead to cor pulmonale. Some of these are:
a. Autoimmune diseases that damage the lungs, such as scleroderma
b. Chronic obstructive pulmonary disease (COPD)
c. Chronic blood clots in the lungs
d. Cystic fibrosis (CF)
 e. Severe bronchiectasis
f. Scarring of the lung tissue (interstitial lung disease)
g. Severe curving of the upper part of the spine (kyphoscoliosis)
h. Obstructive sleep apnea, which causes stops in breathing because of airway
inflammation
i. Idiopathic (no specific cause) tightening (constriction) of the blood vessels of the
lungs
j. Severe left-sided heart failure

SYMPTOMS

 Shortness of breath or lightheadedness during activity is often the first symptom of

cor pulmonale. may also have a fast heartbeat and feel like heart is pounding.
 Over time, symptoms occur with lighter activity or even while you are at rest.
Symptoms you may have are:
 Fainting spells during activity
 Chest discomfort, usually in the front of the chest
 Chest pain
 Swelling of the feet or ankles
 Symptoms of lung disorders, such as wheezing or coughing or phlegm production
 Bluish lips and fingers (cyanosis)

DIAGNOSTIC EVALUATION :

perform a physical exam and ask about symptoms. The exam may find:

 Fluid build up in belly

 Abnormal heart sounds
 Bluish skin
 Liver swelling
 Swelling of the neck veins, which is a sign of high pressure in the right side of the
heart
 Ankle swelling
 These tests may help diagnose cor pulmonale as well as its cause:
 Blood antibody tests
 Blood test to check for a substance called brain natriuretic peptide (BNP)
  Chest x-ray
 CT scan of the chest, with or without an injection of a contrast fluid (dye)
 Echocardiogram
 ECG
 Lung biopsy (rarely done)
 Measurement of blood oxygen by checking arterial blood gas (ABG)
 Pulmonary (lung) function tests
 Right heart catheterization
 Ventilation and perfusion scan of the lungs (V/Q scan)
 Tests for autoimmune lung disease

Treatment

 The goal of treatment is to control symptoms. It is important to treat medical

problems that cause pulmonary hypertension, because they can lead to cor pulmonale.
 Many treatment options are available. In general, the cause of cor pulmonale will
determine which treatment receive.
 If provider prescribes medicines, may take them by mouth (oral), receive them
through a vein (intravenous or IV), or breathe them in (inhaled). will be closely
monitored during treatment to watch for side effects and to see how well the medicine
works . Never stop taking medicines without first talking to provider.

Other treatments may include:

 Blood thinners to reduce the risk of blood clots

 Medicines to manage heart failure symptoms
 Oxygen therapy at home (as in most cases of cor pulmonale, oxygen is low)
 A lung or heart-lung transplant, if medicine does not work

Important tips to follow:

 Avoid strenuous activities and heavy lifting.

 Avoid traveling to high altitudes.
 Get a yearly flu vaccine, as well as other vaccines, such as the pneumonia vaccine,
and the COVID vaccine.
 Stop smoking.
 Limit how much salt you eat.
  limit how much fluid drink during the day.
 Use oxygen if prescribed it.
 Women should not get pregnant.

COMPLICATIONS :

 Cor pulmonale may lead to:

 Life-threatening shortness of breath
 Severe fluid buildup in the body
 Shock
 Death
 ACUTE RESPIRATORY FAILURE

DEFINITION:

The loss of the ability to ventilate adequately or to provide sufficient oxygen to the
blood and systemic organs. The pulmonary system is no longer able to meet the metabolic
demands of the body with respect to oxygenation of the blood and/or CO2 elimination.

CLASSIFICATION:

Type 1 (Hypoxemic ) - PO2 < 50 mmHg on room air. Usually seen in patients with acute
pulmonary edema or acute lung injury. These disorders interfere with the lung's ability to
oxygenate blood as it flows through the pulmonary vasculature.

Type 2 (Hypercapnic/ Ventilatory ) - PCO2 > 50 mmHg (if not a chronic CO2 retainer). This
is usually seen in patients with an increased work of breathing due to airflow obstruction or
decreased respiratory system compliance, with decreased respiratory muscle power due to
neuromuscular disease, or with central respiratory failure and decreased respiratory drive.

