Nursing Patients with Interstitial Lung Disease

3 March, 2008

Author Annette Duck, BSc, SCM, RN, is intertitial lung disease nurse specialist and Association of Respiratory Nurse Specialists committee member, University Hospital of South Manchester NHS Foundation Trust.

Abstract Duck, A. (2008) Nursing patients with interstitial lung disease. Nursing Times; 104: 9, 46–49. Annette Duck considers the important factors for supporting patients with a diagnostic label of interstitial lung disease.

The interstitial lung diseases (ILDs) are a group of over 150 lung disorders. They share common clinical, radiological and pulmonary function features. They usually present with shortness of breath and/or cough. If left untreated they can lead to lung fibrosis or scarring and, ultimately, death.

It is not necessary for nurses to understand the characteristics, pathology or medical management of all 150 types, in order to care and support patients with ILD. As with all illnesses, nurses treat the whole person and not the disease, holistically looking at their unique problems. Patients with ILD often have common problems that need further discussion. The diagnosis and investigation of ILD has been covered in previous NT articles (Duck, 2007a, b).

Diagnosis and providing information

Patients like to feel the clinicians looking after them are familiar with the characteristics of their disease. Sometimes it is not possible to give a definitive diagnosis of ILD and patients can find this distressing. It is vital to have an ‘open and honest’ discussion with the patient, explaining why it has been impossible to arrive at a conclusive diagnosis.

As ILDs are uncommon many GPs or general physicians may only care for a small number of patients with the disease. It is recommended that such patients are referred to a respiratory specialist for full diagnostic work up and management.

A significant number of patients will be given a diagnosis of one of the more common forms of ILD called idiopathic pulmonary fibrosis (IPF). This
form of ILD has a poor prognosis, similar to some types of lung cancer. Most patients will have an understanding of what it means to have a cancer, and this is a useful comparison to help explain their diagnosis. Many patients will not take in the implications of their diagnosis at first presentation and several explanations may be required.

It takes time to obtain a diagnosis of ILD and this can increase worry and anxiety for patients. Fallowfield et al (1995) in their study of patients with cancer identified a ‘strong absolute need for all general information, be it positive or negative’.

Breaking bad news is one of the most important skills a clinician can learn (Buckman, 1992). If patients perceive that information given to them is inadequate or poorly delivered, they may fail to adjust and exhibit signs of anxiety and depression (Fallowfield et al, 1995). If bad news is delivered appropriately, it can improve the therapeutic relationship between patient and clinician.

Ambulatory oxygen

Patients with ILD experience breathlessness on exertion, which is usually associated with hypoxia, and are likely to need ambulatory oxygen before they need oxygen at rest. The British Thoracic Society (BTS, 2006) guidelines for oxygen assessment should be followed.

It is important to assess all patients with breathlessness on exertion for exercise-induced hypoxia, particularly those diagnosed with IPF. IPF progresses rapidly (Wells and du Bois, 1994) and patients are likely to experience exercise-induced hypoxia that can reduce their exercise performance significantly. They should be assessed with either a shuttle walk or six-minute walk test to evaluate whether they are experiencing breathlessness associated with hypoxia (BTS, 2006) (Box 1).

Most patients are reluctant to walk in public with supplementary oxygen due to embarrassment, difficulty transporting oxygen and anxiety about running out of oxygen. This therapy may also be symbolic of dependence and progressive disease.

Patients with an exercise capacity of over 300m may prefer to slow down or stop and rest in preference to using ambulatory oxygen. Patients usually have a threshold at which they will assess the benefit of wearing oxygen in public against social isolation, breathlessness and staying at home.

Using ambulatory oxygen may not stop oxygen desaturation on exercise, particularly in IPF, however, it will raise the baseline oxygen level, maintain higher capillary oxygen levels for longer and enable a faster recovery rate, thus improving exercise performance overall. Oxygen conserver devices attached to cylinders or liquid oxygen units deliver small pulsed doses of oxygen on inspiration, cutting off on expiration, thereby prolonging the life of the cylinder or liquid oxygen unit (Duck, 2006). Although these devices are useful for patients with COPD, who usually only require low flow rates of around 2l/min, they are not useful for patients who need higher flow rates that are equal to or greater than 4l/min with ambulatory oxygen. It is important, therefore, that patients are assessed with and without oxygen conservers before their use is recommended.

IPF is rapidly progressive with a mean survival of about three years from diagnosis (Wells and du Bois, 1994). Patients with IPF should be offered liquid oxygen for ambulatory use outside the home from an early stage, if they meet the BTS guidelines for ambulatory oxygen. Many of these patients generally have a good exercise capacity, but require substantial flow rates to maintain oxygen saturations during activity. As the disease is rapidly progressive, patients often do not have time to become physically deconditioned to exercise, but become limited by breathlessness associated with hypoxia. Correcting hypoxia during exercise means that patients can try and maintain their physical and usual social engagements, which is important to their sense of worth and well-being.

Managing with liquid oxygen outside the home is fundamental to learning how it can help in self-managing strategies with advancing disease and activities of daily living within the home.

Developing self-management strategies with the aid of liquid oxygen can help to avoid emergency admissions to hospital.

Ambulatory oxygen is the single most important supportive treatment we can offer patients with progressive ILD. Increased levels of ambulatory oxygen can mean that patients with advanced disease can maintain a near-normal quality of life. It has been shown that patients can double their exercise performance with adequate supplementary ambulatory oxygen (Hicks et al, 2007).

Box 1 . Shuffle walk and six-minute walk test ·         A shuttle walk test is an exercise assessment test. The patient is instructed to walk at a predetermined pace, which increases with distance and time. Oxygen levels are monitored by pulse oximetry as patients are challenged to exercise to their limits. ·         A six-minute walk test with pulse oximetry is a self-paced walk test and is useful for titrating ambulatory oxygen.

Oxygen delivery devices
Oxygen devices that are useful for patients with ILD include the OxyArm device and high-flow nasal cannula (

Box 2

).

BOX 2 . NEW DEVICES FOR DELIVERY OF OXYGEN High-flow nasal cannula ·         Allows the patient to eat, sleep, talk and drink. ·         The cannula has a slightly wider tubing at the base of entry into the nasal prongs than the traditional nasal cannula. This reduces airway resistance in the nasal cavity that can cause nasal irritation, such as dryness and nose bleeds, when used at more than 4l/min. ·         The manufacturer of the high-flow nasal cannula claims that patients find it comfortable at flow rates of 15l/min. In my experience patients have tolerated 10l/min comfortably. OxyArm device ·         Delivers oxygen via a small cup, attached to a headpiece, strategically positioned in front of the nose and mouth. The oxygen is delivered in a ‘plume’ effect and inhaled on inspiration (Duck, 2006). ·         The device is well tolerated by patients who require a flow of oxygen greater than 4l/min from a nasal cannula. ·         Maintaining adequate oxygen saturations is dependent on the correct positioning of the ‘arm’ piece and flow rates should be individually titrated for the OxyArm using pulse oximetry. ·         The OxyArm is often acceptable to patients who are reluctant to use oxygen with nasal cannula or a mask in public. ·         We do not recommend the OxyArm for sleeping and, in my experience, it is not well tolerated by patients with advanced ILD lung disease who benefit more from the venturi oxygen mask system.

