Influenza

Introduction:

A viral infection affecting the respiratory tract that spreads through droplets. The
virus can be inhaled or picked up from surfaces through direct contact. Infection
can settle into either the upper or lower respiratory tract. The virus causes damage
to the upper layers of cells. The natural defenses of the respiratory tract are com-
promised and it is easier for bacteria to attach to the underlying respiratory tissues.

PROGNOSIS
Influenza symptoms typically run their course within about a week. Current med-
ications help to decrease the length and severity of symptoms associated with
influenza. Some patients will develop secondary infections, such as sinusitis or
viral or bacterial pneumonia following influenza. Patients with pneumonia have an
increased risk of mortality from influenza.

SIGNS AND SYMPTOMS

• Symptoms have an abrupt onset
• Nonproductive cough
• Chills and sweats
• Fatigue and malaise
• Fever over 101°F
• Headache
• Muscle aches (myalgia)
• Watery, nasal discharge
• Sore throat

TREATMENT
Symptomatic treatment to increase patient comfort and medications to shorten
the duration and intensity of symptoms are the focus of patient management.
Medications need to be started early in the symptoms.
• Administer antipyretics for comfort:
• acetaminophen
• Administer antiviral medications:
• zanamivir, oseltamivir
• amantadine, rimantadine

NURSING DIAGNOSES
• Risk for injury
• Impaired gas exchange
• Hyperthermia

NURSING INTERVENTION
• Administer fluids and electrolytes to replace what is being lost due to sweat-
ing and insensible loss from elevated temperature.
• Monitor vital signs.

Acute Respiratory Failure

Introduction:

The lungs are unable to adequately exchange oxygen and carbon dioxide because
of insufficient ventilation. The body is not able to maintain enough oxygen or the
body may not get rid of enough carbon dioxide. A respiratory illness can deterio-rate into acute respiratory failure. Central nervous system depression (due to
trauma or medication) or disease can also lead to acute respiratory failure.

PROGNOSIS
Patients with respiratory failure are not getting enough oxygen. This may be a sudden
event or a decompensation of a chronic respiratory condition such as emphysema or
chronic bronchitis. Supplemental oxygen and bronchodilating medications are used
to enhance airflow to the lungs. The underlying cause needs to be identified and cor-
rected to reverse the problem and return the patient to normal respiratory status.

SIGNS AND SYMPTOMS

• Accessory muscles used to breathe as body works harder to move air
• Difficulty breathing (dyspnea) due to lack of oxygen
• Difficulty breathing when lying down (orthopnea) due to increased work of
breathing in this position; diaphragm has to work harder; posterior chest wall
does not expand well
• Fatigue due to work of breathing and lack of oxygenation
• Coughing may be due to inflammation, bronchospasm, fluid, or underlying
lung condition
• Blood in sputum (hemoptysis) due to irritation of airways
• Respiration greater than 20 breaths per minute (tachypnea) in attempt to get
more air and oxygen into lungs
• Sweating (diaphoresis) as body works harder to move air, using more muscles
• Cyanosis due to hypoxemia
• Anxiety due to air hunger and lack of oxygenation
• Rales (crackles) heard in the lungs if fluid builds up in alveoli and smaller
airways
• Wheezing (rhonchi) due to inflammation within airways
• Diminished breath sounds due to decreased air movement

TREATMENT

• Oxygen therapy to meet body’s needs via nasal canula or mask.
• Administer bronchodilators to enhance airflow through airways in lungs:
• albuterol, levalbuterol, metaproterenol, terbutaline
• Administer anticholinergics to treat bronchospasm:
• ipratropium
• Intubation to maintain patent airway and assist mechanical ventilation.
• Administer anesthetic to ease intubation:
• propofol
• Mechanical ventilation to support respiratory effort.
• omeprazole, esomeprazole, lansoprazole, rabeprazole, pantoprazole
• Administer antibiotics to treat infection (or may be preventative):
• selected according to results of culture and sensitivity study

NURSING DIAGNOSES
• Ineffective breathing pattern
• Ineffective airway clearance
• Anxiety