Type 3 (Peri-operative). This is generally a subset of type 1 failure but is sometimes

considered separately because it is so common.

Type 4 (Shock) - secondary to cardiovascular instability.

CAUSES :

ARF can result from a variety of causes . It can result from primary pulmonary pathologies or
can be initiated by extra-pulmonary pathology. Causes are often multifactorial. Acute
respiratory failure can be caused by abnormalities in:

 CNS ( drugs, metabolic encephalopathy, CNS infections, increased ICP, OSA, Central
alveolar hypoventilation)

 spinal cord (trauma, transverse myelitis)

 neuromuscular system ( polio, tetanus, M.S., M.Gravis, Guillain-Barre, critical care or

steroid myopathy)

 chest wall ( Kyphoscoliosis, obesity)

 upper airways ( obstruction from tissue enlargement, infection, mass; vocal cord
paralysis, tracheomalacia)

 lower airways ( bronchospasm, CHF, infection)

 lung parenchyma ( infection, interstitial lung disease)

 cardiovascular system

CLINICAL MANIFESTATIONS :

Symptoms of respiratory failure depend on the cause. Symptoms may include:

 Shortness of breath or feeling like you can’t get enough air (dyspnea).
 Rapid breathing (tachypnea).
 Extreme tiredness (fatigue).
 Fast heart rate (feeling like the heart’s racing) or heart palpitations.
  Spitting or coughing blood or bloody mucus (hemoptysis).
 Excessive sweating.
 Restlessness.
 Pale skin.
 Bluish skin, lips or nails (cyanosis).
 Headaches.
 Blurred vision.
 Agitation, confusion or being unable to think straight.
 Behavioural changes, not acting like self.

DIAGOSTIC EVALUATION :

Some or all of the following tests to help diagnose respiratory failure:

Pulse oximetry: A sensor slips over the finger to measure the amount of oxygen in the blood.
Providers often check this each time of visit.

Arterial blood gas (ABG) test: A needle is used to take a blood sample from the wrist, arm
or groin to measure the levels of oxygen and carbon dioxide in the blood.

Lung function tests. Also called pulmonary function tests (PFT), physician may ask patient
breathe into a mouthpiece attached to a machine to test how well lungs work.

Imaging. Physician may use X-rays and CT scans to get images of the inside of the body.
These don’t diagnose respiratory failure, but they can help the physician know what’s
causing it.

Electrocardiogram (EKG). An EKG tests how well the heart is working. If indicated as a
heart condition is causing respiratory failure, they get an EKG.

TREATMENT:
MEDICAL MANAGEMENT

 Identify and treat the underlying condition insure early detection; use aggressive
supportive treatment; prevent infection ( intubation and mechanical ventilation).
 As disease progresses, use positive and expiratory pressure PEEP ( neuromuscular
blocking agent such as pancuronium (pavulon and vecuronium) (norcuron) maybe
used to paralyzed patient for easier ventilation.
  Monitor arterial blood gas values , pulse symmetry , and pulmonary function testing.
 Provide circulatory support; treat hypovolemia carefully ; avoid overload
 Provide adequate fluid management ; administer intravenous solutions
 Provide nutritional support; (35 to 45 kilocalories per kilogram daily)
 Pharmacologic therapy may include human recombinant interleukin-1 receptor
antagonist, neutrophil inhibitors, pulmonary- specific vasodilators, surfactant
replacement therapy, antisepsis agents, antioxidant therapy, and corticosteroids (late
in the course of ARDS).

Pharmacologic Intervention

General Comments: Use of genetically engineered surfactant has been studied in

ARDS but has not demonstrated the success that has occurred in premature infants with
surfactant deficiency. Corticosteroids have been widely used in ARDS, yet studies have
not consistently demonstrated any improvement in patient outcomes and remain
controversial. Some evidence exists that prolonged treatment with low-dose
corticosteroids may benefit patients with unresolving ARDS, particularly by reversing
the process of fibroproliferation. If the patient is difficult to ventilate, she or he may
receive skeletal muscle relaxants such as vecuronium (Norcuron), which are
neuromuscular-blocking agents that paralyze the patient’s skeletal muscles. These
medications are used only when the patient’s gas exchange is so poor as to threaten his
or her life. Neuromuscular-blocking agents paralyze the patient without affecting mental
status, so the patient requires sedation to counteract the accompanying fear and anxiety
that occur when the patient is unable to move.
 Nitric oxide Inhalation route a pulmonary vascular vasodilator to decreases pulmonary
vascular resistance with increased perfusion to ventilated areas

