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Chronic Obstructive Pulmonary Disease
Chronic Obstructive
Pulmonary Disease
This course has been awarded
Two (2.0) contact hours.
This course expires on January 20, 2015
Copyright © 2006 by RN.com.
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First Published: June 13, 2006
Updated: January 20, 2009
Updated: January 20, 2012
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Acknowledgements
RN.com acknowledges the valuable contributions of…
…Nadine Salmon, RN, BSN, IBCLC is the Clinical content Specialist for RN.com.
Nadine earned her BSN from the University of the Witwatersrand, Johannesburg, South
Africa. She worked as a midwife in Labor and Delivery, an RN in Postpartum units and
Antenatal units, before moving to the United Kingdom, where she worked as a Medical
Surgical Nurse. After coming to the US in 1997, Nadine worked in obstetrics and
became a Board Certified Lactation Consultant. Nadine was the Clinical Pre Placement
Manager for the International Nurse Staffing division before joining RN.com. When not
writing courses and other educational materials, Nadine is currently pursuing her
master’s degree in Nursing Leadership.
…Susan Herzberger, RN, MSN, original course author, is a free-lance author,
medical-surgical nurse, nursing instructor and private health consultant.
Purpose and Objectives
Define the term COPD and describe the main features of COPD.
1.
2.
3.
4.
5.
6.
Identify patients most at risk for COPD.
Describe the use and interpretation of spirometry.
Show how staging of COPD severity is done.
Describe common management protocols for COPD patients.
Identify characteristics and uses of inhaler medications for COPD patients.
Identify important elements of patient teaching on COPD.
After successful completion of this course, you will be able to:
The purpose of this continuing education course on chronic obstructive pulmonary
disease (COPD) is to update nurses on current goals and management strategies for
COPD patients.
Introduction
Chronic obstructive pulmonary disease (COPD) is one of the most common diseases
you see as a nurse.
It is a slowly progressive and debilitating disease that develops slowly and silently for
years before symptoms appear. COPD mostly affects people in the second half of their
lives. Prevention of COPD is mostly aimed at people in the first half of their lives.
This course will update you on COPD management and patient care goals.
Overview of COPD
The term COPD refers to a group of diseases that cause progressive expiratory airflow
limitation with consequent breathing problems. Gradual loss of lung function makes
breathing so laborious that it can use up to 20% of a person’s energy just to bathe, get
dressed, or even talk (Mayo Clinic, 2005).
Many healthcare personnel misunderstand the term COPD. They confuse it with a
specific disease condition. COPD is defined as an irreversible disease due to
permanent destruction and scarring of pulmonary tissue.
COPD develops through an overlapping of three diseases:
•
•
•
Chronic bronchitis: Creates inflammation, cough, and excessive sputum
production.
Emphysema: Destroys alveoli leading to hyperinflation of lungs.
Co-existent asthma: Increases inflammation, constriction, and mucus production
which compounds dyspnea.
(Centers for Disease Control and Prevention, 2011).
COPD is characterized by increasingly restricted airflow and shortness of breath.
Statistics
COPD is the fourth leading cause of death in the US, and by 2020, this disease is
projected to be the third leading cause of death in the country (U.S. Department of
Health and Human Services, 2008).
In developed countries, the main risk factor for developing COPD is smoking.
Although only a small percentage of smokers develop “clinically significant” COPD,
studies of asymptomatic patients have shown that reduced lung function of any amount
exacts a toll in the form of increased risk of heart disease and shorter lifespan (Ferrara,
A, 2011).
Risk Factors For COPD
The link between COPD and smoking is extremely strong. One out of five smokers
eventually develops the disease, usually after a history of smoking for 15 to 20 years
(Booker, 2005; Braman & Martinez, 2005).
One factor that affects one to three percent of people with COPD is a hereditary
predisposition called alpha-1 antitrypsin (AAT) deficiency (Richmond & Zellner, 2005).
AAT protects normal lung cells from enzymatic destruction in infectious and
inflammatory processes. A deficiency may be inherited or acquired through malnutrition,
liver disease, or nephrotic syndrome (Paguna & Paguna, 2005).
Some people develop COPD through long-term occupational or domestic exposures to
irritants and pollutants. Unfortunately, COPD progresses silently without symptoms until
the fourth or fifth decade of life (Mulroy, 2005; Childers, 2005). By then, half of the
patient’s lung function may be permanently lost (Booker, 2005).