NURSING INTERVENTION
• Monitor respiratory status for rate, effort, use of accessory muscles, sputum
production, and breath sounds.
• Monitor pulse oximetry to check oxygen saturation levels.
• Monitor sputum for changes in color and amount.
• Monitor vital signs for changes.
• Place patient in high Fowler’s or semi-Fowler’s position on bedrest to ease
respiratory effort by allowing optimal diaphragmatic excursion.
• Monitor ventilator settings if appropriate.
• Change patient position every 2 hours to decrease chance of skin breakdown.
• Monitor intake and output of fluids to check for balance.
• Explain to the patient:
• The importance of doing coughing and deep-breathing exercises to fully
expand lungs and enhance the expelling of mucous.
• How to identify the signs of respiratory distress.
• Administer neuromuscular blocking agent to ease mechanical ventilation so
the patient won’t fight ventilator:
• pancuronium, vecuronium, atracurium
• Administer steroids to decrease inflammatory response within lungs:
• hydrocortisone, methylprednisolone, prednisone
• Administer anticoagulant to reduce risk of clot formation:
• heparin, warfarin
• Administer analgesic for discomfort and to decrease myocardial oxygen
demand:
• morphine
• Administer histamine-2 blockers or proton pump inhibitors to reduce chances
of stress-induced gastric ulcer:
• famotidine, ranitidine, nizatidine, cimetidine

Tuberculosis (TB)

Introduction:

An infectious disease spread by airborne route. Infection is caused by inhalation
of droplets that contain the tuberculosis bacteria (Mycobacterium tuberculosis).
An infected person can spread the small airborne particles through coughing,
sneezing, or talking. Close contact with those affected increases the chances of
transmission. Once inhaled, the organism typically settles into the lung, but can
infect any organ in the body. The organism has an outer capsule.
Primary TB occurs when the patient is initially infected with the mycobac-
terium. After being inhaled into the lung, the organism causes a localized reac-
tion. As the macrophages and sensitized T-lymphocytes attempt to isolate and kill
off the mycobacterium within the lung, damage is also caused to the surrounding
lung tissue. A well-defined granulomatous lesion develops that contains the
mycobacterium, macrophages and other cells. Necrotic changes occur within this
lesion. Caseous granulomas develop along lymph node channels during the same
time. These areas create a Ghon’s complex which is a combination of the area ini-
tially infected by the airborne bacillus called the Ghon’s focus and a lymphatic
lesion. The majority of people with newly acquired infections and an adequate
immune system will develop latent infection, as the body walls off the infecting
organism within these granulomas. Disease is not active in these patients at this
point and will not be transmitted until there is some manifestation of the disease.
In patients with inadequate immune response, the tuberculosis will be progres-
sive, lung tissue destruction will continue, and other areas of the lung will also
become involved.
In secondary TB, the disease is reactivated at a later stage. The patient may be
reinfected from droplets, or from a prior primary lesion. Since the patient has pre-
viously been infected with TB, the immune response is to rapidly wall off the infec-
tion. Cavitation of these areas occurs as the organism travels along the airways.
Exposure to TB occurs when a person has had recent contact with a person sus-
pected or confirmed having TB. These patients do not have positive skin test, signs
or symptoms of disease, or chest x-ray changes. They may or may not have disease.
Latent TB infection occurs when a person has a positive tuberculin skin test but
no symptoms of disease. Chest x-ray may show granuloma or calcification.
TB disease is confirmed when a person has signs and symptoms of tuberculo-
sis. The chest x-ray typically has abnormalities in the apical aspects of the lung
fields. In HIV patients other areas may also be affected.

PROGNOSIS
Some patients develop drug-resistant TB, making treatment more difficult. The
drug-resistant TB may be resistant at the time of initial infection, or may develop
as a result of medications during treatment. This occurs either because the treat-
ment was not adequate or not taken appropriately.

SIGNS AND SYMPTOMS
• Weight loss and anorexia
• Night sweats
• Fever, possibly low-grade, due to infection
• Productive cough with discolored, blood-tinged sputum
• Shortness of breath due to lung changes
• Malaise and fatigue due to active illness affecting lungs

TREATMENT
Patients with active TB are initially placed on respiratory isolation as inpatients to
reduce the risk of spreading the organism by droplet infection or aerosolization.
Medications are initiated to treat TB and prevent transmission to others. Treatment
may be initiated for active disease or for those without active disease who have had
recent exposure. Combination therapy is typically used to decrease the likelihood
of drug-resistant organisms. Initial treatment times generally range from 6 to 12
months. Longer treatment plans may be necessary for those with HIV infection or
drug-resistant strains of TB. Some patient populations are monitored closely for
compliance with direct observation of drug treatment. Patient teaching is important
for medication protocol compliance and monitoring for side effects. Repeat sputum
cultures are typically taken to see that the treatment for active disease is effective.
• Administer antitubercular medications to treat and prevent transmission:
• isoniazid, rifampin, pyrazinamide, ethambutol, streptomycin
• Respiratory isolation for in-hospital care—the bacteria is spread by droplet.
• Increase protein, carbohydrates, and vitamin C diet for patients.

