LOWER RESPIRATORY DISORDERS

PLEURAL PAIN
• A common pulmonary manifestations arising from the parietal pleura, which is
richly supplied with sensory nerve endings
• Indicates the presence of pleural inflammation (pleurisy)

Assessment:
• Pain is well localized and may be referred to neck, shoulder or abdomen.
• Upon chest auscultation, often accompanied by pleural friction rub
• Occurs on only one side of the chest, usually in lower lateral portions of the chest
wall
• Aggravated by deep breathing or coughing
• Develops abruptly and is usually severe enough

Medical Management:
• Administration of prescribed analgesics
• If not relieved, physician may perform intercostal nerve block

Nursing Management:
• Turn on the affected side to splint the chest wall. This will lessen the stretch of
pleura
• Teach the client to use his/her hand to splint chest

PLEURISY
• Inflammation of both visceral and parietal pleura

Pathophysiology:
• The pleurae normally reduce the friction between the chest structures as the
lungs expand and contract. Offending pathogens invade the sterile lower
respiratory tract which causes inflammation of the lining of the lung cavity.
Inflammation of the pleurae causes breathing to become painful and less
effective.

Assessment:
• Severe, sharp, knifelike pain when rub together during inspiration
• Pain may become minimal or absent when the breath is held or it may be
localized or radiate to the shoulder or abdomen

Management:
• Objective – To discover the underlying condition causing the pleurisy and to
relieve pain
 • Prescribed analgesics and application of heat and cold provides symptomatic
relief
• Antibiotics are usually prescribed to treat underlying infection or disease

Nursing Management:
• Turn on the affected side to splint the chest wall. This will lessen the stretch of
pleura
• Teach the client to use his/her hand to splint chest

PLEURAL EFFUSION
OVERVIEW:
-collection of fluid in the pleural space located in the visceral and parietal
layers.
-rare, primary disease process that occurs secondary to other diseases
-causes of pleural effusion are either systemic or local
a. systemic diseases
-hydrothorax: heart failure, renal failure, liver failure
-empyema (pus in the pleural cavity): infections, malignancies,
connective tissue disorders
b. local diseases
-hemothorax(blood in the cavity): chest wall injuries, surgery to the chest
-chylothorax: trauma, inflammation(pneumonia,TB), or malignancy

Assessment:
-dyspnea
-diminished or absent breath sounds on affected side
-pain
-limited chest wall movement
-dull or flat sounds on percussion
-symptom analysis of any pain experienced, dyspnea, coughing, vital
signs(elevated temperature), respiratory rate and status(shallow respiratory,
asymmetry), lung sounds(diminished), and percussion for flat or dull sound over
area.
PATHOPHYSIOLOGY
1. Pleural effusion results from:
a. An increase in hydrostatic pressure in the pleural capillaries or
decreased colloid osmotic pressure in the circulatory system that can
lead to excess pleural fluid(transudative)
b. An increased capillary permeability as a result of inflammation,
infection, or malignancy(exudative)
2. The excess pressure exerted by the fluid in the pleural space compresses the
lung and limits its ability to expand, thus compromising gas exchange
3. Amount of fluid in the pleural space can become so large as to displace lung
tissue and result in a compression atelectasis
4. The decreased lung volume on the affected side results in diminished or absent
breath sounds(indicated in the signs and symptoms)

Diagnostic Tests

• chest xray(“white out”-opaque densities of area involved),

• thoracentesis(aspiration of fluid from pleural space)

• culture, sensitivity, and cytological examination of fluid if any removed;

• CT scan

• ultrasonography can determine pleural effusions if needed.

NURSING MANAGEMENT:
1. Medications
a. Antipyretics if fever or pain is present
b. Antibiotics, parenterally or instillation into the pleural space for
repeated effusions
 2. The goal of treatment is to resolve the underlying disease process causing
the problem and prevention of complications such as atelectasis or
pneumothorax
3. Monitos vital signs, especially respiratory rate, rhythm, and use of accessory
muscles
4. Monitor lung sounds and complaints of dyspnea
5. Manage pain if necessary along with bedrest
6. Monitor signs of changing status: tachycardia, hypotension, increasing
shortness of breath

EMPYEMA
• Accumulation of thick, purulent fluid within the pleural space, often with fibrin
development
• Complication of bacterial pneumonia or lung abscess

Pathophysiology:
• Entry of offending pathogens → Invasion of exogenous microorganisms to
respiratory tract→ Multiplication and colonization of microorganisms to sterile
lower respiratory tract → Initiation of Immune response → Results to
inflammation → Increase mucus production and phagocytosis → Accumulation of
exudates in the lungs → Increase in purulent fluid in the lungs→ Pus becomes
thick and almost solidified or loculated (containing cavities) → Fibrothorax
• Empyema most often is due to extension of infection from pneumonia.
Staphylococcal, gram negative and anaerobic infections are common infections
presenting in this mode.
• Anaerobic infections can seed pleura and start as the primary site of infection
without a preceding pneumonitis.
• It could also follow contamination of pleural space from non-sterile pleural taps.

Assessment:
• Chest auscultation - absent or decreased breath sounds
• Percussion – dullness and decreased fremitus
• Acute respiratory infection or pneumonia
• Fever and chills
• Weight loss
• Cough
• Chest pain upon inspiration
• Shortness of breath

Diagnostic Tests:
 • Chest X-ray
• CT scan
• Diagnostic Thoracentesis
• Pleural fluid gram stain and culture

Medical Management:
• Objective: To drain the pleural cavity and to achieve full lung re-expansion
• Antibiotics are prescribed to control the infection
• Needle Aspiration – Thoracentesis
• Tube Thoracostomy – chest drainage using a large diameter intercostal tube
• Open chest drainage via thoracotomy
• Decortication – involves removal of the restrictive mass of fibrin and inflammatory
cells
o Usually not performed until the fibrothorax is relatively solid, so it can be
easily removed

Nursing Management:
• Instruct patient in lung expanding breathing exercises
• Provide care specific to method of drainage of pleural fluid.

