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 EFFUSIONOVERVIEW:

-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 locala. systemic diseases

-hydrothorax: heart failure, renal failure, liver failure -empyema (pus in the pleural cavity): infections, malignancies,

connective tissue disordersb. 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. Medicationsa. Antipyretics if fever or pain is presentb. Antibiotics, parenterally or instillation into the pleural space for

repeated effusions2. 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 dyspnea5. Manage pain if necessary along with bedrest6. 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

cellso 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 months3. 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 oxygenb.) 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 hypoxemiac.) 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 FAILUREOVERVIEW:

-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. Medicationsa. Bronchodilators: methylxanthines (theophylline derivatives)b. Sympathimimetic or anti cholinergic drugs in aerosol form for

bronchodilationc. Corticosteroidsd. Antibiotics if infections existse. Sedatives and analgesia while on mechanical ventilationf. Benzodiazepines: diazepam (valium), lorazepam (ativan), or midazolam

(versed) to decrease respiratory driveg. Neuromuscular blocking agents to suppress the client’s ability to breathe

while on a ventilator2. 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 status4. Administer nebulized inhalation, chest physiotherapy, and suctioning as

needed5. Auscultate breath and lung sounds6. Assess vital signs, respiratory status, nasal flaring, and use of accessory

muscles7. Assess ECG and hemodynamic monitoring8. Maintain nutritional support9. 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 pneumoniab) 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

fremituso 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 hourb. 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 mucusc. 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

PATHOPHYSIOLOGYImpaired 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 unknownb. 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

PATHOPHYSIOLOGYInflammation 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 movements2. Methylxanthines- relax muscles, increase mucus movement, and

increased diaphragm contraction3. Anticholinergics- bronchodilator for those with cardiac diseases4. Corticosteroids- reduce inflammation5. 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 mealsc. excess carbohydrate leads to increased production of carbon dioxide

and can lead to respiratory distressd. 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.) limitedb.) 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 cytologyfiberoptic bronchoscopyfine needle aspirationmagnetic 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 polypsnon-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 CHESTDefinition: 

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 asa 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

HemothoraxDefinition: 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