Department of Medical Nursing, Faculty of Nursing, Chiang Mai University
Teaching Material for 561314: Adult Nursing II
For International Program Nursing Students
Semester I Academic Year 2007
---------------------------------------------------------------------------------------------Principle of Holistic of Nursing Care for Adult with Common Problem in
Respiratory Diseases (Obstructive Pattern)
Assist. Prof. Dr. Nitaya Pinyokham
Obstructive disease is characterized by an increase in airway resistance that is
measured as a decrease in peak expiratory flow rates. In some cases, there is a missmatch between the FEV1/FVC ratio. The normal person exhales most of the inspired
air in the 1st second; this ratio on normal subjects is around 0.8, this means that 80%
of the expired air is expelled the 1st second.
The group of diseases in obstructive lung include emphysema, bronchitis,
asthma, chronic obstructive pulmonary disease (COPD), bronchiectasis, byssinosis,
bronchiolitis, Asbestosis. In this article, only COPD is illustrated its pathophysiology,
predisposing factors, diagnosis, management, and nursing intervention.
2
Normal Lung
Figure 2 COPD Lung
COPD
Chronic obstructive pulmonary disease (COPD), also known as chronic
obstructive airway disease (COAD), is a group of diseases characterized by
limitation of airflow in the airway that is not fully reversible. COPD is the umbrella
term for chronic bronchitis, emphysema and a range of other disorders. It is most
often due to tobacco smoking[1] but can be due to other airborne irritants such as coal
3
dust, asbestos or solvents, as well as preserved meats containing nitrites. [1] COPD is
the fourth leading cause of death in America, claiming the lives of 122,283 Americans
in 2003 and the number of women dying from the disease has surpassed the number
seen in men.
The main symptoms of COPD include dyspnea (shortness of breath) lasting
for months or perhaps years, possibly accompanied by wheezing, and a persistent
cough with sputum production.[2] It is possible the sputum may contain blood
(hemoptysis), usually due to damage of the blood vessels of the airways. Severe
COPD could lead to cyanosis (bluish decolorization usually in the lips and fingers)
caused by a lack of oxygen in the blood. In extreme cases it could lead to cor
pulmonale due the extra work required by the heart to get blood to flow through the
lungs.[3]
COPD is particularly characterized by a ratio of forced expiratory volume over
1 second (FEV1) to forced vital capacity (FVC) being < 0.7 and the FEV1 < 70% of
the predicted value [4] Other signs include a rapid breathing rate (tachypnea) and a
wheezing sound heard through a stethoscope. Pulmonary emphysema is NOT the
same as subcutaneous emphysema, which is a collection of air under the skin that may
be detected by the crepitus sounds produced on palpation.[5]
Pathophysiology
Chronic bronchitis
Bronchitis is inflammation of the bronchi (medium-size airways) in the lungs.
Acute bronchitis is usually caused by viruses or bacteria and may last several days or
weeks.
Bronchitis
Acute bronchitis usually resolves in 7-10 days with no underlying lung
disease. Chronic bronchitis however is dependent on early recognition and smoking
cessation which improves the outcome significantly.
4
Chronic bronchitis is defined in clinical terms as a cough with sputum
production on most days for 3 months of a year, for 2 consecutive years. Chronic
bronchitis is hallmarked by hyperplasia (increased number) and hypertrophy
(increased size) of the goblet cells (mucous gland) of the airway, resulting in an
increase in secretion of mucus which contributes to the airway obstruction.