Nursing Intervention

1. Identify and treat cause of the Acute respiratory distress syndrome

2. Administer oxygen as prescribed.
3. Position client in high fowler’s position.
4. Restrict fluid intake as prescribed.
5. Provide respiratory treatment as prescribed.
6. Administer diuretics, anticoagulants or corticosteroids as prescribed.
7. Prepare the client for intubation and mechanical ventilation using PEEP.
 ADULT RESPIRATORY DISTRESS SYNDROME

Acute respiratory distress syndrome (ARDS) is a lung injury that happens when fluids build
up in small air sacs (alveoli) in the lungs. ARDS prevents the lungs from filling up with air
and causes dangerously low oxygen levels in the blood (hypoxia). Healthcare providers
typically diagnose a person as having mild, moderate or severe respiratory distress syndrome.
They determine that level by comparing the level of oxygen in the blood with the amount of
oxygen that needs to be given to achieve a healthy blood oxygen level.

ARDS prevents other organs such as the brain, heart, kidneys and stomach from getting the
oxygen they need to function. ARDS is dangerous and can lead to several serious and life-
threatening problems.

ARDS typically happens when a person is in the hospital receiving treatment for an infection,
illness or trauma. If they are not hospitalized and experience symptoms of ARDS, get
medical attention immediately.
CAUSES OF ARDS INCLUDE:

Sepsis: Sepsis is the most common cause of ARDS. It can happen when the patient have a
serious infection in the lungs (pneumonia) or other organs with widespread inflammation.

Aspiration pneumonia: Aspiration of stomach contents into the lungs may cause severe lung
damage and ARDS. Aspiration is when food, liquid or other substances get into the airway
and lungs.

Blood transfusions: patients at risk for ARDS if they receive more than 15 units of blood in
a short period of time.

COVID-19: The COVID-19 virus may develop into severe ARDS.

Pancreatitis: Severe inflammation in the pancreas.

Major trauma or burns: Accidents and falls may directly damage the lungs or other organs
in the body and trigger severe inflammation in the lungs.

Inhalational injury: Breathing and exposure to high concentrations of chemical fumes or

smoke.

Drug overdose: An overdose on drugs like cocaine and opioids.

Drowning or near drowning: Drowning causes water to get into the lungs, causing damage.

Some factors that can increase the risk include:

 Being older than 65.

 Tobacco use.
 Substance abuse disorder.
 Having lung disease.

CLINICAL MANIFESTATIONS :

The signs and symptoms of ARDS can vary in intensity, depending on its cause and severity,
as well as the presence of underlying heart or lung disease. They include:

 Severe shortness of breath

 Labored and unusually rapid breathing

  Low blood pressure

 Confusion and extreme tiredness

Another cause of ARDS is pneumonia, which is the infection of the lungs. The common
signs and symptoms include cough, fever, sputum production, chills, and fluid accumulation
in the space surrounding the lungs. Bacteria, viruses, and other pathogens may cause
infection of the lungs.

When the fluid accumulates in the alveoli, they lose their ability to oxygenate the blood
and eliminate carbon dioxide. Patients with ARDS may start having severe shortness of
breath, muscle fatigue, general weakness, low blood pressure, rapid and shallow breathing,
drowsiness or confusion, feeling faint, dry and hacking cough, headaches, and fever.

In severe cases, the lungs may become heavy and unable to expand, with patients
requiring mechanical ventilation due to respiratory failure. With ARDS, other organs may fail
to work properly, leading to multiple organ failure, affecting the heart, kidneys, liver,
bloodstream, and brain.

DIAGNOSTIC EVALUATION :

There's no specific test to identify ARDS. The diagnosis is based on the physical exam, chest
X-ray and oxygen levels. It's also important to rule out other diseases and conditions — for
example, certain heart problems — that can produce similar symptoms.

Imaging

 Chest X-ray. A chest X-ray can reveal which parts of the lungs and how much of the
lungs have fluid in them and whether the heart is enlarged.