Breathlessness with advanced disease

In the latter stages of disease patients become breathless at rest and, when the resting oxygen saturations is less than 93%, they should have arterial blood oxygen levels checked to assess whether they meet the criteria for long-term oxygen therapy (LTOT).

Some patients experience breathlessness without significant hypoxia. These are often patients with no history of smoking and the breathlessness is associated with the small airways becoming stiff as the disease advances. This stiffness makes inspiration difficult, and the patient takes rapid inspiratory breaths and speaks in short sentences with intermittent little coughs.

Breathlessness associated with ‘stiff lungs’ but not extreme hypoxia can sometimes be relieved by increasing the total gas flow of oxygen using the venturi mask system. It is essential that hypoxia as well as breathlessness associated with the ’stiff lungs’ syndrome is corrected. The patient may need to use the 40% or 60% oxygen concentration venturi mask. In the community these masks will require three and four oxygen concentrators, linked together to deliver sufficient oxygen to generate the pressure capable of delivering the required total gas flow.

Strategies for goal setting and positive thinking

Miller (2000) suggests that individuals who have a physical disability have access to multiple resources including social support, psychological stability, knowledge, self-esteem, energy and hope. These should be developed in order to relieve the feelings of powerlessness and loss of control that patients with ILD experience.

Many patients reflect on the past and will grieve about ‘what might have been’. Feeling supported and having opportunities to talk with nurses who are empathetic, acknowledging and understanding can help them to realise what is most important in their lives.

Occasionally, individuals find it difficult to motivate themselves. Nurses are well placed to encourage patients to believe in themselves, by reminding them of who they are and how they once were (Miller, 2000).

All individuals have things they like to do. Nurses can help patients work out ways to do activities that are most important to them and hold some meaning in their lives. If individuals want to do something badly enough they can usually work out ways in which they are most likely to achieve it. I call this model of achievement ‘the four ps’:

·         Priming: Encourage and empower the patient, by asking them how they think they could do whatever it is that they would like to do.

·         Prioritising: Help them to understand that they will not be able to do all the things that they used to do and that now they need to decide on those that are most important.

·         Planning: Advise patients to think about how they are going to do something in light of their breathlessness and reduced exercise abilities.

·         Pacing: Help patients to understand that they should not have an unrealistic expectation of themselves, that they will have good and bad days and will be able to do more on some days compared with others.

Involving a spouse or close friend in this model of care can help maintain a patient’s motivation at home. If the carer is present during an initial interview with the patient, they will usually learn how to manage the despondent moods that are initially experienced by the patient.

Helping patients plan and work out ways to do things that are important to them can help them regain some control over their lives. It can help relieve the feelings of powerlessness that lead to the emotional distress and maladjustment that is often seen in chronic illness. Patients with ILD have travelled independently with supplementary oxygen on public transport, continue to play golf despite being oxygen dependent and even managed to continue singing in a band. Nurses should ask patients what they would like to continue doing and help them work out how to achieve these goals.

Peer support

Patients sometimes feel isolated and alone when dealing with advanced ILD. Support groups allow social comparison and exchange among members, encouraging reassurance about themselves and their reactions to their illness. Stewart et al (2001) note that support groups are most useful when they enhance role functioning, develop new skills, enable coping with stressful transition and ease social isolation.

Box 3

shows how such support groups might work and their benefits.

Box 3 . Starting a support group for patients with ILD The author started a support group for patients with ILD and their carers. The format was agreed by the group and the author acted as facilitator and organiser. It runs every two months and provides an opportunity for patients and carers to exchange ideas, share concerns, discuss problems and provide support to each other. An invited speaker talks about a topic requested by the group and it usually finishes with a relaxation/visualisation session run by a hypnotherapist. Some patients who attend enjoy ‘helping’ others and act as model experts on coping with the condition. Others gain strength from seeing how group members manage and ‘cope’. Simply meeting other people who share similar symptoms and problems helps patients realise that they are not alone.

Palliative care

If channels of communication with patients have been kept open and the health professionals involved have been honest about their prognosis from the beginning, patients often realise when they are approaching the end of their lives as breathlessness and oxygen requirements increase. Some patients will start a conversation about dying overtly, others may skirt around it and active listening skills will be required to understand what might be behind a question.

It is important that patients are assessed for physical aids to enable them to continue with activities of daily living. An occupational therapy and social review will help to identify individual physical and financial needs.

As the disease progresses, oxygen requirements will steadily increase, so that at the end stage patients will be oxygen dependent and probably use a high-flow nasal cannula, usually at 8–10 l/min, alternating with a high oxygen concentration venturi mask (typically 60%). A non-rebreathing mask, which can deliver 80–90% oxygen (Duck, 2006), may be used to complete activities of daily living around the home. A liquid oxygen domiciliary unit kept near to patients and used with a non-rebreathing mask can help them remain in their home.

Patients may describe having ‘panic attacks’ as well as difficulty getting up from a chair and going to the toilet because of breathlessness. These events are probably associated with extreme hypoxia related to minimal exertion and nurses must be aware that a review of management and treatment must be considered at this stage. Patients can be referred to the local palliative care teams at any time, depending on their coping strategies, but should definitely be referred at this stage in the disease trajectory. Referrals can also be made to the local Macmillan or district nursing services, which can review patients in their homes.

Opiates should be used when required to relieve the symptoms of distressing breathlessness even though they have a respiratory depressant effect. Palliative care teams can offer advise and support.

End-of-life care

As with all other terminal illnesses, end-of-life care should be managed with local palliative care services. Patients and their families need to be asked their ‘preferred place of death’ and these preferences should be documented.

Palliative care teams have the knowledge and expertise to relieve distressing symptoms and should work with ILD specialists to ensure that the most distressing symptom of breathlessness is minimised for the patient. The Liverpool Care Pathway (Ellershaw and Wilkinson, 2003) is a useful protocol that can be used to manage end-of-life care either in hospital or in the community.

High-flow oxygen circuit systems are useful for managing symptoms of extreme breathlessness by ensuring patients can have high flow rates and high concentrations of oxygen. They are available in hospital but not in the community and discussions should take place about the preferred place of death before a patient is started on high-flow oxygen systems in hospital. In my experience, it is difficult to remove high-flow oxygen from a patient.

It is imperative that this treatment is used in conjunction with a dying pathway and opiates, so that when maximum flow and oxygen concentrations are reached, breathlessness can be treated by pharmacological means. Midazolam and diamorphine subcutaneous pumps are sometimes needed to control breathlessness, particularly with younger patients who have IPF.

Conclusion

There are now recommendations for the way services for patients diagnosed with ILD are managed (Johnston et al, 2006) and nurses must learn to understand the specific needs of these patients. With better understanding, nurses can develop models of care that will improve patients’ quality of life and benefit those who find it difficult to cope with these lung disorders.

 

Chronic Obstructive Pulmonary Disease (COPD)

WHAT IS COPD?

Chronic obstructive pulmonary disease (COPD) is a condition that makes it difficult to move air into and out of a person’s lungs. Difficulty moving air in the lungs is called “airflow obstruction” or “airflow resistance,” and COPD is characterized by a progressively increasing airflow obstruction that cannot be fully reversed, although it can sometimes be temporarily improved by medications (Wise, 2007). In almost all cases, COPD has been caused by the long-term inhalation of pollutants, especially cigarette smoke (Punturieri et al., 2009).