PULMONARY EMBOLISM

• Is an occlusion of a portion of the pulmonary blood vessels by an embolus

• Embolus – a clot or other plug (thrombus) that is carried by the blood stream
from its point of origin to a smaller blood vessel, obstructing the circulation

Assessment:

• Thrombi originating in the deep calf, femoral, poplitial, or iliac veins

• Emboli from other sources like tumors, air, fat, bone marrow, amniotic fluid,
septic thrombi, and vegetations of the heart with endocarditis

• Major operations predisposing the client to thrombus formation because of

reduced blood flow to pelvis

o Hip surgery

o Knee surgery

o Abdominal surgery
 o Extensive pelvic procedures

• Travelling in cramped position for a long time

• Sitting for long periods

Pathophysiology

Emboli travel to the lungs

Lodge in the pulmonary vasculature

Blood flow obstruction

Decreased perfusion of lung supplied by the obstructed vessel

• If embolus lodges in large vessel, it increases proximal pulmonary

vasculature resistance, causes atelectasis, and eventually reduces CO

• If embolus is in smaller vessel, perfusion is altered but lesser in clinical

manifestations

• PE can lead to right-sided heart failure : once the blood vessels of the
lungs collapse, there is increase pressure in the pulmonary vasculature.
Increased pulmonary pressure increases the workload of the right side of
the heart, leading to failure.

Assessment:

 nonspecific and may not appear until late in the event

 similar to those seen with MI and other CV Diseases

• Tachypnea

• Dyspnea

• Anxiety or fretfulness

• Pleuritic Chest pain (sudden in onset and exacerbated by breathing)

 • Hypoxemia may be present (depending on size of emboli)

• Apprehension

• Cough

• Diaphoresis

• Syncope

• Hemoptysis may occur (indicates alveolar damage)

• Tachycardia

• Fever

• Crackles

• Accentuated heart sounds

Diagnostic Test:

 when PE is suspected, the optimal strategy for diagnosis is an integrated

approach that includes a thorough history and physical examination,
supplemented by selected diagnostic tests:

• PULMONARY ANGIOGRAPHY

- the most definitive means of diagnosis Of PE

- radiopaque contrast agent is injected into the right atrium and pulmonary
artery via a catheter threaded through a peripheral vein
- very invasive, thus reserved for cases in which the index of clinical
suspicion is high despite nondiagnostic findings of other tests
• Pulse Oximetry may be low and unresponsive to inhaled O2

• ABG Analysis indicates arterial hypoxemia (low PAO2) and hypocapnia

(low PACO2) in massive PE

• Severe respiratory alkalosis may occur

• Chest Radiography to rule out other pulmonary diagnosis

• Radioisotope lung scan – IV injection of particles of human serum albumin

with labels iodine 131 or technetium 99m
 • Spiral CT Scan of the chest

• D-dimer plasma test helps exclude PE when the value is below 500 ng/L

Medical Management

1. Maintenance of cardiopulmonary stability is the first priority

• Hypoxemia can be reversed with low flow O2 via nasal cannula

or ET intubation to maintain PAO2 greater than 60mmHg

• Hypotension is treated with fluids and inotropic agents

• Acidosis is corrected with Bicarbonate to prevent its

vasoconstricting effect

2. Anticoagulant therapy

• To reduce the risk of further clots and prevent the extension of

existing clots. Anticoagulants do not break up existing clots

• Anticoagulant are administered until a therapeutic PTT is achieved

o IV Standard Heparin Sodium

o Low-molecular-weight heparin

o Sodium Warfarin – given 3-5 days before heparin is

stopped; taken for 2-6 months

3. Fibrinolytic Therapy

• Thrombolytic agents lyse the clots and restore right-sided heart

function

4. Analgesics for Chest pain

• Morphine is commonly used

Surgical Management
 1. Vena caval interruption with insertion of Greenfield filter

2. Embolectomy – involved surgical removal of emboli from the pulmonary

arteries by either a thoracotomy or an embolectomy catheter

Nursing Management

 Monitor the client closely for hypoxemia and respiratory compromise

 Assess V/S and lung sounds frequently

 Monitor ABG and oximetry values

 Monitor for right-sided heart failure manifestations (peripheral edema,

distended neck veins, liver engorgement)

 Auscultate heart sounds frequently for murmurs or extra heart sounds

 Elevate head of bed to facilitate breathing

 Elevate legs with caution to avoid severe flexure of the hip to prevent
formation of new thrombi

 Emotional support to reduce anxiety and apprehension

Stay with client; provide calm and safe environment

 Early ambulation
 Frequent leg exercises
 Sequential compression stockings
Anticoagulant prophylaxis
 Provide oral care esp. if client is in 02 therapy and breathes through the
mouth

 Observe for signs of bleeding as a side effect of anticoagulants

VENOUS AIR EMBOLISM (VAE)

 The entry of air into the venous system

• May occur in any condition in which an open vein above the right atrium level is
exposed to the atmosphere (e.g. insertion or removal of central venous catheters)
• Large boluses of air (3-8 ml/kg) can cause right ventricular outflow obstruction and
result in cardiogenic shock and circulatory arrest

Assessment:

 severity of manifestations is related to the degree of air entry

• Dyspnea

• Chest pain

• “mill wheel murmur” – a loud, churning, machinery-like murmur heard over

the precordium

• Tachycardia

• Hypotension

• Decreased consciousness

• Circulatory shock

• Sudden death ( with severe VAE)

Preventive Measures

• Carefully prime all intravenous tubings

• Secure all connections in central lines and protect them from being
dislodged

Nursing Management

• If VAE is suspected, any central line procedure in progress is terminated

and clamped

• Promptly place the client in Trendelenburg position and rotate toward the
left lateral decubitus position

 This maneuver helps trap air in the apex of the ventricle, prevents its
ejection into the pulmonary arterial system, and maintains right
ventricular output

• Inform Physician immediately

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

- Referred to by several terms, including shock lung, wet lung, post-traumatic

lung, congestive atelectasis, capillary leak syndrome, and adult hyaline
membrane disease.