 Computerized tomography (CT). A CT scan combines X-ray images taken from

many different directions into cross-sectional views of internal organs. CT scans can
provide detailed information about the structures within the heart and lungs.

Lab tests

A test using blood from an artery in the wrist can measure the oxygen level. Other types of
blood tests can check for signs of infection or anemia. If the doctor suspects that they have a
lung infection, secretions from the airway may be tested to determine the cause of the
infection.

Heart tests

Because the signs and symptoms of ARDS are similar to those of certain heart problems, the
physician may recommend heart tests such as:

 Electrocardiogram. This painless test tracks the electrical activity in the heart. It
involves attaching several wired sensors to the body.

 Echocardiogram. A sonogram of the heart, this test can reveal problems with the
structures and the function of the heart.

Treatment

The first goal in treating ARDS is to improve the levels of oxygen in the blood. Without
oxygen, the organs can't function properly.

Oxygen

To get more oxygen into the bloodstream, the doctor will likely use:

 Supplemental oxygen. For milder symptoms or as a temporary measure, oxygen may

be delivered through a mask that fits tightly over the nose and mouth.

 Mechanical ventilation. Most people with ARDS will need the help of a machine to
breathe. A mechanical ventilator pushes air into the lungs and forces some of the fluid
out of the air sacs.

Fluids

Carefully managing the amount of intravenous fluids is crucial. Too much fluid can increase
fluid buildup in the lungs. Too little fluid can put a strain on the heart and other organs and
lead to shock.
Medication

People with ARDS usually are given medication to:

 Prevent and treat infections

 Relieve pain and discomfort

 Prevent blood clots in the legs and lungs

 Minimize gastric reflux

 Sedate

NURSING MANAGEMENT :

1.Assess and monitor vital signs and respiratory status.

Alterations in respiratory rate and depth along with tachycardia can indicate respiratory
decline.

2. Assess the patient’s level of consciousness.

Altered mental status changes including agitation, confusion, and lethargy are late signs of
impaired gas exchange.

3. Assess ABG levels and oxygen saturation.

Abnormal levels in oxygen saturation (less than 90%) and PaO2 (less than 60 mmHg) can
signal significant oxygenation problems.

4.Encourage the client to perform breathing exercises.

Deep breathing allows optimum lung expansion and promotes oxygenation. Pursed-lip
breathing helps patients with chronic lung diseases breathe with more control.

5. Administer supplemental oxygen at the lowest concentration.

Supplemental oxygenation may be delivered through the use of a nasal cannula or Venturi
mask for defined oxygen delivery.

6. Administer medications.
Treating the underlying cause of acute respiratory failure should occur alongside
oxygenation. This includes administering glucocorticoids, antibiotics, and breathing
treatments.
7. Assist with intubation.
Some patients experiencing acute respiratory failure will require mechanical ventilation for
emergency management. Assist the healthcare provider in preparing the airway.

8.Assess and monitor breath sounds.

Wheezing is indicative of narrowed/obstructed airways. Crackles and rales signal fluid or
mucus filled bronchioles.

9. Assess respiratory rate, depth, and pattern.

Tachypnea, labored breathing, and accessory muscle use signal respiratory distress.

10. Identify those at risk of ineffective airway clearance.

Patients with a history of COPD, cystic fibrosis, or difficulty swallowing/coughing such as
with a stroke, developmental delays, muscular dystrophy, etc., are at a higher risk of
obstructed airways.

11.Obtain a sputum sample.

Attempt to obtain a sample of sputum for testing to determine an underlying infectious
process and appropriate antibiotic regimen.

12. Encourage respiratory device use.

Devices such as an incentive spirometer or flutter valve can be encouraged to mobilize
secretions.

13. Administer medications as indicated.

Bronchodilators open airways while expectorants loosen and thin mucus making it easier to
cough up.

14.Suction as needed.
Patients who cannot clear oral secretions or swallow may need suctioning PRN. Patients with
a tracheostomy often require frequent suctioning to clear secretions.

15.Assess activity intolerance.

The level of activity intolerance ranges from 1-4. Level 1 is the ability to walk at a regular
pace indefinitely with minimal shortness of breath while level 4 is dyspnea and fatigue at rest.
16. Note contributing factors.
Along with respiratory conditions, consider age, weight, and other comorbidities that may
impact activity tolerance.