The specific form that COPD takes can range along a spectrum. At one end of the spectrum, people get emphysema, the destruction of small respiratory units (alveoli and respiratory bronchioles) and the formation of large, useless air spaces in the lung. At the other end of the spectrum, people get chronic bronchitis, narrowed inflamed airways filled with mucus, accompanied by a chronic phlegmy cough. Many people with COPD have a mix of both emphysema and chronic bronchitis.

Regardless of its form, COPD causes dyspnea, i.e., difficulty breathing. The dyspnea of COPD feels like shortness of breath. Early on, shortness of breath occurs only during vigorous exercise. Over the years, however, the dyspnea begins to happen with mild exercise. Later, normal activities of living cause dyspnea. Finally, a person with COPD is short of breath even when sitting quietly. This relentless increase of dyspnea gradually limits a person’s activities, and at some point it becomes hard for a person with COPD to do anything but sit or lie down (Reilly et al., 2008).

Patients with COPD have little or no reserve capacity in their lungs, and they can be living on the verge of hypoxemia. Respiratory infections, increases in inhaled pollution, and the occurrence of other medical problems will further reduce their ability to absorb oxygen and to expel carbon dioxide. These problems can send COPD patients into hypoxemia. Such stresses are unavoidable, so COPD patients suffer repeated episodes of significantly worsened symptoms called “acute exacerbations.” Acute exacerbations resolve slowly over weeks or months even with medical treatment, and sometimes acute exacerbations must be managed in a hospital.

After COPD has become symptomatic, the disease is treated with bronchodilators, which can ease the patient’s dyspnea so that a wider range of activities remains tolerable. However, COPD follows a relentless downward course. Supplemental oxygen therapy can prolong some patients’ lives, and a few select patients can benefit temporarily from lung surgery. Acute exacerbations continue for all patients, and most patients eventually succumb to an acute exacerbation that cannot be reversed (Shapiro et al., 2005).

The Two Major Forms of COPD

The specific form that COPD takes varies from person to person. The predominant forms of COPD are emphysema (destruction of alveoli) and chronic bronchitis (inflammation of the conducting air tubules).

EMPHYSEMA

For some people, COPD causes significant destruction of the terminal airways and air sacs (alveoli); this form of COPD is called emphysema. In emphysema, the overall architecture of the lung is altered dramatically, and the lung becomes honeycombed with useless spaces. These air spaces are created when the walls of the small respiratory airways and their alveoli are torn, allowing neighboring airways and alveoli to merge. In the process, the surrounding capillaries become damaged and the new larger air spaces become useless for gas exchange. Besides reducing the lung area available for gas exchange, emphysema leads to hyperinflated lungs and obstructed airflow (Anthonisen, 2008).

CHRONIC BRONCHITIS

The other main type of COPD involves inflamed airways that become clogged with mucus. Patients with this variant of COPD develop a chronic cough that brings up sputum. This manifestation of COPD is a form of chronic bronchitis, which is defined as a persistent mucus-filled cough that has occurred frequently for at least two years and that is not caused by another disease such as an infection, cancer, or congestive heart failure. It is characterized by an increase in the number and the size of mucus glands in the airways of the lung.

Chronic bronchitis can occur without COPD. More than one-third of smokers have chronic bronchitis, but the disorder is only considered a form of COPD when there is also significant obstruction to airflow within the lungs (Kamanger, 2009).

Airflow Obstruction: The Essence of COPD

In the past, COPD patients with emphysema were said to have type A COPD and were sometimes called “pink puffers.” COPD patients with chronic bronchitis were said to have type B COPD and were sometimes called “blue bloaters.”

Although these names are still used, the division of COPD into two alternative types is too simple because many patients have a mix of emphysema and chronic bronchitis. Currently, the emphasis is on the common feature of all COPD patients: airflow obstruction.

Whether it appears as emphysema, as chronic bronchitis, or as a mixture of the two, COPD is characterized by chronic, worsening, and irreversible airflow obstruction.

Prevention

COPD can be almost entirely prevented by avoiding long-term inhalation of pollutants, mainly cigarette smoke. As they age, all people suffer a decline in their lung functions. Smokers who quit before developing symptoms of COPD can often reduce the decline in their lung functions to nearly normal levels within a few years of remaining smoke free (Lokke et al., 2007).

COPD INCIDENCE

COPD is the most common serious lung disease in the United States. Over the last few decades, there has been an increase in the percent of Americans with COPD. Currently, between 10 and 14 million adults in the United States have a diagnosis of COPD, and an equal number of Americans with COPD may still be undiagnosed. Among people with COPD, significantly more have the chronic bronchitis form than the emphysematous form (Shapiro et al., 2005; ALA, 2009).

Eighty to ninety percent of the people who get COPD have been long-time smokers (ALA, 2009). Therefore, the characteristics of the population of people with COPD are the same as the characteristics of the population of people who have been long-time smokers (Wise, 2007).

Age of Onset

A person’s smoking intensity is measured in pack-years. “One pack-year” means that a person has smoked approximately 1 pack (20 cigarettes) per day for 1 year; smoking 1/2 pack a day for 1 year is equivalent to 1/2 pack-year; and smoking 2 packs a day for 1 year is equivalent to 2 pack-years.

COPD is most common in older people because symptomatic COPD usually takes more than 20 pack-years of smoking to develop. The typical COPD patient has a smoking history of more than 40 pack-years. Today, 21% of adult Americans are smokers, and 1 of 5 high school students has smoked in the last month (CDC, 2009a).

In the United States, 1 of every 7 people between the ages of 55 and 64 has moderate COPD, and 1 of every 4 people older than 75 years has moderate COPD. This is the highest rate of COPD in history because the current generation of older adults has done a record-breaking amount of cigarette smoking. Although many elderly Americans have stopped smoking, even those who quit can develop symptoms of COPD and suffer a greater-than-normal decline in their breathing ability late in life (Hall & Ahmed, 2007).

Gender

More men than women have COPD. Among white Americans, for example, approximately 5% of all men have COPD, while approximately 2% of all women have the disease (Swadron & Mandavia, 2009). The difference between men and women reflects the historical tendency for men to have smoked more heavily than women.

The increased level of smoking by women over the past 30 years is causing the women’s death rate from COPD to rise. Today, more American women than men die from COPD (Anthonisen, 2008; ALA, 2009).

Women are twice as likely to be diagnosed with the chronic bronchitis form of COPD, while men are 1.25 times more likely to be diagnosed with the emphysematous form of COPD (ALA, 2009).

COPD Mortality by Gender: United States 2000–2005
In the twentieth century, COPD caused the deaths of more men than women. Since 2000, however, the statistics have reversed. Currently, COPD kills more women than men each year in the United States. (Source: Drawn from data in CDC, 2008.)

Race

The prevalence of COPD follows the history of the level of smoking in a population. In the United States, higher rates of COPD are found among those who have had the highest levels of smoking: white people, blue-collar workers, and people with less formal education. More Caucasians in the United States die from COPD than people of other races (Wise, 2007; CDC, 2009b).