NURSING DIAGNOSES
• Fatigue
• Ineffective airway clearance

NURSING INTERVENTION
• Monitor respiration for rate, effort, use of accessory muscles, and skin color
changes.
• Increase fluid intake to help liquefy any secretions.
• Record fluid intake and output.
• Explain to the patient:
• How to prevent spreading the disease.
• The importance of finishing all prescribed medication.
• Plan for rest periods during the day.

Pneumothorax

Introduction:

The pleural sac surrounding the lung normally contains a small amount of fluid to
prevent friction as the lungs expand and relax during the respiratory cycle. When air
is allowed to enter the pleural space between the lung and the chest wall, a pnuemo-
thorax develops. This air pocket takes up space that is normally occupied by lung
tissue, causing an area of the lung to partially collapse. If there is a penetrating chest
wound, the patient may have an open pneumothorax, also known as a sucking
chest wound (for the sound it makes during breathing). A closed pneumothorax
may be caused by blunt trauma, post-central line insertion, or post-thoracentesis.
Spontaneous pneumothorax may be secondary to another disease or occur on its
own. As the air accumulates, there may be a partial or complete collapse of the
lung—the more air that accumulates, the greater the area of collapse. If there is a
large enough amount of air trapped between the pleural layers, the tension within
the area increases. This increase in tension results in pushing the mediastinum
toward the unaffected lung, causing it to partially collapse and compromising
venous return to the heart. This is a tension pneumothorax.

PROGNOSIS
Prognosis will vary depending on causes and size of pneumothorax. Any pneumo-
thorax that enlarges or progresses to a tension pneumothorax is a greater risk for
the patient. Tension pneumothorax presents a life-threatening situation. A small
area of pneumothorax may be monitored without intervention while a larger area
requires treatment for resolution of the problem.

SIGNS AND SYMPTOMS

• Sharp chest pain, made worse by activity, moving, coughing, and breathing
• Shortness of breath due to inability to fully expand the lungs during inspiration
• Absent breath sounds over the affected area due to presence of air between
lungs and chest wall
• Subcutaneous emphysema (presence of air in the tissue beneath the skin)—
a crackling feeling beneath the skin on palpation over the area
• Tachycardia (increased heart rate) and tachypnea (increased respiratory rate)
as body attempts to meet needs
• Mediastinal shift and tracheal deviation toward the unaffected side with ten-
sion pneumothorax

TREATMENT
Once identified, a pneumothorax can be treated and completely resolved. A ten-
sion pneumothorax can become a life-threatening condition. Careful monitoring
and early intervention is critical for these patients. A small area may resolve with-
out intervention, but the patient will still be monitored until resolution.
• Bedrest.
• Supplemental oxygen if needed.
• Chest tube connected to suction to re-expand lung if needed.
• Administer analgesic if needed:
• morphine

NURSING DIAGNOSES
• Acute pain
• Ineffective breathing
• Impaired gas exchange

NURSING INTERVENTION
• Place patient in high Fowler’s or semi-Fowler’s position to ease respiratory
effort.
• Monitor drainage of the chest tube for amount and characteristics of output.
Note changes.
• Monitor respirations for rate, effort, use of accessory muscles, skin color, and
breath sounds.
• Teach turning, coughing, and deep-breathing exercises.
• Explain to the patient:
• Disease process.
• Importance of coughing and deep breathing.
• Monitor vital signs for changes.

Pneumonia

Introduction:

Infectious pneumonia may be due to a variety of microorganisms and can be
community-acquired or hospital-acquired (nosocomial). Apatient can inhale bacteria,
viruses, parasites, or irritating agents, or a patient can aspirate liquids or foods. He
or she can also develop increased mucous production and thickening alveolar fluid
as a result of impaired gas exchange. All of these can lead to inflammation of the
lower airways.
Organisms commonly associated with infection include Staphylococcus
aureus, Streptococcus pneumoniae, Haemophilus influenza, Mycoplasma pneumo-
niae, Legionella pneumonia, Chlamydia pneumoniae (parasite), and Pseudomonas
aeruginosa.