Microscopically there is infiltration of the airway walls with inflammatory cells,
particularly neutrophils. Inflammation is followed by scarring and remodeling that
thickens the walls resulting in narrowing of the small airway. Further progression
leads to metaplasia (abnormal change in the tissue) and fibrosis (further thickening
and scarring) of the lower airway. The consequence of these changes is a limitation of
airflow.[10].
Emphysema
Emphysema is a type of chronic obstructive lung disease. It is often caused by
exposure to toxic chemicals or long-term exposure to tobacco smoke.
Emphysema is defined histologically as the enlargement of the air spaces
distal to the terminal bronchioles, with destruction of their walls.[9] The enlarged air
sacs (alveoli) of the lungs reduces the surface area available for the movement of
gases during respiration. This ultimately leads to dyspnea in severe cases. The exact
mechanism for the development of emphysema is not understood, although it is
known to be linked with smoking and age.
Emphysema
The outcome is better for patients with less damage to the lung who stop
smoking immediately. Still, patients with extensive lung damage may live for many
years so predicting prognosis is difficult. Death may occur from respiratory failure,
pneumonia, or other complications.
Predisposing Factors
1) Cigarette smoking. A primary factor of COPD is chronic tobacco smoking.
In the United States, around 90% of cases of COPD are due to smoking[6] (are smoker
5
or former smokers) Not all smokers will develop COPD, but continuous smokers have
at least a 25% risk.[7] If you smoke 30 cigarettes per day you are 20 times more likely
to die from COPD than non-smokers (Asthma Foundation, 2007).
2) Pollutions
-Occupational pollutants. Some occupational pollutants, such as
cadmium and silica, have shown to be a contributing risk factor for COPD.
The people at highest risk for these pollutants include coal workers,
construction workers, metal workers and cotton workers, amongst others.
However, in most cases these pollutants are combined with cigarette smoking
further increasing the chance of developing COPD. These occupations are
commonly associated with other respiratory diseases, particularly
pneumoconiosis (black lung disease).
-Air pollution. Urban air pollution may be a contributing factor for
COPD as it is thought to impair the development of the lung function. In
developing countries indoor air pollution, usually due to biomass fuel, has
been linked to COPD, especially in women.
4) Genetics or family factors. Very rarely, there may be a deficiency in an
enzyme known as alpha 1-antitrypsin which causes a form of COPD and hyper
reactive airways (Asthma Foundation, 2007). Alpha 1-antitrypsin (AAT) is a
substance found in several places throughout the body and is important in preventing
breakdown of cells, particularly those in the lungs and liver. People who are deficient
of this substance are at increased risk of emphysema and cirrhosis of liver (Asthma
Foundation, 2007).
5) Other risk factors. Increasing age, male gender, allergy, repeated airway
infection and general impaired lung function are also related to the development of
COPD. In addition, urbanization, social class, and diet may also have some impact in
development of COPD but their overall effect is not known(Asthma Foundation,
2007). COPD is a common cause of disability of the older people in Thailand. It is
estimated that about half of the acute exacerbation definitely due to bacterial infection
(e.g. Chlamydia pneumoniae and others).
6
Sings and Symptom
The signs and symptoms of chronic obstructive pulmonary disease (COPD)
include:

Cough

Sputum (mucus) production

Shortness of breath, especially with exercise

Wheezing (a whistling or squeaky sound when you breathe)

Chest tightness
The early signs of COPD for which many people seek medical attention before
being formally diagnosed include marked shortness of breath with exertion, a cough
that won’t go away, or frequent respiratory infections. This is often at a point when
the disease is already advanced. Many people might be identified earlier if their
doctors routinely screen all patients who are smokers or previous smokers.
Diagnosis
The diagnosis of COPD is usually suggested by symptoms; it is a clinical
diagnosis and no single test is definitive. A comprehensive history from the patient is
very important with regard to smoking and occupation. Physical examination with a
plethysmograph can reveal the true extent of COPD.
The severity of COPD can be classified as follows using spirometry (see above):
Severity
Post-bronchodilator
FEV1 % predicted
At risk
FEV1 /FVC
>0.7
≥80
Mild COPD
≤0.7
≥80
Moderate COPD
≤0.7
50-80
Severe COPD
≤0.7
30-50
Very Severe
≤0.7
<30 or 30-50 with Chronic
COPD
Respiratory Failure symptoms
7
Management
Although COPD is not curable, it can be controlled in a variety of ways.
1) Smoking cessation
Smoking cessation is one of the most important factors in slowing down the
progression of COPD. Even at a late stage of the disease it can reduce the rate of
deterioration and prolong the time taken for disability and death.[10]
2) Occupational change
Workers may be able to transfer to a significantly less contaminated area of
the company depending on circumstances. Often however, workers may need
complete occupational change.
3) Pharmacotherapy
Bronchodilators
There are several types of bronchodilators used clinically with varying
efficacy: β2 agonists, M3 antimuscarinics, leukotriene antagonists, cromones
and xanthines.[11] These drugs relax the smooth muscles of the airway
allowing for improved airflow. The change in FEV1 may not be substantial,
but changes in the vital capacity are significant. Many patients feel less
breathless after taking bronchodilators.
β2 agonists. There are several highly specific β2 agonists available. Salbutamol
(Ventolin) is the most widely used short acting β2 agonist to provide rapid
relief and should be prescribed as a front line therapy for all classes of
patients. Other β2 agonists are Bambuterol, Clenbuterol, Fenoterol, and
Formoterol. Longer acting β2 agonists such as Salmeterol act too slowly to be
used as relief for dypsnea so these drugs should be used as a secondary
therapy. An increased risk is associated with long acting β2 agonists due to
decreased sensitivity to inflammation so generally the use of a concomitant
corticosteroid is indicated[2][3][4].
8
M3 muscarinic antagonists (anticholinergics. Derived from the deadly agaric
Amanita muscaria, specific antimuscarinics were found to provide effective
relief to COPD. Inhaled antimuscarinics have the advantage of avoiding
endocrine and exocrine M3 receptors. The quaternary M3 muscarinic
antagonist Ipratropium is widely prescribed with the β2 agonist salbutamol.
[5]. Ipratropium is offered combined with salbutamol (Combivent) and with
fenoterol (Duovent). Tiotropium provides improved specificity for M3
muscarinic receptors.
Cromones. Cromones are mast cell stabilizers that are thought to act on a
chloride channel found on mast cells that help reduce the production of
histamine and other inflammatory factors. Chromones are also thought to act
on IgE-regulated calcium channels on mast cells. Cromoglicate and
Nedocromil, which has a longer half-life, are two chromones available.[12]
Leukotriene antagonists. More recently leukotriene antagonists block the
signalling molecules used by the immune system. Montelukast,
Pranlukast, Zafirlukast are some of the leukotrienes antagonists.[13]
Xanthines. Theophylline is the prototype of the xanthine[14] class of drug.
Teas are natural sources of methylxanthines, xanthines and caffeine
while chocolate is a source of theobromine. Caffeine is approximately
16% metabolized into theophylline. Nebulized theophylline is used in
the EMR for treatment of dyspnea (Difficulty in breathing). Patients need
continual monitoring as theophylline has a narrow therapeutic range.
More aggressive EMR interventions include IV H1 antihistamines and IV
dexamethasone.
Corticosteroids
Inhaled corticosteriods (specifically glucocorticoids) act in the inflammatory
cascade and may improve airway function considerably,[10] however the long
term value has not been proven. Corticosteroids are often combined with
9
bronchodilators in a single inhaler. Some of the more common inhaled steroids
in use are beclomethasone, mometasone, and fluticasone.
Salmeterol and fluticasone are combined (Advair), however the reduction in
death from all causes among patients with COPD in the combination therapy
group did not reach the predetermined level of statistical significance.[15][16]
TNF antagonists
Tumor necrosis factor antagonists (TNF) are the most recent class of
medications designed to deal with refractory cases. Tumor necrosis factoralpha is a cachexin or cachectin and is considered a so-called biological drug.
They are considerered immunosopressive with attendant risks. These rather
expensive drugs include infliximab, adalimumab and etanercept.[17]
Vaccination
Patients with COPD should be routinely vaccinated against influenza,
pneumococcus and other diseases to prevent illness and the possibility of
death.[11]
Oxygen therapy: Indicators for O2 therapy are following:

Severe airflow obstruction with FEV1 of less than 30% of predicted.

Cyanosis

Polycythaemia

Peripheral oedema

Elevated jugular venous pressure

Oxygen saturation under 92% when breathing air.

Consider assessment for moderate airflow obstruction (FEV1 30 to 49% of
predicted). Evidence level D

All practices should have a pulse oximeter to identify patients needing LTOT.
Evidence level D

Oxygen concentrators should be used to supply the LTOT at home.
10

Ambulatory oxygen therapy may be of benefit in those who wish to continue
therapy outside the home. Evidence level D.