Mortality Rates

COPD is the fourth leading cause of death in the United States. Between the years 2000 and 2004, there was an average of 120,000 deaths from COPD a year, a frequency of 42 deaths per 100,000 people. Approximately 1/2 of COPD patients die within 10 years of their initial diagnosis (ALA, 2009).

The ten leading causes of death in the U.S. in 2006. (Black column indicates the subset of all heart-related deaths caused specifically by CAD, coronary artery disease.) (Source: National Heart, Lung, and Blood Institute, 2008)

PATHOPHYSIOLOGY OF COPD

COPD and Lung Tissue

COPD is a reactive disease: it is a disease in which the body is turned against itself. In COPD, the body’s reaction to inhaled pollutants (mainly smoke) results in chronic inflammation of the bronchial tree. Inflammation is a natural protective reaction, but it is useless against air pollutants; instead of helping, the persistent inflammatory reactions damage the lungs.

NORMAL LUNGS

Before exploring the details of COPD’s inflammatory damage, here is a review of the structure and function of normal lungs.

Structure

The two lungs comprise millions of microscopic alveoli clustered at the ends of tiny air tubes. The lung tubes begin at the trachea and branch into successively narrower, shorter, and more numerous tubules. The central tubes are the bronchi and bronchioles; the most peripheral tubes are the respiratory bronchioles, which are lined with alveoli. It is through the walls of the alveoli that gases are exchanged between the inspired air and the blood in the surrounding capillaries.

Lung Anatomy
Figure A: Locations of the respiratory structures in the body. Figure B: Enlarged image of airways, alveoli, and their capillaries. Figure C: Location of gas exchange between the capillaries and alveoli. (Source: National Institutes of Health.)

The medium and large bronchi are wrapped with smooth muscle, which tightens to narrow the airways and relaxes to widen the airways. The walls of all the airways are lined by ciliated epithelial cells with interspersed secretory cells, which coat the inner walls of the airways with mucus. All the cilia of the epithelial cells beat in the direction of the trachea and throat, so mucus and trapped particles are continuously moved up and out of the lungs.

Healthy lungs are lightweight, soft, spongy, and elastic. Normally, the chest walls stretch the lungs and keep them expanded to 3 times their relaxed size. When the chest is surgically opened, however, the lungs recoil, as the innate elasticity of the lungs pulls them back to their resting size.

When an adult takes a full breath, the volume of air in the lungs is about 6 liters. During life, the lung is never completely airless: even after a complete exhalation, there are about 2.5 liters of air left (Albertine et al., 2005).

Function

Lungs are the organs through which oxygen is absorbed into and carbon dioxide is expelled from the bloodstream. These gas exchanges occur through the walls of the alveoli and the terminal respiratory airways, which make up the distal-most air spaces inside the lungs.

Maintaining healthy levels of blood gases are the lungs’ primary function, and the lungs contain an extensive capillary system to provide more than the necessary surface for gas exchange. The lung tissue itself is very thin and delicate, and most of the volume inside a normal lung is taken up by air. Since lung tissue is thin and air is light, most of the weight of a lung can be attributed to the blood circulating in it.

People with healthy lungs rarely use all the gas-exchange potential of their lungs. During the most strenuous activity, a healthy person will use only 60% to 70% of their maximal ventilatory capacity. Strenuous exercise does cause temporary dyspnea (shortness of breath), but the 30% to 40% ventilatory reserve quickly relieves the dyspnea of a healthy person after a short rest. Even the dyspnea caused by strenuous exercise in a healthy person is not as debilitating as the dyspnea in a person with severe COPD.

Healthy lungs function less efficiently as they age. As people get older, their chest walls stiffen and their respiratory muscles weaken. Both changes make breathing almost twice as much work for a 70-year-old as for a 20-year-old. The vital capacity (VC or FVC) and the amount of air that can be exhaled in a second (FEV1) gradually and progressively decline during a person’s lifetime. In a healthy person, none of these natural lung changes approaches the dramatic declines caused by COPD. The natural decline in lung function does, however, worsen the already compromised breathing of those elderly people who have COPD (Prendergast & Russo, 2006).

LUNGS WITH COPD

COPD slowly destroys the lung and makes it increasingly difficult for a patient to breathe. The most serious effect of COPD is a progressive obstruction of airflow.

In COPD, the airways leading into the alveoli become narrowed and less flexible, and they are often clogged with mucus. Eventually, many alveoli coalesce into larger, useless airspaces because the walls separating the alveoli become damaged or destroyed.

Development of COPD

Smoke inhalation, sometimes compounded by certain genetic factors, is the primary cause of COPD.

SMOKE: THE MAIN CAUSE

In the industrialized world, cigarette smoking is the main cause of COPD. In underdeveloped countries, smoke from plant products that are burned for indoor cooking or heating is as much a cause of COPD as is cigarette smoking (Shapiro et al., 2005). Other causes of or contributors to COPD include air pollution, second-hand smoke, and occupational exposure to dust and chemicals (ALA, 2009).

In the United States, more than a quarter of all people who have smoked for 25 years or more develop COPD, while another 10% to 20% of smokers have measurably decreased lung function for their age (Lokke et al., 2007). The longer and more intensely people smoke, the more likely they are to develop COPD.

Many long-term smokers eventually develop COPD, but the severity of the disease varies from person to person, even among heavy smokers. People living in the same environment and smoking the same amount can differ in their propensity for developing COPD. Two factors have been suggested as the basis for this difference: airway sensitivity and other specific genetic factors (Swadron & Mandavia, 2009).

Airway Sensitivity

People differ in their airway sensitivities, that is, in how readily their airways constrict when exposed to a variety of irritants such as pollen, dust, and chemicals. Asthma is the most common disease of people who have abnormally sensitive airways. People with COPD also tend to have sensitive and reactive airways. Although asthma and COPD are different diseases, smokers with asthma or with the tendency to develop asthma are more likely to develop COPD and are more likely to have COPD that worsens quickly (Reilly et al., 2008).

AAT Deficiency

Besides airway sensitivity, certain families carry other genetic factors that make them especially susceptible to developing COPD. One of these genetic propensities is alpha1-antitrypsin (AAT) deficiency. AAT is a protein that slows or stops the action of elastase; elastase is an inflammatory enzyme that chews up elastin, an extracellular protein used to build supporting tissues.

An inflammatory reaction in the lung, such as is caused by COPD, produces elastase. Normally, AAT circulating in the blood reduces the damage done by inflammatory elastase. However, a person with an AAT deficiency has little or no protection against inflammatory elastase. AAT deficiency allows the chronic inflammation caused by inhaled smoke to do considerable damage to the lungs; specifically, AAT deficiency fosters the destruction that causes emphysema.

Long-time smokers typically develop COPD when they are 50 to 60 years old. Smokers who are born with AAT deficiency, however, develop symptomatic COPD 10 to 20 years earlier, at an average age of 40 years. Elastase is so destructive that emphysema can even develop ionsmokers if they have a severe AAT deficiency. In the United States, AAT deficiency is the primary cause of only 1% to 2% of cases of COPD because fewer than 1 in 3,000 people are born with severe AAT deficiency (Fairman & Malhotra, 2009).