17.Plan interventions with adequate rest periods.

Patients with respiratory failure are easily fatigued. It is essential to plan care with rest
periods in between to decrease oxygen demand.

18.Increase activities within limitations.

Encourage ambulation and exercise as tolerated. Ensure safety by implementing the use of
assistive devices and gait belts. Increase activity within the patient’s desired abilities.

19.. Ensure adequate oxygen equipment.

Patients may require long-term and continuous supplemental oxygen. Ensure they have
adequate supplies and O2 canisters at discharge.

20. Encourage a healthy lifestyle.

Nutritious diets, appropriate fluid intake, not smoking, and maintaining a healthy weight all
contribute to improved activity tolerance.
 PULMONARY EMBOLISM

A pulmonary embolism is a blood clot that blocks and stops blood flow to an artery in
the lung. In most cases, the blood clot starts in a deep vein in the leg and travels to the lung.
Rarely, the clot forms in a vein in another part of the body.

A pulmonary embolism is a sudden instance of blockage in one or more of the

pulmonary arteries, often caused by a clot that travels to the lungs from other parts of the
body. Pulmonary embolisms are an urgent, potentially life-threatening medical condition that
requires hospitalization and intervention.

CAUSES :

Factors that increase the risk of pulmonary embolism include:

 Injury
 Surgery
 Heart disease
 Cancer
  Pregnancy
 Supplemental estrogen
 Smoking
 Prolonged immobility
 COVID-19

SIGNS & SYMPTOMS :

Pulmonary embolism symptoms may include:

 Sudden shortness of breath — whether you’ve been active or at rest.

 Unexplained sharp pain in the chest, arm, shoulder, neck or jaw. The pain may also be
similar to symptoms of a heart attack.
 Cough with or without bloody mucus.
 Pale, clammy or bluish skin.
 Rapid heartbeat (pulse).
 Excessive sweating.
 In some cases, feeling anxious, lightheaded, faint or passing out.
 Wheezing.

DIAGNOSTIC EVALUATIONS :

The following tests to make a PE diagnosis:

 Blood tests (including the D-dimer test).

 Computed tomography (CT) angiogram.
 Ultrasound of the leg. (This helps identify blood clots in people’s legs, or deep vein
thrombosis, which can move to the lungs and become a PE and cause more damage.)
 A ventilation/perfusion (V/Q) scan, if you’re unable to get contrast for a CT scan. (This
is a nuclear scan that can detect clots in the lung.)
 Other tests the provider may order include:
 Pulmonary angiogram.
 Chest X-ray.
TREATMENT :

Treatment can include medicines, surgery and other procedures, and ongoing care.

Medicines

Medicines include different types of blood thinners and clot dissolvers.

 Blood thinners. These blood-thinning medicines called anticoagulants prevent existing

clots from getting bigger and new clots from forming while the body works to break up
the clots. Heparin is a frequently used anticoagulant that can be given through a vein or
injected under the skin. It acts quickly and is often given along with an oral
anticoagulant, such as warfarin (Jantovin), until the oral medicine becomes effective.
This can take several days.

Newer oral anticoagulants work more quickly and have fewer interactions with other
medicines. Some have the advantage of being given by mouth until they're effective,
without the need for heparin. However, all anticoagulants have side effects, and
bleeding is the most common.

 Clot dissolvers. While clots usually dissolve on their own, sometimes thrombolytics —
medicines that dissolve clots — given through a vein can dissolve clots quickly.
Because these clot-busting medicines can cause sudden and severe bleeding, they
usually are reserved for life-threatening situations.

Surgical and other procedures

 Clot removal. If you have a large, life-threatening clot in the lung, the health care
provider may remove it using a thin, flexible catheter threaded through the blood
vessels.

 Vein filter. A catheter also can be used to position a filter in the body's main vein, the
inferior vena cava, that leads from the legs to the right side of the heart. The filter can
help keep clots from going to the lungs. This procedure is usually only used for people
who can't take anticoagulant drugs or those who get blood clots even with the use of
anticoagulants. Some filters can be removed when no longer needed.
NURSING MANAGEMENT :

1. Administer supplemental oxygen.

Supplemental oxygen is recommended in individuals with oxygen saturation levels under
90%. Unstable patients may require mechanical ventilation.