- Also known as non-cardiogenic pulmonary edema

- Sudden progressive form of respiratory failure characterized by severe

dyspnea, refractory hypoxemia, and diffused bilateral infiltrates.

Assessment:

Etiology:

- Result of ischemia during shock

- Oxygen toxicity

- Inhalation of noxious fumes or fluids

- Inflammation from pneumonia

- Sepsis that traumatizes the alveolar capillary membrane

Risk Factors:

a.) Direct Pulmonary Trauma

- Viral, bacterial, fungal pneumonias

- Lung contusion

- Fat embolus

- Aspiration (e.g. foreign material, drowning, vomitus)

- Massive smoke inhalation

- Inhaled toxins

- Prolonged exposure to high concentrations of oxygen

b.) Indirect Pulmonary Trauma

- Sepsis

- Shock
 - Multisystem trauma

- DIC (Disseminated Intravascular Coagulation)

- Pancreatitis

- Uremia

- Drug overdose

- Anaphylaxis

- Idiopathic

- Prolonged heart bypass surgery

- Massive blood transfusions

- PIH (Pregnancy Induced Hypertension)

- Increased Intacranial pressure

- Radiation therapy

Pathophysiology:

Massive inflammatory response by the lungs

Increases permeability in the alveolar membrane

Resultant of fluid movement in the interstitial and alveolar spaces

Development of non-cardiogenic pulmonary edema

Decreases lung compliance and impairs oxygen transport

3 Phases of ARDS:
 a.) Phase I (Exudative Phase)

- Seen approximately 24 hours after initial insult

- Consists of damage to the capillary endothelium

- Leakage of fluid into the pulmonary interstitium

- Microemboli develops causing increase in pulmonary artery

pressures

- Inflammatory response accompanies pulmonary parenchymal

damage

- Release of toxic mediators, activation of complement, mobilization

of macrophages, release of vasoactive substances from mast cells.

- Further damage to the basement membrane, interstitial space,

alveolar epithelium.

b.) Phase II (Proliferative Phase)

- Begins 7 -10 days later

- Type 1 and type 2 alveolar cells are ultimately damaged

- Results to decreased surfactant production, alveolar collapse, and

atelectasis

- Impaired gas exchange

- Significant hypoxemia

c.) Phase III (Fibrotic Phase)

- Occurs 2 -3 weeks

- Irreversible deposition of fibrin into lung

- Pulmonary fibrosis

- Decreasing lung compliance and worsening hypoxemia

Clinical Manifestations:

- Dyspnea
 - Labored breathing

- Increase respiratory rate

- Hypoxemia

- Compensatory hypocapnia

- Respiratory alkalosis (hyperventilation)

- Metabolic acidosis (increased workload of breathing, hypoxemia)

Treatment and Nursing Interventions:

- Mechanical ventilation (maintain adequate blood oxygen levels)

- ET intubation

- Surfactant therapy

- Nitric oxide (bronchodilation)

- Antioxidants

- Steroids (improvement in pulmonary function)

- Prone position (improve oxygenation)

- Kinetic therapy (improve ventilation)

- Hemodynamic monitoring

- Inotropic Agents (improve cardiac output)

- Antibiotics

- Emotional support

ACUTE RESPIRATORY FAILURE

OVERVIEW:
-defined as the inability of the lungs to maintain adequate oxygenation and
usually manifested by hypoxemia, hypercapnia, and respiratory acidosis
-acute respiratory failure develops suddenly and can be life threatening;
causes can be pulmonary diseases, cardiac diseases, or non-pulmonary
 disorders(infections, injuries); ARF can develop in individuals with normal
lungs
-ABGs reveal a PaO2 less than 50 mmhg, PaCO2 less than 7.35; it is not a
disease process, but a sign of severe dysfunction of the respiratory system
-in the COPD client, a drop of 10-15 mmHg 02 from previous levels indicates
respiratory failure

PATHOPHYSIOLOGY:
1. The lungs are unable to remove CO2 and there is inadequate oxygen inhalation;
severe hypoventilation of the lungs causes a rise in the CO2 level and respiratory
acidosis
2. In chronic respiratory disorders such as emphysema and COPD, breathing
becomes more labred, respiratory muscles weaken, and airway resistance is
increased
3. Clients become extremely exhausted and lose the energy to breathe; ventilation,
diffusion, or perfusion problems may cause respiratory failure
4. As breathing difficulty increases, less oxygen is brought to the alveoli resulting in
less production of surfactant, thus an increased resistance to expansion
5. As fatigue develops and hypoxemia worsens, cardiac output decreases, cardiac
arrhythmias may develop, and vital signs decrease (bradycardia, bradypnea, and
hypotension)
ASSESSMENT:
a. Includes: loss of consciousness, neurovascular assessment, skin color, vital
signs, use accessory respiratory muscles, auscultation of breath sounds, and
ECG pattern
b. Diagnostic Tests: ABGs (mild hypoxia is PaO2 of less than 80 mmHg;
moderate hypoxia is PaO2 of less than 60 mmHg; and severe hypoxia is
PaO2 of less than 40 mmHg); chest xray (shows that of the underlying
disease process), ECG (dysrhythmias), hemodynamic monitoring, sputum for
C&S

SIGNS AND SYMPTOMS:

-hypoxemia
-hypercapnia
 -dyspnea
-neurologic changes (restlessness, apprehension, impaired judgment, and motor
skills)
-cyanosis
-diaphoresis
-cool skin
-initial vital signs changes (tachycardia, hypertension, tachypnea)