THE LUNG’S INFLAMMATORY RESPONSE TO SMOKING

Cigarette smoking causes COPD by inciting a chronic inflammatory response to the pollutants in the smoke. Over time, this persistent inflammation leads to destruction of lung tissue, accumulation of mucus, and thickening of small airways (Reilly et al., 2008).

In COPD, inflammation begins with the activation of local macrophages in the lung tissue; in fact, the gradual and progressive accumulation of macrophages throughout the lungs is a characteristic feature of COPD. Activated macrophages also attract neutrophils (polymorphonuclear leukocytes) from the bloodstream. The greater the number of neutrophils that invade the lung tissue, the faster lung function declines.

Enzymatic Destruction of Terminal Airways

When responding to irritants, both macrophages and neutrophils secrete proteases. Normally, the destructive action of proteases is held in check by a sufficient concentration of antiproteases, such as alpha1-antitrypsin (AAT), which circulate in the bloodstream and which are also released by neighboring epithelial cells. Antiproteases limit the damage that short-term inflammation inflicts on local tissues.

In COPD, there is an imbalance between proteases and antiproteases. Cigarette smoke is a strong and continuous stimulant of inflammation, and in the lungs of a chronic smoker proteases are constantly being released. Meanwhile, the normal protective function of the local antiproteases is hampered because smoke in the lungs leads to an accumulation of free radicals, superoxide anions, and hydrogen peroxide, all of which reduce the effectiveness of antiproteases.

The resulting imbalance of proteases and antiproteases frees at least some of the proteases to damage local tissues by degrading elastin and other structural molecules in the walls of the airways and the alveoli. At first, holes appear in the walls, and later the weakened walls are ripped apart by the force of breathing. Alveoli, which were formerly small chambers with capillary-coated walls, merge into large wall-less air spaces. When these spaces become >1 cm in diameter, they are called “bullae,” and a lung filled with bullae is said to be emphysematous.

The progressive destruction of lung tissue leads to the emphysematous form of COPD, which is characterized by:

• Destruction of alveoli
• Loss of lung elasticity
• Loss of lung supporting tissue
• The collapse of small airways

Fibrosis and the Narrowing of Small Airways

The hallmark of COPD is the increased resistance it causes for airflow in the lungs. In the chronic bronchitis form of COPD, much of the airflow obstruction comes from a progressive thickening and stiffening of the small airways.

The pathologic process underlying the narrowing of airways is fibrosis. With fibrosis, excess collagen accumulates in and around the airways, making them fatter and more rigid. Again, chronic inflammation is at the root of the problem. Extra collagen is secreted as a natural repair response to tissue damage. In COPD, the lung is continuously damaged by chronic inflammation, and this damage is met by continuing fibrosis in an attempt to fix the damaged tissue.

The chronic bronchitis form of COPD includes other changes in the small airways. These changes reduce airway volume still further. Specifically:

• Mucus cells proliferate and become larger; this generates excess mucus.

• The smooth muscle in the airway walls thickens.

• The airway walls bulge with invading inflammatory cells.

Functional Effects of COPD

REDUCED FEV1

When inhaling, a person stretches his or her chest and lung tissues. During exhalation, the elastic recoil of the chest and lungs is a major contributor to the force that pushes air out of the lungs.

In COPD, fibrosis reduces lung elasticity. Therefore, a patient with COPD needs to replace the lost elastic force with extra muscular effort. Moreover, the extra effort must be sustained for a longer time. The narrowed airways in lungs with COPD carry smaller volumes of air, and people with COPD take longer to empty their lungs.

The extent of airway obstruction can be quantified for COPD patients. One standard assessment measures the patient’s FEV1, the volume of air that can be pushed out of the lungs during the first second after a full inhalation. (See “Lung Function Tests” below.) A persistent, irreversible low FEV1 is the most characteristic objective finding in COPD.

HYPERINFLATION OF THE LUNGS

In COPD, the difficulty of breathing is worsened by excessively expanded (hyperinflated) lungs. Most people with COPD have some degree of emphysema, and part of each breath flows into nonfunctioning spaces where it is unusable. To get sufficient oxygen into their system, people with COPD need to take larger breaths.

People with COPD also take longer exhaling, and after taking a large breath, there is not enough time to fully exhale the air. Excess air remains in their lungs during each breathing cycle.

Wasted air space and excess residual air lead to hyperinflated lungs. Hyperinflated lungs change the shape of the chest and diaphragm, making the mechanics of breathing more difficult. With hyperinflated lungs, breathing can be exhausting.

HYPOXEMIA AND HYPERCAPNIA

Together, the obstructed airflow and the hyperinflated lungs of COPD make breathing hard work. When COPD is severe, just the breathing required for slow walking can use a third of the body’s total oxygen intake.

In COPD, patients may not have enough energy to pull in all the oxygen they need or to expel all the carbon dioxide they produce. Compounding the problem of maintaining adequate gas exchange, COPD destroys alveoli and the small capillaries that surround them, making each breath even less effective. As a result, people with severe COPD become chronically hypoxemic (too little circulating oxygen) and hypercapnic (too much circulating carbon dioxide). People with moderate COPD become hypoxemic during modest exercise, and as the disease worsens, they can become unable to exercise at all (Gold, 2005b).

PULMONARY HYPERTENSION

COPD also affects the blood vessels in the lung. COPD:

• Destroys lung capillaries
• Thickens the walls of small pulmonary blood vessels

• Constricts lung arteries due to chronic hypoxia and acidemia

• Constricts lung arteries due to the physical pressure of hyperinflated lungs

These changes increase the arterial resistance inside the lungs. More force is needed to push blood through the lungs, and the person develops pulmonary hypertension. In a normal adult lung, the mean pulmonary artery pressure is <16 mm Hg. In a lung with pulmonary hypertension, the mean pulmonary artery pressure is >20 mm Hg.

Pulmonary hypertension is especially hard on the right ventricle of the heart, which hypertrophies in response. As the strain on the right ventricle persists, the heart can fail. Heart failure secondary to lung problems is called cor pulmonale, and COPD is the leading cause of cor pulmonale (Weitzenblum & Chaouat, 2009).

DAMAGE BEYOND THE LUNGS

Patients with COPD have problems with organ systems other than their lungs. COPD leads to chronic hypoxemia, it drains energy reserves, and it is a source of chronic inflammation. These problems cause total body muscle weakness and weight loss.

Chronic hypoxemia strains the heart and reduces the ability of the heart’s ventricles to respond to the demands of exercise.

Chronic inflammation initiates a generalized prothrombotic condition in the circulation. This makes blood clots more likely to form, and patients with COPD are at increased risk for developing myocardial infarctions, strokes, deep-vein thromboses, and pulmonary emboli.

In addition, people with COPD have a high incidence of clinical depression. The depression is not only a psychological reaction to their increasingly restricted lifestyles. The metabolic and inflammatory changes of COPD make depression more likely biochemically.

DYSPNEA AND ITS SPIRALING EFFECTS

Over the years, patients with COPD become less and less able to do even modest exercise without developing dyspnea. Dyspnea, the feeling of breathlessness, is a common symptom. It comes from a mix of three sensations:

• The urge to breathe. This sensation is triggered by exercise or by the metabolic results of exercise—hypoxemia, hypercapnia, and metabolic acidosis.

• Difficulty breathing. This sensation is produced by excess chest movement and by unusual effort required by the muscles of respiration during breathing.