COPD affects more than the lungs. Gas exchange abnormalities create problems all over the
body, especially in the heart and brain.
Risk Factors For COPD
Cardiovascular disease commonly co-exists with COPD. Pulmonary hypertension is
inevitable and this leads to cor pulmonale (Right-sided heart failure caused by
respiratory disease).
COPD invites a host of other health problems. COPD patients are generally poor
surgical risks (Braman & Martinez, 2005). Pneumonia and pneumothorax can
complicate post-operative care. Patients who have severe COPD bear the additional
burden of restrictive and expensive use of oxygen therapy. In the most advanced stage,
patients must face end-of-life decisions about the use of ventilatory support.
Pathology & Presentation of COPD
In response to the triggers of smoke and/or air pollutants, inflammatory processes with
long-reaching consequences are set in motion (GOLD, 2005). Lung cells that are not
protected by adequate AAT deteriorate more rapidly in response to irritants (Richmond
& Zellner, 2005).
Inflammation in the lungs creates excessive mucus secretion and ciliary dysfunction. It
eventually scars the bronchial tube linings. Elasticity that normally keeps the airways
open is then lost. Simultaneously, hyper-responsiveness (asthma) constricts the
bronchioles further. Irreversible structural changes eventually occur. Small airways
become narrowed due to fibrosis and muscle hypertrophy. Alveolar walls collapse
leaving larger spaces where air is trapped.
Initially, COPD develops without noticeable symptoms. Eventually, dyspnea and
productive coughing cause patients to seek healthcare. Some patients complain of
orthopnea, difficulty breathing while lying flat on their backs. Most patients complain of
coughing, wheezing, excessive sputum, shortness of breath (SOB), and incapacity for
physical activity (Childers, 2005; Mayo Clinic, 2005; Mulroy, 2005).
As the disease progresses, frequent cycles of exacerbation occur. Chronic symptoms
intensify, accompanied by fever and a change in color or tenacity of sputum. In one of
three cases, the cause of exacerbation cannot be identified (GOLD, 2005). Most often
the episodes follow influenza and colds. Excess mucus favors the growth of bacteria,
supporting secondary respiratory infections. Air pollution and seasonal allergies are also
triggers.
Diagnosis
The diagnosis of COPD is made from the patient’s history of smoking or occupational
exposure, from clinical symptoms of chronic productive cough and shortness of breath
(SOB), and from diagnostic testing.
The diagnosis of COPD depends primarily on establishing the presence of diminished
airflow through spirometry testing, as well as excluding all
other possible causes for decreased airflow, such as lung cancer, asthma, tuberculosis
or other infectious processes (Ferrara, A, 2011).
Additional diagnostic tests used to verify suspicions of COPD include:
•
•
•
•
•
•
•
Pulmonary function tests
Chest x-ray to rule out other causes
Arterial blood gas (ABG) analysis
Pulse oximetry
Sputum exam
CT scan
Serum protein electrophoresis, followed by AAT determination and genetic
phenotyping
(Mayo Clinic, 2005; Paguna & Paguna, 2005).
COPD is a functional diagnosis, as most people seek medical attention only when activities of
daily living (ADL) are significantly affected by shortness of breath (Ferrara, A, 2011).
Pulmonary function tests
Pulmonary function tests:
•
•
•
•
Determine the cause of SOB
Confirm or rule out a diagnosis
Monitor the effects of respiratory medications
Evaluate a patient’s surgical risk
To prepare your patient for a pulmonary function test advise your patient of the
following:
• Avoid smoking and drinking alcohol for four hours prior to the test
• Avoid eating a big meal for two hours before the test
• Avoid exercise for half an hour before the test
• Empty the bladder right before testing
• Wear loose clothing
• Expect to be fatigued
(American Thoracic Society, 2011)
Three types of pulmonary function tests are done to evaluate COPD:
•
•
•
Spirometry is the first test done. This 30-minute test measures airflow in terms of
vital lung capacity.
Diffusion studies take 15 minutes and measure how well oxygen moves from the
lungs into the blood. Arterial blood gases may be drawn simultaneously.
Body plethysomography, a 15-minute test, is conducted in an enclosed clear
plastic box. It measures how much air is left in the lungs between inhalation and
exhalation.
Spirometry
Spirometry is a simple test that can be performed in an office setting. It involves taking a
deep breath and releasing it forcefully into a mouthpiece. The spirometer records the
volume of air released over time (Ferrara, 2011).