PROGNOSIS
Prognosis will vary depending on patient’s age, preexisting lung disease, infect-
ing organism and response to antibiotics. Patients at risk for pneumonia are: older
patients; those with respiratory disease; patients with comorbid conditions such
as heart, liver, or kidney disease; and patients who develop complications (such as
atelectasis or pleural effusion). Patients at greater risk for complications from
pneumonia will be treated within the hospital, while those at lower risk may be
treated at home. Patients with respiratory rates over 30, tachycardia, altered men-
tal status, or hypotension also are considered higher-risk.
Patients without other coexisting conditions, who do not appear to have the
higher-risk symptoms listed above, can usually be safely treated as outpatients.
Patients with comorbidities (higher-risk coexisting symptoms) or who appear ill
are usually treated in the hospital. Some require critical care treatments and must
be closely monitored. There is still a significant mortality rate from pneumonia,
despite the recognition of pneumonia and use of antibiotics.

SIGNS AND SYMPTOMS

• Shortness of breath due to inflammation within the lungs, impairing gas
exchange
• Difficulty breathing (dyspnea) due to inflammation and mucus within the
lungs
• Fever due to infectious process
• Chills due to increased temperature
• Cough due to mucous production and irritation of the airways
• Crackles due to fluid within the alveolar space and smaller airways
• Rhonchi due to mucus in airways; wheezing due to inflammation within the
larger airways
• Discolored, possibly blood-tinged, sputum due to irritation in the airways or
microorganisms causing infection
• Tachycardia and tachypnea as the body attempts to meet the demand for
oxygen
• Pain on respiration due to pleuritic inflammation, pleural effusion, or atelec-
tasis development
• Headache, muscle aches (myalgia), joint pains, or nausea may be present
depending on the infecting organism

TREATMENT
Supplemental oxygen is given to help meet the body’s needs. Antibiotics
are given for the most likely organism (empirically) until the sputum culture

results are returned. Patients may need bronchodilators to help open the
airways.
• Administer oxygen as needed.
• For bacterial infections, administer antibiotics such as macrolides (azithro-
mycin, clarithromycin), fluoroquinolones (levofloxacin, moxifloxacin),
beta-lactams (amoxicillin/clavulanate, cefotaxime, ceftriaxone, cefuroxime
axetil, cefpodoxime, ampicillin/sulbactam), or ketolide (telithromycin).
• Administer antipyretics when fever >101 for patient comfort:
• acetaminophen, ibuprofen
• Administer brochodilators to keep airways open, enhance airflow if needed:
• albuterol, metaproterenol, levalbuterol via nebulizer or metered dose
inhaler
• Increase fluid intake to help loosen secretions and prevent dehydration.
• Instruct the patient on how to use the incentive spirometer to encourage deep
breathing; monitor progress.

NURSING DIAGNOSES
• Risk for aspiration
• Impaired ventilation
• Ineffective airway clearance

NURSING INTERVENTION
• Monitor respiration for rate, effort, use of accessory muscles, skin color, and
breath sounds.
• Record fluid intake and output for differences, signs of dehydration.
• Record sputum characteristics for changes in color, amount, and consistency.
• Properly dispose of sputum.
• Explain to the patient:
• Take adequate fluids—3 liters per day—to prevent excess fluid loss through
the respiratory system with exhalation.
• Use of incentive spirometer.

Lung Cancer

Introduction:

Lung cancer is the abnormal, uncontrolled cell growth in lung tissues, resulting in
a tumor. A tumor in the lung may be primary when it develops in lung tissue. It
may be secondary when it spreads (metastasizes) from cancer in other areas of the
body, such as the liver, brain, or kidneys. There are two major categories of lung
cancer—small cell and non-small cell. Repetitive exposure to inhaled irritants
increases a person’s risk for lung cancer. Cigarette smoke, occupational exposures,
air pollution containing benzopyrenes, and hydrocarbons have all been shown to
increase risk.
• Small cell:
• Oat cell—fast-growing, early metastasis
• Non-small cell:
• Adenocarcinoma—moderate growth rate, early metastasis
• Squamous cell—slow-growing, late metastasis
• Large cell—fast-growing, early metastasis

PROGNOSIS
Lung cancer is the leading cause of cancer death. Many patients with lung cancer
are diagnosed at a later stage, leading to the long-term (5-year) survival rate of less
than 20 percent. Earlier diagnosis is more beneficial for treatment and outcome.
The longer the cancer has been in the lungs, the greater the likelihood of metasta-
sis to other areas.