2. Resuscitate volume aggressively.

The most prevalent cause of death in patients with hemodynamically unstable PE is acute
right ventricular (RV) failure. Aggressive volume resuscitation can cause the RV to
overextend and lower cardiac output (CO). Thus, only patients with collapsing prominent
veins (inferior vena cava) should receive intravenous fluid resuscitation. Hemodynamic
support may include the use of vasopressors.

3. Consider life-saving measures.

Extracorporeal membrane oxygenation (ECMO) is an example of a mechanical
cardiopulmonary support device used in instances of high-risk, severe PE when other therapy
has failed or if the patient cannot tolerate thrombectomy.

4. Understand the need for anticoagulation.

It is crucial to understand that anticoagulation is the cornerstone of PE treatment. It also
relieves chest and calf pain by promoting good blood flow to the affected area.

5. Administer anticoagulants as ordered.

PE can be treated with anticoagulation using:

Low-molecular-weight heparin (LMWH)

Unfractionated heparin (UFH)

6. Monitor for bleeding.

There is a risk of bleeding with any anticoagulant. Monitor for bloody stools, bruising,
hemoptysis (coughing up blood), and epistaxis (bloody nose).

7. Consider NOACs.
Deep vein thrombosis (DVT) and PE are now treated and prevented with non-vitamin K
antagonist oral anticoagulants (NOAC). Dabigatran, apixaban, and rivaroxaban are examples
of NOACs. They are also called ―DOACs,‖ or direct oral anticoagulants.
8. Monitor for PTT/INR.
The dosage of warfarin used daily to maintain proper blood thinning is determined by the
INR (international normalized ratio). Blood tests are not required to check the effectiveness
of the dosage of DOACs. IV unfractionated heparin is monitored through routine PTT (partial
thromboplastin time) law draws to ensure therapeutic levels.

9. Assist in catheter-directed treatment.

With catheter-directed thrombolytic therapy, the clot-busting medication is delivered directly
into the pulmonary artery at the location of the clot.

10. Surgically remove the clot.

The clot is removed using a catheter placed into the pulmonary artery. It is done through
thrombectomy (removal of thrombus) or embolectomy (removal of embolus).

11. Consider vena cava filters.

The risk of recurrent PE decreases after placing a permanent vena cava filter. Vena cava
filters are recommended for patients:

With a contraindication to anticoagulants

Still experiencing VTE, and anticoagulants are no longer working

12. Wear compression stockings.

In those with a prior history of a clot, compression stockings may aid in preventing recurrent
DVT. Legs are steadily compressed by compression stockings, which improves blood flow
via the veins and muscles of the legs. Compression stocks are a low-cost method for
preventing blood from pooling in the legs before and after surgery.

13. Encourage early ambulation.

Following surgery, ambulation can aid in preventing pulmonary embolism and speed up
recovery in general. Encourage the patient to get up and move around on the day of their
surgery if not contraindicated.

14. Elevate the legs.

Elevating the patient’s legs at night and whenever sitting is therapeutic. Pillows can be used
to elevate the legs and feet.
15. Use pneumatic compression.
Thigh-high or calf-high cuffs used in pneumatic compression therapy automatically inflate
and deflate every few minutes. The legs’ veins are massaged and constricted, increasing
blood flow and circulation.

16. Increase fluid intake.

Dehydration can lead to the formation of blood clots. Water is the best liquid to prevent blood
clots. Avoid alcohol due to the effects of fluid loss.

17. Move periodically.

When on a long car ride, stop and stretch. On a plane, bend the knees and pump the feet to
promote circulation.

18. Avoid sitting still.

Every 15 to 30 minutes, advise the patient to reposition, move the ankles in circles, and lift
the toes when sitting for a long time. Emphasize the need to move even when sitting to
promote circulation.

19.Assess respiratory status.

The blood supply to the lungs is restricted by pulmonary embolism, which reduces oxygen
levels and raises blood pressure in the pulmonary arteries. The lungs are affected based on the
clot size and the presence of an underlying lung or heart disease. The symptoms of a
pulmonary embolism can vary but usually result in chest pain with breathing, shortness of
breath, and coughing.

20. Auscultate for lung sounds.

Bibasilar crackles or wheezing lung sounds are expected for patients with pulmonary
embolism.