Two spirometry values are important in COPD diagnosis and staging:
•
•
Forced vital capacity (FVC) is the total amount of air exhaled.
FEV1 (forced expiratory volume in 1 second) is the amount of air forcibly exhaled in
the first second of the test.
The ratio of FEV1 to FVC (FEV1/FVC) indicates pattern of airflow that is normal,
restricted, or obstructed. A low FEV1/FVC ratio indicates obstructed airflow.
Compared with the total volume of air exhaled, the amount exhaled in the first second is
low, which indicates narrowed airways (Ferrara, 2011).
What spirometry values confirm COPD?
Results from spirometry are given in percentages of the predicted normal value based
on age, height and weight, race, and sex. COPD patients have less than 80% FEV1 and
less than a 70% FEV1 to FVC ratio (Paguna & Paguna, 2005; GOLD, 2005). The
severity of COPD is staged according to these values and does not rely totally on the
presence of clinical symptoms.
When a patient’s FEV1 is less than 60%, a reversibility test may be conducted to
exclude asthma as the reason for the poor performance. A bronchodilator is given by
nebulizer and the test is repeated. If airflow obstruction completely resolves, COPD is
ruled out. However, the reversibility test is controversial (Booker, 2005). Studies show
that 16 to 23% of asthmatics have irreversible airflow obstruction (Martinez et al., 2005).
If the effect of a bronchodilator in testing improves lung function by 20%, patients may
be put on long-term usage (Paguna & Paguna, 2005).
Stages of COPD
Spirometry defines the stage of COPD so that appropriate interventions can be made to
halt disease progression. COPD staging aids in treatment decisions and is important in
predicting the course of the disease (Ferrara, 2011).
Patients with more advanced stages suffer more frequent exacerbations and
deteriorating quality of life. Frequent exacerbations often require hospitalization, an
intolerance of exercise develops, as well as an incapacity for work, a restricted social
life, and sleep disorders.
Staging is based on spirometry testing after the administration of a bronchodilator
(Ferrara, 2011). A higher stage implies a higher risk of death (Ferrara, 2011).
The Bode Index
Spirometry provides a good tool for evaluating lung function, but a more comprehensive
tool to define a patient’s overall health and accurately predict the risk of death from
COPD, is the Bode Index (Ferrara, 2011).
The BODE index (Body-mass index, airflow Obstruction, Dyspnea and Exercise
capacity) combines measurements of the patient’s systemic health (the 6-minute
walking test and the body-mass index) with the patient’s perception of his or her
condition (the dyspnea score) and an objective measure of pulmonary dysfunction
(FEV1).
The BODE index assigns a score from 0 to 3 (inclusive) variables: FEV1, exercise (in
the form of the 6-minute walking test), dyspnea, and body-mass index (BMI). The
maximum total score of the BODE index is 10. The patient’s risk of death increases with
increasing total score (Ferrara, 2011).
Managing COPD
COPD, like other chronic diseases, cannot be cured. However, disease management is
essential to limit disease progression. What can be done for COPD patients when they
are in a stable condition? The most effective intervention is the promotion of smoking
cessation.
Current treatment options for COPD relieve symptoms and provide supportive care, by
slowing down the rate of decline in lung function and the number of exacerbations
(Ferrara, 2011). The goals of COPD treatments include risk reduction, improved health
status and quality of life, and minimization of the frequency and severity of acute
exacerbations (Ferrera, 2011).
COPD is generally managed with:
•
•
•
Bronchodilators and often corticosteroids, both administered by inhalation.
A pulmonary rehabilitation program.
Eventually, long-term oxygen therapy.
Current protocol for COPD management
Stage 0:
At Risk
Stage 1:
Mild COPD
Stage 2:
Moderate
COPD
Stage 3:
Severe
COPD
Stage 4:
Very
Severe
COPD
Normal spirometry.
Chronic productive cough.
FEV1 greater than 80% of predicted value.
Ratio less than 70%.
With or w/out symptoms.
FEV1 less than 50 to 80% of predicted
value.
Ratio less than 70%.
With or w/out symptoms.
FEV1 less than 30 to 50% of predicted
value.
Ratio less than 70%.
With or w/out symptoms.
FEV1 less than 30 % of predicted value or
less than 50% predicted plus chronic
respiratory failure.