NURSING MANAGEMENT:
1. Medications
a. Bronchodilators: methylxanthines (theophylline derivatives)
b. Sympathimimetic or anti cholinergic drugs in aerosol form for
bronchodilation
c. Corticosteroids
d. Antibiotics if infections exists
e. Sedatives and analgesia while on mechanical ventilation
f. Benzodiazepines: diazepam (valium), lorazepam (ativan), or midazolam
(versed) to decrease respiratory drive
g. Neuromuscular blocking agents to suppress the client’s ability to breathe
while on a ventilator
2. Administer oxygen therapy as ordered (usually low levels) or maintain
mechanical ventilation with PEEP; high oxygen levels may cause
hypoventilation
3. Administer parenteral therapy, monitor fluid and electrolyte status
4. Administer nebulized inhalation, chest physiotherapy, and suctioning as
needed
5. Auscultate breath and lung sounds
6. Assess vital signs, respiratory status, nasal flaring, and use of accessory
muscles
7. Assess ECG and hemodynamic monitoring
8. Maintain nutritional support
 9. Monitor pulse oximetry
-

INFLUENZA

- “flu”

- Refers to an acute viral infection of the respiratory tract

- Epidemic

Assessment:

Risk Factors:

- Very young children

- Older adults

- Institutional settings

- People with chronic diseases

- Health care personnel

Types:

- Type A (most prevalent)

- Type B (can reach epidemic levels, but the disease produced is generally
milder)

- Type C (never been connected with a large epidemic)

Clnical Manifestations:

- Fever

- Myalgias

- Hacking cough

- 2 – 3 days of chills

- Anorexia

- Sore throat
 - Runny nose

- Nasal congestion

- Light sensitive

- Nausea and vomiting

- Diarrhea

Treatment or Nursing Responsibilty:

- Adequate rest periods

- Increase fluid intake

- Acetaminophen

- Saline gargles

- Vaccination

Pathophysiology:

Direct inhalation of toxic substances or allergens or virus

Virus comes In contact with oropharyngeal or respiratory mucosa

Virus multiplication occurs in the regional lymph nodes

Localizes in small blood vessels in the oropharygeal mucosa

Subsequently infects adjacent cells or alveolar cells

PNEUMONIA

DEFINITION

-an inflammatory process in lung parenchyma usually associated with a marked

increase in interstitial and alveolar fluid

-second most common but has the highest mortality

Assessment:

Types:
 • Segmental pneumonia-involve one or more lobe segments of the lungs

• Lobar pneumonia-involve one or more entire lobes

• Bilateral pneumonia- lobes in both lungs

Classification

• Bronchopneumonia- involves terminal bronchioles and alveoli

• Insterstitial (reticular)- involves inflammatory process within the lung tissue

surrounding the air spaces or vascular structures rather than the air passages
themselves

• Alveolar(acinar) pneumonia- fluid accumulation in the distal air spaces

• Necrotizing pneumonia- death of a portion of lung tissue surrounded by viable

tissue

• Infectious

a) Community acquired pneumonia

b) Hospital acquired pneumonia(Nosocomial)-resistant to antibiotics

ETIOLOGY AND RISK FACTORS

Causes: bacteria, viruses, mycoplasms, fungal agents and protozoa

-may also result from aspiration of foods, fluids or vomitus or from inhalation of
toxic or caustic chemicals, smoke, dusts or gases

Major risk factors include the following:

• Advanced age

• History of smoking

• Upper respiratory tract infection

• Tracheal intubation

• Prolonged immobility

• Immunosuppressive therapy

• A nonfunctional immune system

 • Malnutrition

• Dehydration

• Homelessness

• Chronic disease states(diabetes,heart disease, chronic lung disease, renal

disease and cancer)

• Others: dysphagia, exposure to air pollution, altered consciousness,

inhalation of noxious substances, aspiration of food, liquid or aspiration of
foreign gastric material

SIGNS AND SYMPTOMS

• Fever

• Chills

• Sweats

• Fatigue

• Cough

• Sputum production and

• Dyspnea

• Less common symptoms: hemoptysis, pleuritic chest pain and headache

PATHOPHYSIOLOGY

Sterptococcus pneumonia, a major cause of bacterial pneumonia, generally

resides in the nasopharynx . Viral infections increase attachment of Sterptococcus
pneumonia to the receptors in the respiratory epithelium. Once inhaled into the alveolus
pneumococci infect type II alveolar cells. They multiply in the alveolus and invade
alveolar epithelium. Pneumococci spread from alveolus through the pores of Kohn,
thereby causing inflammation and consolidation along lobar compartments. Inflamed
and fluid-filled alveolar sacs cannot exchange oxygen and carbon dioxide effectively.
Alveolar exudates tends to consolidate.

DIAGNOSTIC TESTS
 • Chest radiograph- provides information about the location and extent of the
pneumonia consolidation

• Sputum and culture analysis-definitive diagnosis

• Fiberoptic bronchoscopy

• Transcutaneous needle aspiration/ biopsy

• ABG measurements

• Chest x-ray

• CBC

Assessment:

o percussion-dullness

o Auscultation- crackes and whispered pectoriloquy, increased tactile

fremitus

o Unequal chest wall expansion

MEDICAL MANAGEMENT

• Antibiotic therapy- broad spectrum

• Mucolytics

• Expectorants

• Antitussives

• Fluid and electrolyte management

• Nutritional support

• Oxygen therapy

• Chest physiotherapy and nasotracheal suctioning

NURSING INTERVENTIONS

• Place client in upright position during feeding and 30 minutes thereafter

 • Perform respiratory assessments every 4 hours including the rate and character
of respirations, auscultation of breath sounds and assessment of skin and nail
beds to determine the severity of hypoxia.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

a. ASTHMA
- also known as “reactive airway disease”
- disorder of the bronchial airways characterized by periods of reversible bronchospasm
- this involves biochemical, immunologic, endocrine, infectious, autonomic, and
psychological factors
- Etiology/Risk Factors: Inherited disorder, environmental factors (viral infection,
allergens, pollutants), excitatory states (stress, laughing, crying), exercise, changes in
temperature, strong odors
- component of triad disease: asthma, nasal polyps, and allergy to aspirin
- involves inflammatory process that produces mucosal edema, mucus secretion, and
airway inflammation