21. Review ABG analysis.

Suspicion for pulmonary embolism increases in patients with unexplained hypoxemia and a
normal chest radiograph. The ABG analysis reveals respiratory alkalosis and hypocapnia.

22. Obtain chest X-ray.

A blood clot will not show on a chest X-ray, but this imaging is useful when a patient
presents with acute dyspnea to rule out other possible diseases.
 PULMONARY HYPERTENSION

Pulmonary hypertension is high blood pressure in the arteries of the lungs. It makes
the right side of the heart work harder than normal.

CAUSES :

The right side of the heart pumps blood through the lungs, where it picks up oxygen.
Blood returns to the left side of the heart, where it is pumped to the rest of the body.

When the small arteries (blood vessels) of the lungs become narrowed, they cannot
carry as much blood. When this happens, pressure builds up. This is called pulmonary
hypertension.

The heart needs to work harder to force the blood through the vessels against this
pressure. Over time, this causes the right side of the heart to become larger. This condition is
called right-sided heart failure, or cor pulmonale.

Pulmonary hypertension may be caused by:

 Autoimmune diseases that damage the lungs, such as scleroderma and rheumatoid
arthritis
 Birth defects of the heart
 Blood clots in the lung (pulmonary embolism)
 Heart failure (of the left side of the heart)
  Heart valve disease
 HIV infection
 Low oxygen levels in the blood for a long time (chronic)
 Lung disease, such as COPD or pulmonary fibrosis or any other severe chronic lung
condition
 Medicines (for example, certain diet drugs)
 Obstructive sleep apnea

In rare cases, the cause of pulmonary hypertension is unknown. In this case, the condition
is called idiopathic pulmonary arterial hypertension (IPAH). Idiopathic means the cause of a
disease is not known. IPAH affects more women than men.

If pulmonary hypertension is caused by a known medicine or medical condition, it is called

secondary pulmonary hypertension.

PULMONARY HYPERTENSION FUNCTIONAL CLASSIFICATION

Once a diagnosis of pulmonary hypertension is confirmed, the condition is classified

according to how the symptoms affect you and the ability to do everyday tasks.

Pulmonary hypertension may fall into one of the following groups:

Class I. Pulmonary hypertension is diagnosed, but there are no symptoms during rest or
exercise.

Class II. There are no symptoms at rest. Everyday chores or activities such as going to work
or the grocery store may cause some shortness of breath or mild chest pain. There's a slight
limitation of physical activity.

Class III. It's comfortable at rest, but doing simple tasks such as bathing, dressing or
preparing meals causes fatigue, shortness of breath and chest pain. The ability to do physical
activity becomes very limited.

Class IV. Symptoms occur at rest and during physical activity. Any type of activity causes
increasing discomfort.
SIGNS AND SYMPTOMS :

 Shortness of breath or light headedness during activity is often the first symptom. Fast
heart rate (palpitations) may be present. Over time, symptoms occur with lighter
activity or even while at rest.
 Other symptoms include:
 Ankle and leg swelling
 Bluish colour of the lips or skin (cyanosis)
 Chest pain or pressure, most often in the front of the chest
 Dizziness or fainting spells
 Fatigue
 Increased abdominal size
 Weakness
 People with pulmonary hypertension often have symptoms that come and go. They
report good days and bad days.

DIAGNOSTIC EVALUATION :

 Abnormal heart sounds

 Feeling of a pulse over the breastbone
 Heart murmur on the right side of the heart
 Larger-than-normal veins in the neck
 Leg swelling
 Liver and spleen swelling
 Normal breath sounds if pulmonary hypertension is idiopathic or due to congenital
heart disease
 Abnormal breath sounds if pulmonary hypertension is from other lung disease

In the early stages of the disease, the exam may be normal or almost normal. The condition
may take several months to diagnose. Asthma and other diseases may cause similar
symptoms and must be ruled out.

Tests that may be ordered include:

 Blood tests
 Cardiac catheterization
 Chest x-ray
 CT scan of the chest
  Echocardiogram
 ECG
 Lung function tests
 Nuclear lung scan
 Pulmonary arteriogram
 6-minute walk test
 Sleep study
 Tests to check for autoimmune problems

TREATMENT :

Treatment may include:

Medicines to relax blood vessels. Also called vasodilators, these medicines help open
narrowed blood vessels and improve blood flow. The medicine comes in many forms. It may
be breathed in, taken by mouth or given by IV. Some types are given continuously through a
small pump attached to the body.