Ratio less than 70%.
(GOLD, 2005)
Avoidance of risk factors.
Influenza vaccine.
Add short-acting
bronchodilator PRN.
Add regular use of one or more
long-acting bronchodilators.
Add rehabilitation.
Add inhaled
glucocorticosteroids if having
repeated exacerbations.
Add long-term oxygen therapy
if in chronic respiratory failure.
Consider surgical treatments.
Bronchodilators
Bronchodilators are the foundation of COPD treatment.
Two main classes of bronchodilators are used to treat COPD:
•
•
Agonists: Beta-agonist agents relax airway smooth muscles and improve airflow.
Anticholinergics: Block acetylcholine, a neurotransmitter that activates respiratory
muscles.
Since COPD patients with moderate-to-severe disease develop shortness of breath with
normal daily activities, they need medications that last throughout the day. Short-acting
drugs that require multiple applications reduce patient compliance and may increase
undesirable side effects.
Therefore, the most common clinical approach for patients with anything beyond mild
COPD is to prescribe long-acting bronchodilators for daily use, and to prescribe
short-acting agents as “rescue” medications for particularly severe episodes of dyspnea
(Ferrera, 2011). COPD patients with mild disease are treated on an “as-needed”
schedule.
Inhaled Corticosteroids
Inhaled corticosteroids (ICS) reduce both the frequency and severity of acute
exacerbations of COPD, and are preferable to the use of systemic steroids, which have
many adverse effects and are not recommended for long-term treatment (Ferrera,
2011).
Commonly prescribed inhaled steroids for COPD treatment include:
•
•
Budesonide (Entocort EC)
Fluticasone
(Porter et al, 2010 in Ferrera, 2011).
Use of inhalers
Ask your patients to demonstrate how they are using their inhalers at each visit. Proper
use ensures maximum benefit of this primary intervention. Improper use may be due to
shakiness, weakness, or confusion. There are three ways of administering medication
designed for inhalation:
•
•
•
Metered dose inhalers (MDIs).
Aerolizers.
Dry-powder inhalers (DPIs).
The MDIs are gas-propelled inhalers. They are preferably used with a spacer to ensure
the maximum dosage of medicine goes directly into the lungs, not into the mouth and
throat. The open-mouthed method for using a MDI is preferred over the closed-mouth
method, when no spacer is used (University of Pittsburgh Medical Center, 2005).
Aerolized medicine may be delivered with a nebulizer. This machine changes liquids
into a mist. Nebulizers are not regularly used by COPD patients but may be employed in
the ED during an exacerbation.
DPIs are propelled through inhalation. The discus and turbuhaler models require
techniques different from MDIs (NHLBI, 1997).
Your patients may have several different kinds of inhalers at home. In an episode of
dyspnea requiring relief, teach them to use their inhalers in this order:
1. Fast-acting, relief inhaler.
2. Regular, maintenance inhaler.
3. Steroid inhaler.
Teach patients to avoid the side effects of inhalant steroids by rinsing and gargling after
each use. This applies to combination inhalers that have steroids in them.
Combination Therapy
Although the use of a long-acting bronchodilator or ICS are helpful in patients with
moderate-to-severe COPD, the combination of these agents yield more
impressive results (Ferrera, 2011).
Combinations of β-agonists with corticosteroids are now available in a single inhaler.
Salmeterol/fluticasone is sold in the U.S. under the trade name Advair
(available as a dry powder or metered-dose inhaler), and budesonide/formoterol
(available as a metered dose inhaler) is sold in the U.S. under the trade name
Symbicort.
In various studies, the LABA/ICS combination has better anti-inflammatory effect than
either drug used independantly (Ferrera, 2011). The possible side effects
of combination therapy are outweighed by improved quality of life, survival benefits and
reduction in acute exacerbations.
There is also evidence from several trials that the addition of an anticholinergic to the
combination of LABA/ICS might provide even greater benefit for patients (Mapel et al,
2010 in Ferrera, 2011).
Medications
Patients often use a combination of medications, some for fast relief, some with a long
duration, and some just for exacerbations. Some formulations combine different types of
bronchodilators or bronchodilators with different speeds of onset. Some combine
bronchodilators and anti-inflammatories (Capriotti, 2005; Hanania, 2004). Experts now
report that the combination of a long-acting beta2-agonist with an inhaled
glucocorticosteroid controls COPD better than a combination of a short-acting
beta2-agonist with an anticholinergic (GOLD, 2005).