• Anxiety. This sensation can be caused by a fear of suffocating or by a memory of past discomfort with breathlessness. (The anxiety of dyspnea can also come from entirely different sources of stress that are happening at the time.) (Stulbarg & Adams, 2005)

Breathlessness is upsetting. It stops people from exercising, and it is the main reason that people with COPD limit their activities. Dyspnea on exercise gets worse as COPD progresses. Patients begin to spend all their time either sitting in a chair or lying in bed, and after months of inactivity, COPD patients become deconditioned as their muscles and circulatory system settle into sedentary states.

It is a spiraling problem: dyspnea causes lack of exercise, lack of exercise causes deconditioning, and deconditioning makes it harder to exercise. When they have become deconditioned, COPD patients get severe leg tiredness and leg discomfort when they try to exercise. Leg problems become yet another limiting factor when deconditioned people with COPD attempt to exercise.

To break this cycle, people with COPD must exercise. Pulmonary rehabilitation, which includes gradually increasing, supervised training regimens, can reverse muscle weakness, reduce leg pain, and increase exercise tolerance (see “Pulmonary Rehabilitation” below).

CLINICAL APPEARANCE OF STABLE COPD

The “Typical” COPD Patient

The “typical” patient with moderate to severe COPD is an elderly white male with a history of smoking at least one pack of cigarettes a day for more than 40 years. He complains of general tiredness and becomes short of breath when exercising. His legs bother him when walking, so he spends most of his time sitting. If you ask him to exhale quickly, it takes him an unnaturally long time.

Other aspects of the “typical” picture range along a spectrum:

• If this person is on the emphysematous end of the spectrum, he will tend to be thin and have a wide, barrel-shaped chest. He will always feel out of breath. When he coughs, he will not produce much sputum. On chest examination, this person’s breath sounds will be distant and relatively clear.

• If this person is on the chronic bronchitis end of the spectrum, he will tend to be of normal weight or overweight. He will cough frequently and will bring up sputum. On chest examination, his breath sounds will include rales (dry crackles), rhonchi (wet crackles), and wheezes. A COPD patient with chronic bronchitis will get more respiratory infections thaormal (Punturieri et al., 2009).

Chief Complaints

Patients with COPD usually present with the complaints of dyspnea and coughing.

DYSPNEA

Dyspnea during mild exercise is the most common reason that people with COPD first seek out a doctor. This dyspnea will have appeared gradually over a period of years. The dyspnea of COPD reflects at least two sensations:

• The urge to breathe. COPD patients have airway obstruction, and they cannot fully empty their lungs before they need to take another breath. The residual air, which keeps the lungs hyperinflated, dilutes the oxygen content of the newly inhaled air. Thus, these people feel hypoxemic.
• Difficulty breathing. COPD patients have hyperinflated lungs. Their chests remain overly expanded in the resting state (i.e., after exhaling). It is difficult for the respiratory muscles to expand their chest farther when attempting to take a new breath. Thus, these people put an unusual effort into breathing.

Sometimes, a COPD patient will come to the doctor reporting that a recent illness has triggered dyspnea. Illnesses, especially respiratory illnesses, worsen dyspnea. If the patient actually has COPD, a careful review of the history of the patient’s exercise tolerance usually turns up evidence of increasing dyspnea before the illness (Reilly et al., 2008).

COUGH

While dyspnea is the symptom that most often brings COPD patients to a doctor, coughing is the most common symptom found in patients with early COPD. The cough of COPD is usually worse in the mornings. Early in the disease, the cough produces only a small amount of colorless sputum (i.e., mucus and lung secretions that are expelled into the throat by coughing). Coughing typically begins earlier in the development of COPD than dyspnea, but unlike dyspnea, coughing does not limit the patient’s daily activities.

Coughing is stimulated by irritation of the bronchial tree. The sudden onset of new coughing is usually caused by irritation from a respiratory infection and is accompanied by fever, tachycardia, and tachypnea. This type of cough typically lasts less than 3 weeks, although in some people, coughs can hang on as long as 2 months after a respiratory illness. The coughing of COPD, however, occurs intermittently for years.

Medical History

HISTORY OF THE CHIEF COMPLAINT

As a rule, the health system first sees COPD patients when they are in their late forties to mid-fifties and with chief complaints of dyspnea and excessive coughing. In retrospect, their symptoms have been going on for at least a decade, with coughing having shown up first. At one time, the dyspnea had only beeoticed during heavy exertion, but eventually it began to interfere with even mild activities.

Many COPD patients will report that typical respiratory infections are now occurring more frequently, lasting longer, and seeming more severe: colds bring on breathlessness, wheezing, coughing, and sometimes the production of colored (yellow, green, or blood-tinged) sputum (Kamangar, 2009).

SMOKING

The key element in the history of a COPD patient is smoking. The first symptoms of COPD appear after about 20 pack-years of smoking, and the disease usually becomes clinically significant after 40 pack-years of smoking.

OTHER IMPORTANT INFORMATION

Besides asking about chronic diseases and heart conditions, a few other specific problems should be explicitly investigated when taking the history of a patient with COPD:

• Allergy history. Asthma and other allergic syndromes that affect the respiratory system can worsen (or mimic) COPD.

• Symptoms of GERD. Gastroesophageal reflux disease (GERD) can cause chronic cough and can sometimes be confused with chronic bronchitis.

• Symptoms of clinical depression. Depression is more common in people with chronic illnesses such as COPD (Anthonisen, 2008).

Physical Exam

A patient with mild COPD may have no signs of the disease when sitting quietly, and their physical exam may be normal. In contrast, the physical exam of a person with severe COPD can be diagnostic (Shapiro et al., 2005; Swadron & Mandavia, 2009).

GENERAL APPEARANCE

• Patients with emphysematous COPD are typically thin but barrel-chested. They tend to breathe through pursed lips, and they sit leaning forward in a “tripod position”; this posture widens the chest as much as possible by supporting the upper body on the elbows or the extended arms.

• 
  
  

The tripod position. Patient leans forward, resting on elbows or hands, in an effort to expand the chest and ease breathing. (Source: Jason M. McAlexander, MFA. © 2007, Wild Iris Medical Education.)

• Patients with chronic bronchitis COPD are typically of normal weight or overweight. They have a productive cough and may be cyanotic. At rest, their rate of respiration is high, often more than 20 breaths per minute. Patients may present as dull and irritable because their state of consciousness can be clouded by hypoxemia.

WEIGHT

The patient’s weight will influence the treatment recommendations. Obesity worsens the symptoms of COPD. On the other hand, many COPD patients—especially patients with the emphysematous form of COPD—are cachectic and underweight and have wasted muscles. In these cases, nutritional therapy will be important.

CHEST

A COPD patient with chronic bronchitis but little emphysema may have a normal-sized chest. Significant emphysema, however, leads to a wide, barrel-shaped chest with a flattened diaphragm. In a patient with emphysema, the chest remains perpetually in the position of inhalation. To take a new breath, emphysematous patients must expand their chests beyond the normal position of inhalation; this requires using accessory respiratory muscles of the shoulder, neck, and back.