Short bursts of oxygen therapy for episodes of breathlessness should only be
used if all other methods fail. Evidence level C.
Pulmonary rehabilitation
Pulmonary rehabilitation is a program of disease management, counseling and
exercise coordinated to benefit the individual.[18] Pulmonary rehabilitation has
been shown to relieve difficulties breathing and fatigue. It has also been
shown to improve the sense of control a patient has over their disease as well
as their emotions.[19]
Diet
A recent French study conducted over 12 years with almost 43,000 men
concluded that eating a Mediterranean diet "halves the risk of serious lung
disease like emphysema and bronchitis". [6]
Surgery
For some people with severe COPD, surgery may be recommended. Surgery is
usually done for people who have:

Severe symptoms

Not had improvement from taking medicines

A very hard time breathing most of the time
The two types of surgeries considered in the treatment of severe COPD are:
bullectomy and lung volume reduction surgery (LVRS).
Prognosis
A good prognosis of COPD relies on an early diagnosis and prompt treatment.
Most patients will have improvement in lung function once treatment is started,
however eventually signs and symptoms will worsen as COPD progresses. The
median survival is about 10 years if two-thirds of expected lung function was lost by
diagnosis.
11
Nursing Intervention
Nursing diagnosis: Impaired gas exchange
Definition of impaired gas exchange: By the process of diffusion the
exchange of oxygen and carbon dioxide occurs in the alveolar-capillary membrane
area. The relationship between ventilation (airflow) and perfusion (blood flow) affects
the efficiency of the gas exchange. Normally there is a balance between ventilation
and perfusion; however, certain conditions can offset this balance, resulting in
impaired gas exchange. Chronic conditions such as chronic obstructive pulmonary
disease (COPD) put these patients at greater risk for hypoxia.
Characteristics
Confusion, Somnolence, Restlessness, Irritability, Inability to move
secretions, Hypercapnia, Hypoxia
Expected Outcomes
Patient maintains optimal gas exchange as evidenced by normal
arterial blood gases (ABGs) and alert responsive mentation or no further
reduction in mental status.
Ongoing Assessment
1. Assess respirations: note quality, rate, pattern, depth, and breathing effort.
Both rapid, shallow breathing patterns and hypoventilation affect gas
exchange. Shallow, "sighless" breathing patterns postsurgery (as a result of
effect of anesthesia, pain, and immobility) reduce lung volume and
decrease ventilation.
2. Assess lung sounds, noting areas of decreased ventilation and the presence
of adventitious sounds.
3. Assess for signs and symptoms of hypoxemia: tachycardia, restlessness,
diaphoresis, headache, lethargy, and confusion.
12
4. Assess for signs and symptoms of atelectasis: diminished chest excursion,
limited diaphragm excursion, bronchial or tubular breath sounds, rales,
tracheal shift to affected side. Collapse of alveoli increases physiological
shunting.
5. Assess for signs or symptoms of pulmonary infarction: cough, hemoptysis,
pleuritic pain, consolidation, pleural effusion, bronchial breathing, pleural
friction rub, fever.
6. Monitor vital signs. With initial hypoxia and hypercapnia, blood pressure
(BP), heart rate, and respiratory rate all rise. As the hypoxia and/or
hypercapnia becomes more severe, BP may drop, heart rate tends to
continue to be rapid with arrhythmias, and respiratory failure may ensue
with the patient unable to maintain the rapid respiratory rate.
7. Assess for changes in orientation and behavior. Restlessness is an early
sign of hypoxia. Chronic hypoxemia may result in cognitive changes such
as memory changes.
8. Monitor ABGs and note changes. Increasing PaCO2 and decreasing PaO2
are signs of respiratory failure. As the patient begins to fail, the respiratory
rate will decrease and PaCO2 will begin to rise. In those with COPD, have
a significant decrease in pulmonary reserves, and any physiological stress
may result in acute respiratory failure.
9. Use pulse oximetry to monitor oxygen saturation and pulse rate. Pulse
oximetry is a useful tool to detect changes in oxygenation. Oxygen
saturation should be maintained at 90% or greater. This tool can be
especially helpful in the outpatient or rehabilitation setting where patients
at risk for desaturation from chronic pulmonary diseases can monitor the
effects of exercise or activity on their oxygen saturation levels. Home
oxygen therapy can then be prescribed as indicated. Patients should be
assessed for the need for oxygen both at rest and with activity. A higher
liter flow of oxygen is generally required for activity versus rest (e.g., 2 L
at rest, and 4 L with activity). Medicare guidelines for reimbursement for
home oxygen require a PaCO2 less than 58 and/or oxygen saturation of