Systemic medications are not commonly used in COPD because of the risk for more
serious side effects. However, exacerbations may make them necessary. Orally
administered theophylline requires monitoring by blood test. It can cause nausea and
vomiting, arrhythmias, and seizures (ATS, 2005). Long-term prednisone causes weight
gain, skin bruising, osteoporosis, hyperglycemia, muscle weakness, and pedal edema.
Some other pharmaceutical treatments used in COPD are:
•
•
•
•
Influenza vaccines, which reduce illness and deaths about 50%.
Weekly intravenous plasma administration to correct documented alpha-1
antitrypsin deficiencies.
Antibiotics as needed for bacterial infections.
Opioids as needed for pain management in advanced COPD (GOLD, 2005;
Richmond & Zellner, 2005)
Pulmonary rehabilitation
Encourage your newly diagnosed patients to participate in a rehabilitation program. This
involves a two month commitment to exercise training, nutritional counseling, and
COPD education. Patients learn how to ease their exhalations with pursed lip breathing.
In the rehabilitation program, patients learn how to do controlled coughing to save
energy and oxygen. They learn practical tips such as eating smaller, more frequent
meals. They are taught to monitor outdoor air quality prior to excursions. Additional
patient education topics include breathing and coughing techniques, tips on conserving
energy, planning for acute exacerbations, simple exercises to do at home and use of
oxygen therapy (Ferrera, 2011).
Rarely, COPD patients may have surgical interventions to prolong life (Childers, 2005).
Lung volume reduction surgery is sometimes an option to improve exercise capacity in
patients with emphysema predominantly located in the upper lobes. The success of this
operation generally benefits patients for a few years. Bullectomy may be performed for
localized restructuring. In this surgery, larger, distended airspaces are removed to allow
healthy alveoli to expand. Lung transplantation is another possibility.
Oxygen Therapy
Patients in very severe, stage four COPD, require long-term oxygen therapy for most
activities of daily living. The patient’s clinical practitioner prescribes oxygen. The
prescription indicates:
•
•
•
•
The source of oxygen (liquid or gas)
How it will be delivered (usually via a nasal cannula)
When it is to be used
The flow rate (usually less than 3L/min)
In some patients with COPD, the body tries to compensate for the constant
lack of oxygen by producing high levels of red blood cells and relying on the hypoxic
drive (chronically high CO2 levels and relative oxygen deficiency stimulate respiration in
the patient with COPD). This is in contrast to the normal person where the blood level of
CO2 drives respiration. In these patients high doses of oxygen can inadvertently reduce
respiration and cause respiratory depression. Thus oxygen therapy in the COPD patient
must be closely monitored, and maintained at less than 4 L/minute.
High levels of oxygen in COPD patients can lead to CO2 retention in the blood. This,
however, is not normally a concern in stable patients receiving oxygen therapy at home.
The decision to begin oxygen therapy should come after patients have been stable on a
treatment regimen for at least 30 days (Ferrera, 2011).
Managing Exacerbations
On assessment, the patient should be observed for a change in alertness, as a first sign
of impending crisis. Locate previous measurements of lung function and arterial blood
gases in the medical record. When the patient is able to cooperate with testing,
spirometry will be done for comparison. Meanwhile, arterial blood gases, chest x-ray,
ECG, and hematocrit will be done to establish a current diagnosis and direct treatment.
The decision to admit to the hospital or discharge to home hinges on the need for
assisted ventilation. This will be necessary when arterial blood gases show no
improvement despite medical therapy and oxygenation (ATS, 2004). Non-invasive
positive pressure ventilation (NPPV) is given to reduce the labor of breathing and
improve arterial blood gases. It is given through a nasal or face mask.
NPPV is a form of life support and administered on a medical unit, often in the ICU.
Patients often self-manage their exacerbations at home, and may not report these
sporadic episodes to their practitioners. COPD patients may take prescribed oral
steroids during the first 72 hours. If this measure fails, patients may present to the ED.
Safe Oxygen Delivery
Patients with COPD have a lower than normal respiratory drive in response to chronic
hypercapnia, elevated CO2. COPD patients in exacerbation are muscularly fatigued
from labored breathing.
Assisted Ventilation
Some COPD patients require endotracheal intubation or tracheostomy.
These conventional methods of ventilatory assistance are initiated with patients who
exhibit:
•
•
•
•
•
•
•
Cardiovascular instability.
