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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. All Rights Reserved. Reproduction and distribution of these materials are prohibited without the express written authorization of RN.com.

First Published: June 13, 2006 Updated: January 20, 2009 Updated: January 20, 2012

IMPORTANT INFORMATION RN.com strives to keeps its content fair and unbiased. The author has no conflicts of interest to disclose. The planners of the educational activity have no conflicts of interest to disclose. (Conflict of Interest Definition: Circumstances create a conflict of interest when an individual has an opportunity to affect Education content about products or services of a commercial interest with which he/she has a financial relationship.) There is no commercial support being used for this course. Participants are advised that the accredited status of RN.com does not imply endorsement by the provider or ANCC of any products/therapeutics mentioned in this course. The information in the course is for educational purposes only. There is no “off label” usage of drugs or products discussed in this course.

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.

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