SIGNS AND SYMPTOMS
• Coughing due to irritation from mass. Presence of mucous or exudate may
not be until later in disease.
• Coughing up blood (hemoptysis).
• Fatigue.
• Weight loss due to the caloric needs of the tumor, taking away from the needs
of the body.
• Anorexia.
• Difficulty breathing (dyspnea) caused by damaged lung tissue. The patient
begins to have respiratory problems later in the disease.
• Chest pains as mass presses on surrounding tissue; may not be until late in
disease.
• Sputum production.
• Pleural effusion.

TREATMENT
Treatment is focused on resolution of the tumor. Surgical removal is appropriate
for some patients, but not always necessary. Chemotherapy and radiation are both
methods that are used to destroy the cancerous cells. Oxygen therapy is used to aid
in meeting the current needs of the body, but not all patients will require supple-
mental oxygen therapy. Attention to nutrition is important to meet the demands of
the body. Pain control is an integral component of care in any type of cancer treat-
ment. Appropriate pain management needs to be individualized for the patient.
• Surgical removal of affected area of the lung (wedge resection, segmental
resection, lobectomy) or total lung (pneumonectomy).
• Radiation therapy to decrease tumor size.
• Chemotherapy often with a combination of drugs:
• cyclophosphamide, doxorubicin, vincristine, etoposide, cisplatin
• may see relapse after treatment
• Oxygen therapy to supplement the needs of the body.
• High-protein, high-calorie diet to meet the needs of the body.
• Administer antiemetics to combat side effects of chemotherapy:
• ondansetron, prochlorperazine
• Administer analgesics for pain control:
• morphine, fentanyl

NURSING DIAGNOSES
• Anxiety
• Activity intolerance
• Impaired gas exchange

NURSING INTERVENTION
• Monitor respiratory status, looking at rate, effort, use of accessory muscles,
and skin color; auscultate breath sounds.
• Monitor pain and administer analgesics appropriately.
• Monitor vital signs for changes, elevated pulse, elevated respiration, change
in BP, and elevated temperature, which may signal infection.
• Monitor pulse oximetery for decrease in oxygenation levels.
• Assist patient with turning, coughing, and deep-breathing exercises.
• Place patient in semi-Fowler’s position to ease respiratory effort.
• Explain to the patient:
• The importance of taking rest periods.

Bronchitis

Introduction:

Increased mucus production, caused by infection and airborne irritants that block
airways in the lungs, results in the decreased ability to exchange gases. There are
two forms of bronchitis: acute bronchitis, where blockage of the airways is re-
versible, and chronic bronchitis, where blockage is not reversible. Patients with
acute bronchitis are symptomatic typically for 7 to 10 days often due to viral (but
sometimes bacterial) infection. Patients with chronic bronchitis will have symp-
toms of a chronic productive cough for at least 3 consecutive months in 2 consec-
utive years. There is increased mucous production, inflammatory changes, and,
ultimately, fibrosis in the airway walls. The patient with chronic bronchitis has an
increased incidence of respiratory infection.

PROGNOSIS
Patients with acute bronchitis who have a resolution of symptoms and respiratory
status will return to normal condition. Chronic bronchitis is classified as a chronic
obstructive pulmonary disease (COPD), which is often linked to smoking and has
a progressive pattern. Shortness of breath is initially present only with exertion,
and eventually is present even at rest. Patients with chronic bronchitis often develop
right-sided heart failure and peripheral or dependent edema. Patients will have
acute exacerbations of chronic bronchitis.

SIGNS AND SYMPTOMS

• Cough due to mucous production and irritation of airways.
• Shortness of breath.
• Fever in acute episodes due to infection.
• Accessory muscles are used for breathing—as respiratory effort increases,
additional muscles are necessary to assist.
• Productive cough due to irritation of airways. Mucous is a protective reac-
tion of the respiratory system.
• Weight gain secondary to edema in chronic bronchitis is due to right-sided
heart failure.
• Wheezing due to inflammation within the airways.