88% or less on room air. Oxygen delivery is then titrated to maintain an
oxygen saturation of 90% or greater.
13
10. Assess skin color for development of cyanosis. For cyanosis to be present,
5 g of hemoglobin must desaturate.
11. Monitor chest x-ray reports. Chest x-rays may guide the etiological factors
of the impaired gas exchange. Keep in mind that radiographic studies of
lung water lag behind clinical presentation by 24 hours.
12. Monitor effects of position changes on oxygenation (SaO2, ABGs, SVO2,
and end-tidal CO2). Putting the most congested lung areas in the dependent
position (where perfusion is greatest) potentiates ventilation and perfusion
imbalances.
13. Assess patient’s ability to cough effectively to clear secretions. Note
quantity, color, and consistency of sputum. Retained secretions impair gas
exchange.
Therapeutic intervention
1. Maintain oxygen administration device as ordered, attempting to maintain
oxygen saturation at 90% or greater. This provides for adequate
oxygenation.
2. Avoid high concentration of oxygen in patients with COPD. Hypoxia
stimulates the drive to breathe in the chronic CO2 retainer patient. When
applying oxygen, close monitoring is imperative to prevent unsafe
increases in the patient’s PaO2, which could result in apnea.
NOTE: If the patient is allowed to eat, oxygen still must be given to the
patient but in a different manner (e.g., changing from mask to a nasal
cannula). Eating is an activity and more oxygen will be consumed than
when the patient is at rest. Immediately after the meal, the original oxygen
delivery system should be returned.
3. For patients who should be ambulatory, provide extension tubing or
portable oxygen apparatus. These promote activity and facilitate more
effective ventilation.
4. Position with proper body alignment for optimal respiratory excursion (if
tolerated, head of bed at 45 degrees). This promotes lung expansion and
improves air exchange.
14
5. Routinely check the patient’s position so that he or she does not slide
down in bed. This would cause the abdomen to compress the diaphragm,
which would cause respiratory embarrassment.
6. Position patient to facilitate ventilation/perfusion matching. Use upright,
high-Fowler’s position whenever possible. High-Fowler’s position allows
for optimal diaphragm excursion. When patient is positioned on side, the
good side should be down (e.g., lung with pulmonary embolus or
atelectasis should be up).
7. Pace activities and schedule rest periods to prevent fatigue. Even simple
activities such as bathing during bed rest can cause fatigue and increase
oxygen consumption.
8. Change patient’s position every 2 hours. This facilitates secretion
movement and drainage.
9. Suction as needed. Suction clears secretions if the patient is unable to
effectively clear the airway.
10. Encourage deep breathing, using incentive spirometer as indicated. This
reduces alveolar collapse.
11. For postoperative patients, assist with splinting the chest. Splinting
optimizes deep breathing and coughing efforts.
12. Encourage or assist with ambulation as indicated. This promotes lung
expansion, facilitates secretion clearance, and stimulates deep breathing.
13. Provide reassurance and allay anxiety:
a. Have an agreed-on method for the patient to call for assistance
(e.g., call light, bell).
b. Stay with the patient during episodes of respiratory distress.
14. Anticipate need for intubation and mechanical ventilation if patient is
unable to maintain adequate gas exchange. Early intubation and
mechanical ventilation are recommended to prevent full decompensation
of the patient. Mechanical ventilation provides supportive care to maintain
adequate oxygenation and ventilation to the patient. Treatment also needs
to focus on the underlying causal factor leading to respiratory failure.
15. Administer medications as prescribed. The type depends on the etiological
factors of the problem (e.g., antibiotics for pneumonia, bronchodilators for
15
COPD, anticoagulants/thrombolytics for pulmonary embolus, analgesics
for thoracic pain).
Education and Continuity of Care
1. Explain the need to restrict and pace activities to decrease oxygen
consumption during the acute episode.
2. Explain the type of oxygen therapy being used and why its maintenance is
important. Issues related to home oxygen use, storage, or precautions need
to be addressed.
3. Teach the patient appropriate deep breathing and coughing techniques.
These facilitate adequate air exchange and secretion clearance.
4. Assist patient in obtaining home nebulizer, as appropriate, and instruct in
its use in collaboration with respiratory therapist.
5. Refer to home health services for nursing care or oxygen management as
appropriate.
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?plan=23
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