PATHOPHYSIOLOGY:
Exposure to extrinsic allergens and irritants IgE is produced by B lymphocytes
IgE antibodies attach to mast cells and basophils in bronchial walls release of
chemical mediators of inflammation leads to capillary dilation edema of the
airway (to dilute and wash away allergens)
capillary constriction closes airway (prevents inhalation of
allergens)

- s/sx: dyspneic, marked respiratory effort, nasal flaring, pursed-lip breathing, use of
accessory muscles, wheezing, bronchospasm (continuous coughing)
a. Early-phase reaction, develop immediately and last about an hour
b. Delayed (late phase) reaction, same manifestations as with early phase, do
not begin until 4 to 8 hours after exposure and may last for hours or
days
- diagnostic test: Arterial blood gas (ABG) analysis, pulse oximetry
- Status Asthmaticus, severe, life threatening complication of asthma
-it is an acute episode of bronchospasm that tend to intensify
-leads to acute cor pulmonale (right-sided heart failure)
-pneumothorax commonly develops
-if continues, hypoxemia worsens and acidosis begins. If not treated or reversed,
respiratory or cardiac arrest ensues

b. Chronic Bronchitis
- results from inflammation of the bronchi leading to increased mucus production,
chronic cough, and scarring of the bronchial lining
- initially affects the larger bronchi but eventually all the airways are involved
- Etiology/Risk factors: smoking, air pollution, second-hand smoke, hx of childhood
respiratory tract infections, heredity, occupational exposure to certain pollutants
- compared to acute, manifestation continues for at least 3 months of the year for 2
consecutive years
- characterized by the following:
a. increase in the size and number of submucous glands in the large bronchi
(increases mucus production)
b. increase number of goblet cells, which also secrete mucus
c. impaired ciliary function, which reduces mucus clearance
- mucociliary defenses are impaired, there’s increased susceptibility to infection which
will result to greater mucus production, and bronchial walls become inflamed and
thickened

PATHOPHYSIOLOGY
Impaired mucous defenses presence of thick mucus and inflamed bronchi
obstruction of airways (esp. during expiration) airways collapse, air is then trapped
in the distal portion of the lungs reduced alveolar ventilation fall in
PaO2/increased levels of PaCO2, polycythemia (compensation to hypoxemia)

c. EMPHYSEMA
- A disorder in which the alveolar walls are destroyed which leads to permanent
overdistention of the airspaces. As a result, air passages are obstructed.
-Etiology/risk factors:
a. exact cause is unknown
b. bronchial spasm, infection, irritation or combination of the three (may be
contributory)
c. children who suffer from bronchitis or asthma (susceptible)
- Some forms may result from a breakdown in the lung’s normal defense mechanisms
(Alpha1-antitrypsin [AAT]) against certain enzymes
- highest occurrence among heavy cigarette smokers, esp. those exposed to polluted
air
- difficult expiration is the result of destruction of the walls (septa) between alveoli,
partial airway collapse and loss of elastic recoil
- 3 types:
a. Centriacinar (centrilobular) emphysema
- most common type; produces destruction in the bronchioles, usually in the
upper lung regions
- inflammation begins in the bronchioles and spreads peripherally but the
alveolar sac remains intact
- occurs most often on smokers

b. Panacinar emphysema
- destroys the entire alveolus; most commonly involves the lower portions of
the lung
- generally observed in individuals with AAT deficiencies

c. Paraseptal (distal acinar) emphysema

 - primarily involves the distal airway structures, alveolar ducts, and alveolar
sacs
- localized around the septa of the lungs or pleura, resulting in isolated blebs
along the lung periphery
- believed to be the likely cause of spontaneous pneumothorax
- diagnosis is primarily accomplished through spirometry

PATHOPHYSIOLOGY
Inflammation of bronchi, excessive mucus production, loss of elastic recoil of airways,
and collapse of the bronchioles Alveoli destroyed and the alveolar surface
decreases Increase dead space or area where no gas exchange Impaired
oxygen diffusion Hypoxemia Later, impaired elimination of CO2
Hypercapnia and respiratory acidosis

Assessment:
• progressive dyspnea on exertion
• dypnea at rest
• enlarged anteroposterior diameter
• hyperresonant sounds to percussion
• over inflation and flattened diaphragms
• compensated respiratory acidosis
• enlarged heart and ventricular lift
• lip cyanosis, neck vein distension
• pitting peripheral edema
• ECG shows right heart strain pattern and right axis deviation

diagnostic test
• chest x-ray
• Arterial blood gas (ABG) analysis
• ECG

• COMPLICATIONS OF COPD
a. Respiratory tract infections-because of the alteration of respiratory defense
mechanisms and decreased immune resistance
b. Spontaneous Pneumothorax-from rupture of an emphysematous bleb
- s/sx worsens at night causing sleep-onset dyspnea and frequent or early-morning
awakenings
- decreased respiratory muscle tone and activity during sleep may lead to
hypoventilation

MANAGEMENTOF COPD

• Improve ventilation
-bronchodilators, to reduce airway obstruction
1. Beta- agonists- bronchodilation, increase ciliary movements
 2. Methylxanthines- relax muscles, increase mucus movement, and
increased diaphragm contraction
3. Anticholinergics- bronchodilator for those with cardiac diseases
4. Corticosteroids- reduce inflammation
5. Mast-cell inhibitor- prevents release of chemical mediators
-long-term oxygen therapy via nasal cannula
-ventilatory supports via endotracheal tube or tracheostomy

• Remove bronchial secretions

-pulmonary hygiene (to rid lungs from secretions, reduce risk for infection)
-nebulized bronchodilators and positive-pressure air flow or positive end-
expiratory pressure devices (increase caliber of airways)
-Postural drainage and chest physiotherapy (moves secretions from which they
can be expelled)