TREATMENT

Acute bronchitis is treated in the short term with symptomatic treatment and
antibiotics when a bacterial infection is present. Chronic bronchitis is treated with
a combination of medications to keep the airways open, reduce inflammation
within airways, and prevent complications or exacerbations.
• Administer beta2-agonists by inhaler or nebulizer to dilate the bronchi:
• terbutaline, albuterol, levalbuterol
• formoterol, salmeterol
• Administer anticholinergics which allow for relaxation of bronchial smooth
muscle:
• ipratropium, tiotropium inhaler
• Administer steroids to decrease inflammation within the airways
• hydrocortisone, methylprednisolone systemically
• beclomethasone, triamcinolone, fluticasone, budesonide, flunisolide inhalers
• prednisolone, prednisone orally
• Administer methylxanthines to enhance bronchodilation:
• aminophylline
• theophylline (Theo-Dur)
• Administer diuretics to reduce fluid retention in patients who develop right-
sided heart failure:
• furosemide, bumetanide
• Administer expectorant to help liquefy secretions:
• guaifenesin
• Administer antibiotics in acute exacerbation of chronic bronchitis:
• selected by culture and sensitivity study or given empirically
• Administer antacid, H2 blocker, or proton pump inhibitor to decrease the
amount of acid in stomach, reducing possible ulcer formation due to stress
of disease or medication effects.
• antacids: aluminum hydroxide/magnesium hydroxide, calcium carbonate
• H2 blockers: ranitidine, famotidine, nizatidine, cimetidine
• proton pump inhibitors: omeprazole, lansoprazole, esomeprazole, rabepra-
zole, pantoprazole
• Administer vaccines—to decrease chances of infection:
• influenza
• pneumonia
• Give 3 liters of fluid per day to help liquefy secretions
• Oxygen: 2 liters per minute via nasal canula to help meet body’s needs; low
flow rates help reduce dyspnea while avoiding CO2 retention.
• Increase protein, calories, and vitamin C in diet to meet body’s needs.
• Administer the incentive spirometer or flutter valve to encourage coughing
and expelling of mucous.
• Nocturnal negative pressure ventilation used for hypercapnic (elevated CO2
levels) patients.

NURSING DIAGNOSES
• Ineffective airway clearance
• Activity intolerance
• Ineffective breathing pattern

NURSING INTERVENTION
• Monitor respirations looking at rate, effort, use of accessory muscles, skin
color; listen to breath sounds.
• Place patient in high Fowler’s position to ease respiration.
• Weigh the patient daily. Excess fluid due to heart failure will increase weight.
Notify physician, NP, or PA of weight gain of 2 pounds in 24 hours.
• Have the patient perform the turning, coughing, and deep-breathing exer-
cises to enhance lung expansion and expel mucous.
• Monitor sputum for changes in color or amount, which may signal infection
in patients with chronic bronchitis.
• Monitor intake and output.
• Increase fluids to keep mucous thinner and easier to expel.
• Explain to the patient:
• How to administer oxygen.

Bronchiectasis

Introduction

Bronchi and bronchioles become abnormally and permanently dilated, caused by
infection and inflammation. This results in excessive production of mucous that
obstructs the bronchi. There is some obstruction of the airways and a chronic
infection. The changes within the lung can be localized or generalized. The lung
may develop areas of atelectasis where thick mucous obstructs the smaller air-
ways, making the mucous difficult to expel. This results in inflammation and
infection of the airways and leads to bronchiectasis.

PROGNOSIS
Early diagnosis and appropriate treatment of infections are essential for manage-
ment. Postural drainage and chest physical therapy aid in movement of mucous
from the airways. The difficulty in breathing is caused by excess mucus similar to
patients with Chronic Obstructive Pulmonary Disease (COPD) (emphysema or
chronic bronchitis).

SIGNS AND SYMPTOMS
• Difficult breathing (dyspnea) due to the mucous production and irritation
within the airways.
• Productive, foul-smelling odorous cough, due to thick, difficult-to-expel,
tenacious mucous, often with bacterial colonization.
• Cough may be worse when lying down.
• Recurrent bronchial infections.
• Hemoptysis (blood-tinged or bloody mucous).
• Loss of weight because patients are not eating well, due to respiratory
changes and foul-smelling mucous with cough. Increased respiratory effort
requires more calories to meet normal requirements.
• Crackles or rhonchi on inspiration due to mucous build-up.
• Anemia of chronic disease.
• Cyanosis.
• Clubbing of the fingers.

TREATMENT
Treatment is focused on getting enough oxygen to meet current needs of the patient,
expel mucous, and treat infections.
• Supplemental oxygen to help meet body’s needs.
• Postural drainage to assist with drainage of secretions.
• Chest PT to loosen secretions.
• Remove excessive secretions during a bronchoscopy.
• Administer bronchodilators to help keep airways open:
• albuterol, levalbuterol
• Administer antibiotics to treat infection:
• selected based on the results of a culture and sensitivity study

NURSING DIAGNOSES
• Ineffective airway clearance
• Imbalanced nutrition: less than what the body requires
• Impaired gas exchange
NURSING INTERVENTION
• Monitor respiratory rate, effort, breath sounds, skin color, and use of acces-
sory muscles.
• Perform chest percussion to help loosen secretions.
• Explain to the patient:
• That family member can perform chest PT.
• How to do postural drainage.
• How to administer oxygen.
• How to properly administer medications.