Respiratory arrest.
Copious secretions.
Complications such as pneumonia or sepsis.
Impaired mental status.
Craniofacial traumas or abnormalities.
Worsening acidosis and tachypnea (over 35 breaths/minute) despite NPPV (ATS,
2012).
End-of-Life Care
Page
The last year of a COPD patient’s life is heavily loaded with intensifying symptoms:
• Breathlessness that is unrelieved, or at best only partially relieved
• Weakness and fatigue
• Depression
• Pain
(Elkington, et al., 2005)
It can be difficult to recognize the point when chronic care becomes palliative care for
COPD patients (ATS, 2012). However, hospitalizations at least twice a year and inability
to leave home provide clues. Often patients know intuitively that they might die soon.
Statistics show that one-third to one-half of stage four COPD patients die within two
years of being admitted for an acute exacerbation (Ellkington et al., 2005).
Patients, their families, and their practitioners must make crucial decisions regarding life
support with invasive ventilation. No one finds such decisions easy, but making the
decisions in advance may afford some peace before the end of the patient’s life is
imminent.
Advise your patients to do advance care planning while they are medically stable.
Inform them of how the decision to intubate is based on the prediction of reversibility of
an exacerbation, the patient’s wishes, and available resources (GOLD, 2005).
Encourage them to have Advance Directives in place for influencing decisions on
respiratory support and terminal sedation. It is not possible to know in advance if an
exacerbation can be reversed in advanced stages of COPD. Practitioners are guided by
the patient’s wishes, expressed in advance (ATS, 2012).
Smoking Cessation
Foremost among what your patients need to know is how to stop smoking, if they
haven’t already done so. This effort at any stage of COPD will slow down the loss of
lung function. Lung capacity may even return to the normal decline that goes along with
aging, if COPD is not too advanced. This benefit is much less if patients continue to be
exposed to residential or workplace irritants and pollutants in the air (Braman &
Martinez, 2005; GOLD, 2005).
Offer current smokers treatment options at every visit. Practical counseling is effective.
Other pharmacotherapies that can be offered include:
• Nicotine gum
• Nicotine inhalers
• Nasal sprays
• Transdermal patches
• Sublingual tablets or lozenges.
• Some patients may need an antidepressant to make the transition
(GOLD, 2005).
Case Study: Carol
She is already on a regime that includes a combination inhalant of a long-acting
beta2-agonist with a corticosteroid. She is admitted for 24 hours and given NPPV. Then
she is discharged with prescriptions for a short-term course of oral steroids and an
antibiotic. Carol’s pulmonary function tests done during hospitalization show she is in
stage 3 COPD. Your goal with her is to capitalize on what she considers her success
strategies for improving quality of life. You also prepare her for the eventuality of
long-term oxygen therapy.
Carol Smith, age 69, is in the ED with an exacerbation of COPD. You see her sitting
erect and bending forward with her arms resting on an overbed table. There is a tremor
in her hands. Her neck is extended. She breathes through pursed lips in a soft whistle.
Dyspnea prevents her from talking to you. You learn from her spouse that she is sick for
the fifth day with an upper respiratory infection.
Case Study: John
John Jefferson's stage 4 COPD is complicated by co-existing cor pulmonale and type 2
diabetes. John has an Advance Directive in his chart, written over a year ago. You
assess his pain level and he indicates that it is an eight on a scale of one to ten. His
family is gathered to say goodbye, recognizing that an escalation of the current dosage
of morphine and/or the discontinuance of life support will most likely end his life.
John Jefferson, age 77, is hospitalized for ventilatory support. His COPD is at the most
severe stage with 90% of his lung function gone. John smoked for 40 years before
quitting at age 60. He also inhaled a lot of dust particles and pollutants during his job as
a highway construction worker.
You first meet John in the context of his family. John is unable to communicate. Despite
intubation and life support, he seems alert and aware of the discussion taking place
about him.
Conclusion
Society often places blame on the COPD patient for having a preventable disease. It
inflicts guilt over smoking.
As a nurse, you can take a broader perspective, knowing that all people struggle with
the odds when making lifestyle choices.
You will have the opportunity to care for many COPD patients at varying stages of
disease severity. You may admire a patient struggling to maintain an acceptable quality
of life despite the debilitation.
Your focus on attainable goals will contribute greatly to the patient’s quality of life.