• Reduce complications
-prophylaxis for Deep Vein Thrombosis for clients who are immobilized,
polycythemic, or dehydrated
-vaccines (reduces chances of serious illnesses)

• Promote exercise
-aerobic exercises (like walking) are used to enhance cardiovascular fitness and
train respiratory muscles to function more effectively
-assess ABG first and supplemental oxygen during exercise if client becomes
severely hypoxemic
-breathing exercises
a. encourage diaphragmatic and pursed-lip breathing
b. discourage rapid, shallow panic breathing
• Improve general health
-have client to stop smoking
-minimize exposure to second-hand smoke, occupational dusts and chemicals,air
pollution, and known allergens
-adequate nutrition to maintain respiratory strength
a. consult a clinical dietitian to assist client in modifying diet and meet
caloric needs
b. offer small frequent small meals rather than large meals
c. excess carbohydrate leads to increased production of carbon dioxide
and can lead to respiratory distress
d. adjust oxygen delivery devices so that mouth is not obstructed but
oxygen is delivered to the nose during eating

PULMONARY EDEMA

- Abnormal accumulation of fluid in the lung tissue, the alveolar space, or both, it is
a severe, life-threatening condition
Assessment:

Clinical manifestations

- Increased respiratory distress:

• dyspnea
• air hunger
• central cyanosis
- May feel anxious and agitated
- Presence of cough
- Confused and stuporous

Diagnostic tests and findings

- Auscultation(reveals crackles)
- Chest x-ray(increased interstitial markings)
- O2 saturation decreases
- Arterial blood gas analysis(hypoxemia)

Medical management

- Management focuses on correcting the underlying disorder

- Vasodilators
- Inotropic medications
- Afterload and preload agents
- Contractility medications

Nursing Management

- Assist on oxygen administration and intubation and mechanical ventilation

- Administer medications

PULMONARY HYPERTENSION

- exists when the systolic pulmonary artery pressure exceeds 30 mmHg ar the
mean pulmonary artery pressure exceeds 25 mmHg at rest or 30 mmHg with
activities

Assessment:

Clinical Manifestations

- Dyspnea
 - Weakness
- Fatigue
- Syncope
- Occasional hemoptysis
- Signs of Right-sided heart failure

Diagnostic tests

- Complete and thorough physical examination

- Chest X-ray
- Pulmonary function studies
- Electrocardiogram
- Echocardiogram
- Ventilation-perfusion scan
- Sleep studies
- Autoantibody tests
- Liver function testing
- Cardiac catheterization
-
Medical Management

- Oxygen administration
- Chest Physical Therapy
- Bronchial hygiene maneuver
- Bed rest
- Sodium restriction
- Diuretic therapy
- ECG monitoring

Nursing Management

- assess respiratory and cardiac status

- administer medication

CHEST TRAUMA

- Results from an injury of the chest can be classified as blunt or penetrating

Blunt chest trauma results from sudden compression or positive pressure i
inflicted to the chest wall. Penetrating trauma occurs when a foreign object
penetrates the chest wall

Assessment

- determine the ff:

 • time elapsed since injury occurred
• mechanism of injury
• level of responsiveness
• specific injuries
• estimated blood loss
• recent drug or alcohol use
• prehospital treatment
- physical examination

Diagnostic tests

- chest x-ray
- CT scan
- Complete blood count
- Clotting studies
- Type and cross-match
- Electrolytes
- Oxygen saturation
- Arterial blood gas analysis
- ECG

Medical Management

- drain intrapleural fluid and blood

- maintain patent airway

OCCUPATIONAL LUNG DISEASE

PNEUMOCONIOSIS

- refers to a nonneoplastic alteration of lung resulting from inhalation of mineral

or inorganic dust.

Clinical manifestation

- dyspnea
- cough
- prolonged illness culmination in respiratory failure

SILICOSIS

- is a chronic fibrotic pulmonary disease caused by inhalation of silica

dust
Clinical Manifestations

- dyspnea
- fever
- cough
- weight loss
- hypoxemia
- severe air-flow obstruction
- right sided-heart failure
Medical Management

- supportive therapy is directed at managing complications and

preventing infection

ASBESTOSIS

- is a disease characterized by diffuse pulmonary fibrosis from the

inhalation of asbestos dust.

Assessment:

Clinical Manifestations

- progressive dyspnea
- persistent, dry cough
- mild to moderate chest pain
- anorexia
- weight loss
- malaise
Medical Management

- directed at controlling infection and treating lung disease

- avoid additional exposure to asbestos
- stop smoking

COAL WORKER PNEUMOCONIOSIS

- “black lung disease”

- Variety of respiratory diseases found in coal workers who have inhaled coal
dust over the years

Assessment:

Clinical Manifestations
 - chronic cough
- sputum production
- dyspnea

Medical Management

- treatment focuses on early diagnoses and management of

complications

LUNG CANCER (bronchogenic Carcinoma)

Definition:
a disease of uncontrolled cell growth in tissues of the lung. This growth may lead
to metastasis, which is the invasion of adjacent tissue and infiltration beyond the lungs.
The vast majority of primary lung cancers are carcinomas of the lung, derived from
epithelial cells. Lung cancer is the leading cancer killer among men and women in the
unite states. For men the incidence of lungcancer has remained relatively constant and
in women it has begun to plateau after a continues rise over the past 30 years. In the
70% of the patients with lung cancer, the disease has spread to regional lymphatics and
other sites by the time of diagnosis making the long term survival rate low.

Classification and Staging:

• 2 Major Categories:
a.)small cell lung cancer
-arises in the major bronchi and spread by infiltration along the
bronchialwall.
-accounts for 20%-25% of all bronchogenic cancers(Baldwin, 2003)
-represents 15%-20% of tumors.

* types:
a.) limited
b.) extensive
b.) non-small cell lung cancer (NSCLC)
-represents 75%-80% of tumors.