Asthma

Introdcuction

The airways become obstructed from either inflammation of the lining of the air-
ways or constriction of the bronchial smooth muscles (bronchospasm). A known
allergen, for example, pollen—is inhaled, causing activation of antibodies that rec-
ognize the allergen. Mast cells and histamine are activated, initiating a local inflam-
matory response. Prostaglandins enhance the effect of histamine. Leukotrienes also
respond, enhancing the inflammatory response. White blood cells responding to the
area release inflammatory mediators.
Astimulus causes an inflammatory reaction, increasing the size of the bronchial
linings; this results in restriction of the airways. There may be a bronchial smooth
muscle reaction at the same time. There are two kinds of asthma:
• Extrinsic asthma, also known as atopic, caused by allergens such as pollen,
animal dander, mold, or dust. Often accompanied by allergic rhinitis and
eczema; this may run in families.
• Intrinsic asthma, also known as nonatopic, caused by a nonallergic factor
such as following a respiratory tract infection, exposure to cold air, changes
in air humidity, or respiratory irritants.

PROGNOSIS
Triggers for the asthmatic patient can often be identified and avoided. Patients can
learn to check peak flow levels and manage symptoms in conjunction with their
caregiver. Well controlled asthma typically has temporary, reversible exacerba-
tions that can be controlled with medications, often in an outpatient setting. With
frequent attacks, a mild exposure to a known trigger will often be sufficient to
exacerbate an attack. Patients who do not respond to medications or who use med-
ications improperly may die during an asthma attack.

SIGNS AND SYMPTOMS

• Wheezing initially present on expiration continues throughout respiratory
cycle as inflammation progresses. Air has difficulty moving through the nar-
rowed airways, making noise. Not all asthmatics will have wheezing.
• Asymptomatic between asthma attacks. Symptoms resolve when there is no
inflammation present.
• Difficulty breathing (dyspnea) as airways narrow due to inflammation. This
is typically progressive as inflammation increases.
• Respiration greater than 20 breaths per minute (tachypnea) as the body
attempts to get more oxygen into the lungs to meet physiologic needs.
• Use of accessory muscles to breathe as the body tries harder to get more air
into the lungs.
• Tightness in the chest due to narrowing of the airways (bronchoconstriction).
• Cough.
• Tachycardia—heart rate greater than 100, as the body attempts to get more
oxygen to the tissues.

TREATMENT
The focus of treatment is to return the respiratory status to normal, deliver ade-
quate oxygen, and limit the number of recurrences. Patient education should focus
on understanding the disease, its management, and when emergency care may be
necessary.
• Administer supplemental oxygen to help meet body’s needs.
• Identify and remove allergens and known triggers to avoid causing an asthma
attack.
• Give patient 3 liters/day of fluid to help liquefy any secretions.
• Administer short-acting beta2-adrenergic drugs to bronchodilate:
• albuterol, pirbuterol, metaproterenol, terbutaline, levalbuterol
• Administer long-acting beta2-adrenergic drugs to manage symptoms day to
day; keep airways open, not for acute symptoms:
• salmeterol, formoterol
• Administer leukotriene modulators to reduce local inflammatory response in
lung to reduce exacerbations; does not have immediate effect on symptoms:
• zafirlukast, zileuton, montelukast
• Administer anticholinergic drugs
• ipratropium inhaler, tiotropium handihaler
• Administer antacid, H2 blocker, or proton pump inhibitor to decrease the
amount of acid in the stomach, reducing the possibility of ulcers due to stress
of disease or medication effects.
• Antacids: aluminum hydroxide/magnesium hydroxide, calcium carbonate
• H2 blockers: ranitidine, famotidine, nizatidine, cimetidine
• Proton pump inhibitors: omeprazole, lansoprazole, esomeprazole, rabepra-
zole, pantoprazole
• Administer mast cell stabilizer to retain an early component of the initial
response to allergens, which will prevent further reactions from occurring;
this is not for acute symptoms. This is useful for pretreatment for allergen
exposure or chronic use to improve control of symptoms.
• cromolyn, nedocromil
• Administer steroids to decrease inflammation, which will help open airways;
these are not for acute symptoms:
• hydrocortisone, methylprednisolone intravenously
• beclomethasone, triamcinolone, fluticasone, budesonide, flunisolide, mo-
metasone inhalers
• prednisolone, prednisone orally
• Administer methylxanthines to assist with bronchodilation, often used when
other medications not effective:
• aminophylline, theophylline