Appendix One: Open-Mouth Method For Using An Inhaler
Open-Mouth Method For Using An Inhaler
When instructing a patient in the open-mouth method of using an inhaler, encourage the
patient to follow these steps:
1.Remove the cap. Hold the inhaler upright.
2.Check to be sure the mouth piece is free of any foreign object.
3.Shake the inhaler.
4.Tilt the head back slightly. Breathe out slowly.
5.Place the inhaler 1 to 2 inches in front of an open mouth (the width of 2 fingers).
6.Press down on the canister firmly as you start to breathe in slowly. (Press down until
the medicine is released.)
7.Breathe in slowly for a count of 3 to 5 seconds.
8.Hold your breath for a slow count to 10 (10 seconds).
9. If more puffs are prescribed, the ideal is to wait between doses, to make the medicine
more effective. For bronchodilators that are short-acting beta agonists, it is best to wait
10 minutes between doses. But it is often only practical to wait 3 to 5 minutes. For other
inhalers, try to wait 1 minute between puffs.
10. Rinse and gargle with mouth wash or with water after using any steroid inhaler
(even when it’s combined with another medicine).
UPMC, (2011).
Appendix Two: Closed-Mouth Method For Using An Inhaler
Closed-Mouth Method
Note: This method is not preferred over the spacer or open-mouth methods. Less
medicine reaches the airways with the closed-mouth method. Direct the patient to follow
these steps:
1.Remove the cap. Hold the inhaler upright.
2.Check to be sure the mouth piece is free of any foreign object.
3.Shake the inhaler.
4.Tilt the head back slightly. Breathe out slowly.
5.Place the inhaler in your mouth. Close your mouth.
6.Press down on the canister firmly as you start to breathe in slowly. (Press down until
the medicine is released.)
7.Breathe in slowly for a count of 3 to 5 seconds.
8.Hold your breath for a slow count to 10 (10 seconds).
9.If more puffs are prescribed, the ideal is to wait between doses. For bronchodilators
that are short-acting beta agonists, it is best to wait 10 minutes between doses, but it
may be more practical to wait 3 to 5 minutes. For other inhalers, try to wait 1 minute
between puffs.
10.Rinse and gargle with mouth wash or with water after using any steroid inhaler (even
when it’s combined with another medicine).
UPMC (2011).
Appendix Three: Spacers
Spacers
The use of a spacer device offer several benefits. When a spacer is used, more
medicine reaches the lungs, and less medicine is deposited on the tongue and the back
of the mouth. Side effects also are fewer and milder.
There are several types of spacers available. It’s important that the patient follows the
instructions on the package insert for their particular spacer. Instruct the patient to follow
these steps:
1.Remove the caps. Check to be sure the inhaler and spacer are free of any foreign
object.
2.Attach the inhaler to the spacer.
3.Shake well.
4.Tilt the head back slightly. Sit upright, and breathe out normally.
5.Place the mouth piece into your mouth. Close your lips around it.
6.Press down on the canister firmly until the medicine is released. This will put 1 puff of
the medicine into the spacer.
7.Breathe in slowly for a count of 3 to 5 seconds. Many spacers whistle if you inhale too
fast.
8.Hold your breath for a slow count to 10 (10 seconds).
9.Remove the spacer from your mouth, and then breathe out slowly.
10.If more puffs are prescribed, the ideal is to wait between doses. This will make the
medicine more effective.
11. Rinse and gargle with mouth wash or with water after using any steroid inhaler
(even when it’s combined with another medicine).
(UPMC, 2011).
Resources
At the time this course was constructed all URL's in the reference list were current and accessible.
rn.com. is committed to providing healthcare professionals with the most up to date information available.
National Heart, Lung and Blood Institute
http://www.nhlbi.nih.gov
American Lung Association
http://www.lungusa.org.
American Thoracic Society
http://www.thoracic.org
National Lung Health Education Program
http://www.nlhep.org
National Jewish Medical and Research Center
http://www.nationaljewish.org
Cleveland Clinic Foundation
http://www.clevelandclinic.org.
American College of Chest Physicians
http://www.chestnet.org.
American Association for Respiratory Care
http://www.yourlunghealth.org.
References
At the time this course was constructed all URL's in the reference list were current and accessible.
rn.com. is committed to providing healthcare professionals with the most up to date information available.
© Copyright 2006, AMN Healthcare, Inc.
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