*types:
a.) Squamous cell cancer
-usually morecentrally located and arises more commonly in the
segmental and subsegmental bronchi.
-represents 20%-30%of tumor in NSCLC.

b.) Adenocarcinoma
-most prevalent carcinoma of the lung in both men and women.
 -occurs peripherally as peripheral masses or nodules and often
metastasizes.
- represents 30%-40% of tumors in NSCLC, including
bronchoalveolar carcinoma.

c.) Bronchoalveolar cell cancer

- found in terminal bronchi and alveoli
- usually slow growing

d.) Large cell carcinoma

-also called undifferentiated carcinoma.
- fast growing tumor that tends to arise peripherally.
- represents 10% of tumors in NSCLC.

Assessment:

Risk factors:
-tobacco smoke
-secondhand/passive smoker
-environmental and occupational exposures
-gender
-genetics
-dietary deficits
-COPD
-TB

clinical manifestations:
-develops insidiously and is asymptomatic until late in its course
-signs and symptoms depends on its location and size of tumor, the degree of
obstruction and the existence of metastases to regional or distant sites.
*dry persistent cough without sputum
*change in chronic cough
*dyspnea
*hemoptysis
*chest or shoulder pain(late manifestation)
*recurring fever (early symptom in some patient)
*hoarseness
*dysphalgia
*head and neck edema
*symptoms of pleural or pericardial effusion
*weakness
*anorexia
*weight loss

Diagnostic findings:
sputum cytology
 fiberoptic bronchoscopy
fine needle aspiration
magnetic resonance imaging(MRI)
positron emission tomography(PET)
biopsy

Medical management:
*surgical mgt: lobectomy, pneumonectomy
*radiation therapy:
*chemotherapy

CYSTIC FIBROSIS
− most common fatal autosomal recessive disease among caucasian population.
− caused by a mutation in the gene for the protein cystic fibrosis transmembrane
conductance regulator (CFTR). This gene is required to regulate the components
of sweat, digestive juices, and mucus. Although most people without CF have
two working copies of the CFTR gene, only one is needed to prevent cystic
fibrosis. CF develops when neither gene works normally. Therefore, CF is
considered an autosomal recessive disease.
− Diagnosed in infancy and early childhood.

Assessment:
Clinical manifestations:
pulmonary manifestations:
− productive cough
− wheezing
− hyperinflation of lung fields on chest x-ray
− sinusitis
− nasal polyps
non-pulmonary manifestations:
− gastrointestinal problems( pancreatic insufficiency, recurrent abdominal pain,
biliary cirrhosis, vitamin deficiency, weight loss)
− CF-related diabetes
− genitourinary problems( male and female infertility)
− clubbing of digits

Diagnostic findings:
− elevated sweat chloride concentration
− pilocarpine iontophoresis sweat test
− genetic evaluation

Medical management:
− antibiotic agents
− bronchodilators
 − anti- inflammatory agents
− supplemental oxygen
− lung transplantation
− gene therapy

FLAIL CHEST
Definition:

is a life-threatening medical condition that occurs when a segment of the chest wall
bones breaks under extreme stress and becomes detached from the rest of the chest
wall. It occurs when multiple adjacent ribs are broken in multiple places, separating a
segment, so a part of the chest wall moves independently. The number of ribs that must
be broken varies by differing definitions: some sources say at least two adjacent ribs are
broken in at least two places, some require three or more ribs in two or more places.
The flail segment moves in the opposite direction as the rest of the chest wall: because
of the ambient pressure in comparison to the pressure inside the lungs, it goes in while
the rest of the chest is moving out, and vice versa. This so-called "paradoxical motion"
can increase the work and pain involved in breathing. Studies have found that up to half
of people with flail chest die. Flail chest is invariably accompanied by pulmonary
contusion, a bruise of the lung tissue that can interfere with blood oxygenation. Often, it
is the contusion, not the flail segment, that is the main cause of respiratory failure in
patients with both injuries.

Assessment:

Signs and Symptoms:

• During normal inspiration, the diaphragm contracts and intercostal muscles push the
rib cage out. Pressure in the thorax decreases below atmospheric pressure, and air
rushes in through the trachea. However, a flail segment will not resist the decreased
pressure and will appear to push in while the rest of the rib cage expands.
• During normal expiration, the diaphragm and intercostal muscles relax, allowing the
abdominal organs to push air upwards and out of the thorax. However, a flail segment
will also be pushed out while the rest of the rib cage contracts.
The constant motion of the ribs in the flail segment at the site of the fracture is incredibly
painful, and, untreated, the sharp broken edges of the ribs are likely to eventually
puncture the pleural sac and lung, possibly causing a pneumothorax.

Treatment:
Treatment of the flail chest initially follows the principles of Advanced Trauma Life
Support. Further treatment includes:
• Good analgesia including intercostal blocks, avoiding narcotic analgesics as much as
possible. This allows much better ventilation, with improved tidal volume, and increased
blood oxygenation.
• Positive pressure ventilation, meticulously adjusting the ventilator settings to avoid
barotrauma.
• Chest tubes as required.
• Adjustment of position to make the patient most comfortable and provide relief of pain.
Surgical fixation is usually not required. A patient may be intubated with a double lumen
tube. In a double lumen endotracheal tube, each lumen is connected to a different
ventilator. Usually one side of the chest is affected more than the other, so each lung
may require drastically different pressures and flows to adequately ventilate.

Pathophysiology and management:

Flail chest occurs when a series of adjacent ribs are fractured in at least 2 places,
anteriorly and posteriorly. This section of the chest wall becomes unstable and it moves
inwards during spontaneous inspiration. The physiological impact of a flail chest
depends on multiple factors, including the size of the flail segment, the intrathoracic
pressure generated during spontaneous ventilation, and the associated damage to the
lung and chest wall. Treatment varies with the severity of the physiologic impairment
attributable to the flail segment itself. Immediate surgical fixation may decrease
morbidity, but conservative treatment with positive pressure ventilation is preferred
when multiple injuries to the intrathoracic organs are present.