Examples of vasodilators to treat pulmonary hypertension include epoprostenol (Flolan,

Veletr), treprostinil (Remodulin, Tyvaso, others), Iloprost (Ventavis) and selexipag (Uptravi).

Soluble guanylate cyclase (sGC) stimulators. This type of medicine relaxes the pulmonary
arteries and lowers pressure in the lungs. Examples include riociguat (Adempas). Do not take
these medicines if you're pregnant.

Medicines to widen blood vessels. Medicines called endothelin receptor antagonists reverse
the effect of a substance in the walls of blood vessels that causes them to narrow. Such
medicines include bosentan (Tracleer), macitentan (Opsumit) and ambrisentan (Letairis).
They may improve energy level and symptoms. Do not take these medicines if you are
pregnant.

Medicines to increase blood flow. Medicines called phosphodiesterase 5 (PDE5) inhibitors

may be used to increase blood flow through the lungs. These medicines also are used to treat
erectile dysfunction. They include sildenafil (Revatio, Viagra) and tadalafil (Adcirca, Alyq,
Cialis).

High-dose calcium channel blockers. These medicines help relax the muscles in the walls of
blood vessels. They include amlodipine (Norvasc), diltiazem (Cardizem, Tiazac, others) and
nifedipine (Procardia). Although calcium channel blockers can be effective, only a small
number of people with pulmonary hypertension improve while taking them.

Blood thinners. Also called anticoagulants, these medicines help prevent blood clots. One
example is warfarin (Jantoven). Blood-thinning medicines slow the clotting process. The
medicines can increase the risk of bleeding. This is especially true if you're having surgery or
a procedure that enters the body or creates an opening in the skin. Talk to the health care
team about the risk.

Digoxin (Lanoxin). This medicine helps the heart beat stronger and pump more blood. It can
help control irregular heartbeats.

Water pills, also called diuretics. These medicines help the kidneys remove excess fluid from
the body. This reduces the amount of work the heart has to do. Diuretics also may be used to
reduce fluid buildup in the lungs, legs and belly area.

Oxygen therapy. Breathing pure oxygen is sometimes recommended as a treatment for

pulmonary hypertension. This treatment may be suggested if you live at a high altitude or
have sleep apnea. Some people with pulmonary hypertension need oxygen therapy all the
time.

Surgery or other procedures

If medicines do not help control the symptoms of pulmonary hypertension, surgery may be
recommended. Surgeries and procedures to treat pulmonary hypertension may include:

Atrial septostomy. This treatment may be recommended if medicines don't control pulmonary
hypertension symptoms. In an atrial septostomy, a doctor creates an opening between the
upper left and right chambers of the heart. The opening reduces the pressure on the right side
of the heart. Potential complications include irregular heartbeats called arrhythmias.

Lung or heart-lung transplant. Sometimes, a lung or heart-lung transplant may be needed,

especially for younger people who have idiopathic pulmonary arterial hypertension. After a
transplant, medicine must be taken for life to help reduce the chance of rejection.

NURSING MANAGEMENT :

 Avoid adding salt at the table or using ―seasoning salt.‖

 Avoid smoked, cured, salted and canned meat products.
  Buy foods that are ―low sodium‖ or ―low salt.‖
 Limit fast foods and prepared foods.

Other dietary changes include:

 Eat foods high in fiber (like whole grains, bran, fruits and vegetables).
 Eat foods high in potassium (like dried fruits, bananas and oranges).
 Eat foods high in magnesium (like peanuts, tofu and broccoli).
 Limit foods that contain refined sugar, saturated fat and cholesterol.

Seek medical attention if conditions like

 A fast heart rate (120-150 beats per minute) that won’t go down.
 Fainting spells with loss of consciousness.
 Hickman catheter complications with intravenous prostacyclins. These include
infection, catheter displacement, solution leak, bleeding and IV pump malfunction.
 Shortness of breath that doesn’t go away when rest.
 Sudden and severe chest pain.
 Sudden and severe headache.
 Sudden weakness or paralysis in the arms or legs.