LUNGS

The chest of an emphysematous patient is unusually resonant to percussion, and the breath sounds are distant. At the other end of the spectrum, the chest of a chronic bronchitis patient can have dull spots when percussed, and their lungs will be noisy with rales, rhonchi, and wheezing.

The common feature of all forms of COPD is airway obstruction, which worsens as the disease becomes more severe. A simple, direct measure of airway obstruction is the time it takes a patient to exhale an entire lungful of air. A normal person has a forced expiratory time (FET) of <3 seconds. An FET of >4 seconds suggests obstruction. An FET of >6 seconds indicates considerable airway obstruction, at the level of moderate-to-severe COPD.

HEART

COPD can injure the heart in two major ways:

• The chronic inflammatory state of COPD predisposes a person to develop coronary artery disease. Therefore, the history and physical examination of a patient with COPD should look for evidence of ischemic heart problems.

• COPD can cause pulmonary hypertension, which strains the right ventricle of the heart. Pulmonary hypertension will intensify the pulmonary component of the second heart sound. In addition, pulmonary hypertension can cause tricuspid valve insufficiency, which can be heard as a holosystolic murmur loudest along the left sternal border. When pulmonary hypertension causes right-sided heart failure (cor pulmonale), the patient will have jugular venous distension and edema of the legs and ankles.

Laboratory Findings

The key chemistry values in a person with COPD are the levels of blood gases—oxygen and carbon dioxide—and the pH of the blood.

BLOOD OXYGEN LEVELS

The severity of a patient’s COPD can be estimated by the degree that the blood gases deviate from normal. In the early stages of the disease, the amount of oxygen in arterial blood is usually withiormal limits. Oxygen concentration in arterial blood is measured as its partial pressure (PaO₂), and a normal oxygen partial pressure (or oxygen tension) is 80 to 100 mm Hg.

As COPD worsens, the PaO₂ can drop below 60 mm Hg; this level signals respiratory distress to the brain, and it strongly activates the respiratory centers. When the PaO₂ is below 60 mm Hg, a person hyperventilates in an attempt to reverse the hypoxemia by breathing in more air. Unfortunately, hyperventilation due to hypoxemia expels too much carbon dioxide from the bloodstream, and this causes respiratory alkalosis, a pH imbalance in the blood. Hypoxemia with alkalosis is found in the middle phase of the course of COPD.

In later stages of COPD, the patient does not have the energy to hyperventilate, so carbon dioxide builds up in the blood. Now the hypoxemia is accompanied by hypercapnia (excess blood carbon dioxide), and the patient develops chronic respiratory acidosis, an ominous sign. Hypoxemia with acidosis is found in the late phase of the course of COPD (Kamangar et al., 2009; Swadron & Mandavia, 2009).

Arterial Blood Gases

Early in the course of COPD, arterial blood gases do not need to be checked regularly. However, an early set of baselines values should be taken because they can be used as a comparison to evaluate the degree of change brought by an acute exacerbation.

Pulse Oximetry

Accurately measuring a person’s blood oxygen tension requires drawing arterial blood and testing it in a laboratory. Pulse oximetry is a quicker, noninvasive way to test blood oxygenation. A pulse oximeter has a small probe that can be clipped onto a patient’s finger or earlobe. Using measurements of transmitted light, the oximeter determines the percent of the patient’s hemoglobin that is saturated with oxygen.

Pulse oximeters are not as accurate as direct oxygen tension measurements from arterial blood gases, and the percent of hemoglobin saturation measured by an oximeter is not the same as a person’s PaO₂. Nonetheless, the two values are related. A person with a normal PaO₂ (80–100 mm Hg as determined from blood gases) will have a hemoglobin saturation ≥96% (as determined by pulse oximetry); a person with hypoxemia of 60 mm Hg will have a hemoglobin saturation of approximately 86%.

HEMATOCRIT

Routine blood analyses are not needed to manage most cases of COPD. Some people with severe COPD produce excess red blood cells (polycythemia) in response to their chronic hypoxia. This leads to hematocrit readings of >52% in men (normal is 43–52%) and >48% in women (normal is 37–48%).

ALPHA1-ANTITRYPSIN LEVELS

Patients who develop emphysema at an early age (under 40 years old) and nonsmokers of any age who develop emphysema are usually tested for their blood levels of the enzyme alpha1-antitrypsin (AAT). Deficiency of this enzyme makes a person unusually susceptible to emphysematous COPD. AAT deficiency is not common. When it is found, the patient and family should be educated about the genetics of this disease. It is sometimes possible to treat AAT deficiency with replacement doses of the enzyme.

Imaging Studies

COPD is a disease that is defined functionally: COPD causes progressively worsened airflow obstruction in the lungs. Therefore, breathing measurements are better diagnostic indicators of the disease than are static pictures of the lung. Nonetheless, imaging studies play a role in evaluating COPD patients.

The most commonly used images for evaluating and managing COPD are chest x-rays and computed tomography (CT) scans. Other modalities that are sometimes used include magnetic resonance imaging (MRI) and optical coherence tomography (OCT) (Coxson et al., 2009).

CHEST X-RAYS

Chest x-rays are used to rule out other causes of airway obstruction, such as mechanical obstruction, tumors, infections, effusions, or interstitial lung diseases. In acute exacerbations of COPD, chest x-rays are used to look for pneumothorax, pneumonia, and atelectasis (collapse of part of a lung) (Wise, 2007).

In its later phases, COPD produces a number of changes that can be seen in chest x-rays:

• When COPD includes significant emphysema, the chest is widened, the diaphragm is flattened, and the lung fields have fainter and fewer vascular markings. Emphysema can make the heart look long, narrow, and vertical, and the airspace behind the heart can be enlarged.

• When COPD includes significant chronic bronchitis, chest x-rays have a “dirty” look. There are more vascular markings and more nonspecific bronchial markings, and the walls of the bronchi look thicker thaormal when viewed end-on. Often, the heart appears enlarged (Swadron & Mandavia, 2009).

COMPUTED TOMOGRAPHY (CT) SCANS

CT scans are now the imaging technique of choice for lung evaluations (Coxson et al., 2009). CT scans, especially high-resolution scans, are better than chest x-rays at resolving the details of the lung abnormalities caused by COPD. Specifically, CT scans can help define which areas of a patient’s lungs are predominately emphysematous and which are predominately bronchiolitic. CT scans are also better than chest x-rays at identifying other diseases, such as tumors or infections, that may be complicating a patient’s COPD. Late in the disease, CT scans are used to evaluate COPD patients who are to be treated surgically.

CT SCANS AND RADIATION EXPOSURE

In developed countries, medical imaging is the source of most of the radiation to which the average person is exposed—other than the natural background radiation of the environment. Of the common medical imaging techniques, CT scans give the highest dose of radiation.

Cancers caused by radiation tend to take many years to develop, and radiation damage is often cumulative; therefore, CT scans pose the most danger to young people. “Based on radiation exposure issues, CT uses should be strongly constrained in children, used cautiously in young adults, and used prudently in older adults… . [I]n all cases, it is recommended that CT radiation dose be adjusted on the basis of the size of the patient to be as low as necessary to answer the clinical question posed” (Coxson et al., 2009).