FRACTURED STERNUM

Definition:

A person with a sternum fracture has a broken sternum, caused by an injury. Most
sternum fractures are caused by motor vehicle accidents. A sternum fracture may occur
when the driver's chest strikes the steering wheel during the accident.

Assessment:

The most common symptom of a fractured sternum includes chest pain over the center
of the chest. The pain may be worse during movement or during a deep breath.
Additional symptoms may include bruising, swelling, and tenderness over the sternum.
Symptoms of a severe sternum fracture include difficulty breathing and a deformed
chest.

Causes:

With increased use of seat belts and shoulder restraints, incidence has increased, but
overall severity of injuries has decreased.
Presumably, incidence has increased because all of the deceleration forces are
concentrated into a nonelastic 2-inch strap that transmits this force directly to the
sternum.
Effects of airbags on incidence of sternal fractures are not fully known, though literature
suggests a decreased incidence when these are deployed.

Pathophysiology:

Most sternal fractures are caused by blunt anterior chest trauma, although stress
fractures have been noted in golfers, weight lifters, and other participants in noncontact
sports. Insufficiency fractures caused by abnormally decreased bone density or
weakened bone can occur spontaneously in patients with osteoporosis or osteopenia
(particularly in older persons), those on long-term steroid therapy, or those with severe
thoracic kyphosis. Cardiopulmonary resuscitation commonly causes rib and sternal
fractures, something that must be considered during the recovery process from the
illness that led to the cardiac arrest.

Management:

Treatment for a fractured sternum may include rest, cold compresses, narcotic pain
medication, or nonsteroidal anti-inflammatory medications for pain. Treatment for a
severe sternum fracture may include heart monitoring, oxygen therapy, and surgery to
repair the fracture.

Pulmonary Tuberculosis

- is an infectious disease that primarily affects the lung parenchyma. It also

may
be transmitted to other parts of the body, including the meninges, kidneys,

bones and lymph nodes.

- primary infectious agent: M.tuberculosis

Assessment:
Clinical Manifestations

- symptoms are insidious

- low-grade fever
- cough
- night sweats
- fatigue
- weight loss
- cough may be productive or mucopurulent

Diagnostic Tests

A. tuberculin skin test

- The Mantoux test is used to determine whether a person has been infected

With the TB bacillus

Interpretation of results:

>the size of the induration determines the significance of the reaction:

1. 0-4mm – not significant

2. 5mm greater – may be significant

3. 10mm greater – significant

B. QuantiFERON-TB Gold (QFT-G) Test

Pharmacologic Therapy

A. Isoniazid

B. Rifampin

C. Rifabutamin

D. Pyrazinamide

E. Ethambutol

Nursing Management

- promote airway clearance

- promoting activity and adequate nutrition
- adherence to medical regimen
- monitoring and managing potential complications
Atelectasis

- refers to closure or collapse of alveoli

- may be acute or chronic

Assessment:

Clinical Manifestations

- is usually insidious
- cough
- sputum production
- low-grade fever
- dyspnea
- tachycardia
- tachypnea
- pleural pain

Diagnostic Tests

- chest x-ray (reveals patchy infiltrates or consolidated areas)

- O2 saturation may demonstrate a low saturation of hemoglobin with oxygen

Medical Management

- Endotracheal Intubation
- Mechanical ventilation
- Bronchoscopy

Nursing Management

- frequent turning
- early ambulation
- voluntary deep-breathing maneuvers
- use of incentive spirometer
- improve ventilation
- lung volume expansion maneuvers
- coughing
 - positive end-expiratory pressure
- suctioning

PNEUMOTHORAX

- it is the presence of air in the pleural space that prohibits complete lung expansion
- lung expansion occurs when the pleural lining of the chest wall and the visceral lining
of the lung maintain negative pressure in the pleural space
- if the continuity of the system is lost, pneumothorax will result
- it may be closed or open

a. closed, air may escape into the pleural space from a puncture or tear in the
internal respiratory structure such as the bronchus, bronchioles, or alveoli
- a fractured rib may also be a reason

b. open, air may enter the pleural space directly through a hole in the chest wall
or diaphragm
- may be classified as
a spontaneous pneumothorax, may be idiopathic (primary) or as a result of
another lung illness such as COPD, tuberculosis, or cancer (secondary)

b. traumatic pneumothorax, results in a collapsed lung caused either by blunt

force trauma to the chest wall or by the creation of an open sucking chest wound
caused by a motor-vehicle accident, gun or knife wound or a diagnostic procedure such
as thoracentesis

c. tension pneumothorax, develops when air is trapped in the pleural space

during inspiration and cannot escape during expiration
- intrapleural pressure becomes greater than the lung nbbn tissue pressure,
resulting in compression of the lung and surrounding structures.

Assessment:
• Marked severe dyspnea
• Tachypnea
• Subcutaneous emphysema in the neck and upper chest
• Progressive cyanosis
• Acute chest pain on affected area
• Hyperresonance upon percussion on the affected area
• Tachycardia
• Asymmetrical chest wall movement
 • Diminished or absent breath sound
• Extremes restlessness and agitation

Diagnostic Test:
• Chest X-ray

Medical Management:
• Large bore chest tubes are inserted on affected side at the fifth
intercostals space anterior to the midaxillary line.
• Suction drainage should be established.
• Thoracentesis to remove air.
• VATS- video Assisted Thoracotomy surgery

Hemothorax
Definition: a small amount of blood (<300ml) in the pleural space may cause no clinical
manifestation and may require no intervention with the blood being reabsorbed
spontaneously

Assessment:
• Respiratory Distress
• Shock
• Mediastinal Shift
• Dullness upon percussion
• Restlessness
• Tachypnea

Diagnostic Test:
• Chest X-ray
• Aspiration of blood from the pleural space
• Thoracentesis

Management:
• Video assisted thoracotomy surgery
• Fluid replacement through blood transfusion
• Thoracotomy
• Thoracentesis