NURSING DIAGNOSES
• Impaired gas exchange
• Ineffective airway clearance
• Ineffective tissue perfusion

NURSING INTERVENTION

• Monitor respiration: patient’s respiratory status can continue to deteriorate;
look at respiratory rate, effort, use of accessory muscles, skin color, breath
sounds.
• Place patient in high Fowler’s position to ease respirations.
• Monitor vital signs, look for changes in BP, tachycardia, tachypnea.
• Explain to the patient:
• How to use a peak flow meter.
• How to use the metered dose inhaler or dry powder and in which order to
take inhaled medication.
• Avoid exposure to allergen.
• How to recognize the early signs of asthma.
• How to perform coughing and deep-breathing exercises.

Asbestosis

Introduction
Asbestos fibers enter the lungs, causing inflammation in the bronchioles and in the
walls of the alveoli. After inhalation, the fibers settle into the lung tissue. Fibrosis
develops and ultimately pleural plaques form. The changes within the lung result
in a restrictive lung disease. The damage to the lung causes impairment in breath-
ing and air exchange.

PROGNOSIS
It may take a decade or longer from the time of exposure before symptoms begin
to develop. Some patients have worked in occupations known for asbestosis ex-
posure (mining, shipyards, fireproofing, and construction before the mid-1970s),
for 10 or 15 years prior to symptom development. There is an increased risk of
lung cancer (mesothelioma) in patients with history of asbestosis exposure, espe-
cially if the patient has also smoked. Mesothelioma may develop 2 to 4 decades
postexposure.

SIGNS AND SYMPTOMS
• Difficulty breathing (dyspnea) on exertion and at rest due to changes in the
lung tissue
• Chest pain or tightness due to changes within the lung tissue and restrictive
air movement
• Dry cough due to irritation within the lungs
• Frequent respiratory infections due to changes within the lung, increasing
susceptibility to infection
• Respiration greater than 20 breaths per minute (tachypnea) due to decreased
vital capacity
• Rales or crackles when listening to breath sounds

TREATMENT
There is no specific treatment for asbestosis, nor is there a cure.
• Flu vaccine and pneumoccocal vaccine to reduce chance of illness.
• Oxygen therapy (1 to 2 liters per minute) to ease breathing discomfort by in-
creasing available oxygen to meet body’s needs.
• Administer antibiotics for exacerbations of respiratory symptoms—to treat
infectious process based on results of culture and sensitivity study or
empirically.

NURSING DIAGNOSES
• Fatigue
• Impaired gas exchange
• Imbalanced nutrition: less than the body requires

NURSING INTERVENTION
• Administer chest percussion and vibration to loosen and expel secretions.
• Explain to patient:
• How to avoid infections (reduced exposure to others with an infection and
vaccines administered according to physician’s orders).
• Proper use of oxygen therapy.

How the Respiratory System Works

The respiratory system has the following basic functions:
• Movement of air in and out of the lungs
• Exchange of oxygen and carbon dioxide
• Helping maintain acid-base balance
Ventilation moves air in (inspiration) and out (expiration) of the lungs. Dur-
ing inspiration, air flows in through the nose and passes into the nasopharynx.
Air is then drawn through the pharynx, larynx, trachea, and bronchi. The bronchi
branches (bifurcates) right and left into smaller tubes called bronchioles that ter-
minate in alveoli. The airways are lined with mucous membranes to add moisture
to the inhaled air. There is a thin layer of mucous in the airways that helps to trap
foreign particles, such as dust, pollen, or bacteria. Cilia—small, hair-like projec-
tions—help to move the mucous with the foreign material upward so it can be
coughed out.
Alveoli are air-filled sacs containing membranes coated with surfactant. The
surfactant helps the alveoli to expand evenly on inspiration and prevents collapse
on exhalation. Carbon dioxide and oxygen are exchanged; a higher concentration
of gas moves to the lower area of concentration. A higher concentration of carbon
dioxide in the hemoglobin moves across the membrane into the alveoli and is
expired by the lung. Higher concentration of oxygen in the alveoli crosses the
membrane and attaches to the hemoglobin which is then distributed by the circu-
latory system throughout the body.
Lungs are contained within a pleural sac in the thoracic cavity and operate on
negative pressure. The visceral pleura is close to the lungs and the parietal pleura
is close to the chest wall. There is a pleural space between these two layers that
contains a small amount of fluid to prevent friction with chest movement on inspi-
ration and expiration.