Lung Function Tests

Pulmonary function tests are used to assess the extent of a patient’s airway obstruction. When COPD is diagnosed, baseline pulmonary function values should be recorded. Later tests can be used to measure the progression of the disease and to evaluate the effectiveness of treatments (Gold, 2005a). For COPD, the two general classes of breathing tests are (1) measurements of lung volumes, and (2) measurements of airflow rates and volumes.

LUNG VOLUME

In COPD, airway obstruction makes it difficult to fully empty the lungs. The air that remains keeps the lungs inflated even after a complete exhalation; this makes it more difficult for a patient to pull in sufficient air during the next breath. As a result, the total air volume contained by the lungs increases, although the effective volume of air—the amount of air actually breathed in and out—decreases.

The effective volume of air is called the vital capacity (VC); specifically, VC denotes the largest volume of air that can be exhaled after a full inhalation. Usually, this volume is measured by having a patient take as large a breath as possible and then exhale as quickly and forcefully as possible. With these testing instructions, the result is more accurately called the forced vital capacity (FVC) (Wanger & West, 2005).

AIRFLOW RATES

Besides limiting the effective volume of air in the lungs, COPD also slows the movement of air inside the lungs. This slowing can be measured directly. Measurements of the rate of air movement during breathing are called spirometric measurements; more specifically, spirometry measures the volume of air exhaled in a defined period of time (Miller et al., 2005).

A small, handheld spirometry device can be used for quick office or clinic tests. (Source, National Institutes of Health.)

Office spirometers come in a variety of forms. (Source: Dougherty, n.d.)

The most common spirometric measurement used for COPD is the one-second forced expiratory volume (FEV1). This is the maximum amount of air that a patient can breathe out in the first second of a forced exhalation after having taken a full breath.

Spirometry is helpful in evaluating the severity of airflow obstruction in patients with symptomatic COPD. On the other hand, spirometry does not add much to the evaluation of asymptomatic patients with COPD, because treatments (other than smoking cessation) are not typically begun until after a patient becomes symptomatic (Qaseem et al., 2007).

Ranking the Severity of COPD

People with normal lungs can expel most of the air in their lungs within 1 to 2 seconds. The amount of air forcefully exhaled in the first second (the FEV1) is about 3/4 of a healthy person’s vital capacity (the FVC).

If someone could exhale the lungs’ entire vital capacity in 1 second, their FEV1/FVC ratio would be 1.00. A normal person has an FEV1/FVC ration between 0.70 and 0.80; in other words, a person with normal lungs can exhale between 70% and 80% of their vital capacity in the first second. This ratio, FEV1/FVC (the percent of the vital capacity that can be exhaled in one second), declines as a person ages, but even elderly people will have FEV1/FVC >0.70 if their lungs are normal.

In COPD, airway obstruction restricts the rate of exhaling, and people with COPD cannot get a normal amount of air out of their lungs in one second. People with COPD have FEV1/FVC <0.70. When a person has an FEV1/FVC <0.70 and a history of  more than 20 pack-years of smoking, they can be given a presumptive diagnosis of COPD (Wagner & West, 2005).

A person who has a history of >20 pack-years of smoking and an FEV1/FVC <0.70 is almost certain to have COPD.

The four basic stages of COPD are mild, moderate, severe, and very severe. Patients with COPD have an abnormally low one-second exhaled percent of vital capacity (i.e., FEV1/FVC <0.70). COPD is staged by the degree to which the FEV1/FVC is below 0.70 when corrected for the person’s age, gender, and body build (Wise, 2007; Swadron & Mandavia, 2009).

STAGING OF COPD
Stage	Severity	FEV1/FVC
*Predicted FEV1 values adjusted for a person’s age, gender, height, and weight can be calculated from published equations (Pellegrino et al., 2005). Sources: Modified from Rabe et al., 2007; Ries, 2008; and Gold, 2009.
I	Mild	FEV1/FVC <0.70 and FEV1 ≥80% predicted value*
II	Moderate	FEV1/FVC <0.70 and 50% ≤ FEV1 <80% predicted value*
III	Severe	FEV1/FVC <0.70 and 30% ≤ FEV1 <50% predicted value*
IV	Very Severe	FEV1/FVC <0.70 and FEV1 <30% predicted value* or FEV1 <50% predicted value plus chronic respiratory or heart failure

Differential Diagnosis, including Asthma

Dyspnea and chronic cough are the presenting symptoms of a number of conditions other than COPD (Gonzales & Nadler, 2010). These conditions include pneumothorax, pulmonary emboli, pneumonia, lung infections, atelectasis, interstitial lung disease, sarcoidosis, effusions, lung masses, upper-airway or foreign-body obstructions, and congestive heart failure. Most of these conditions can be identified using imaging studies, such as chest x-rays, and clinical signs. Anemia or metabolic acidosis can also cause chronic dyspnea, and both of these can be identified by blood studies.

UNLIKELY TO HAVE COPD

As a quick diagnostic rule, a combination of three negative findings gives a high likelihood that the patient does not have COPD. The triad is:

• The patient has never smoked.
• The patient reports no wheezing.
• No wheezing is heard on physical examination.

Source: Qaseem et al., 2007.

Asthma, which is another common obstructive airway disease, is high on the list of differential diagnoses for conditions presenting with both dyspnea and cough. Asthma usually cannot be distinguished from COPD by chest x-rays, clinical signs, or blood studies.

Patients with asthma have hypersensitive airways that are always slightly inflamed, edematous, and filled with immune cells (characteristically, eosinophils). Certain inhaled allergens and a variety of stresses can trigger these primed immune cells, causing a flare of the disease—an asthmatic attack—that brings on edema, mucus, and narrowed airways. Like COPD, asthmatic attacks will obstruct airways and impede airflow; but unlike COPD, the airway restrictions of an asthmatic attack can be, at least in young people, quickly and almost entirely reversed by bronchodilators.

As people with asthma age, however, their airway obstruction sometimes becomes more fixed and less reversible. Clinically, these people’s disease begins to share more features with COPD, and the two diseases may be hard to distinguish. Determining which disease is present can be important for a patient’s treatment. For example, the dyspnea of asthmatic patients tends to improve markedly when the patient is given steroids, but the chronic dyspnea of most COPD patients does not improve following steroids (Jeffery, 2008).

Some useful distinctions between asthma and COPD include (Barnes, 2008):

• Asthma usually appears in people <30 years of age, while COPD typically appears in people >40 years of age.
• Asthmatic attacks are reversed quickly and completely by medications, while the symptoms of COPD are reversed only modestly and temporarily by medications.
• Asthma often runs in families, while COPD usually does not.
• Only 20% to 30% of asthmatic patients have been smokers, and those who smoke have less than a 20 pack-year history. On the other hand, 90% to 95% of COPD patients have been smokers, and most have greater than a 20 pack-year history of smoking.

LONG-TERM TREATMENT OF COPD

COPD is a life-long disease. It requires special medical treatment during acute exacerbations, and after the disease reaches the level called “moderate COPD,” it requires daily medications and permanent adjustments to a patient’s lifestyle. Gross (2008) and Gold (2009) are guides to the management of COPD.

The goals of long-term COPD treatments are:

• Slow the progression of the disease
• Ease the symptoms
• Increase the patient’s ability to be mobile and to do activities of daily living
• Prevent acute exacerbations

Education is important. All COPD patients should learn about their disease and should understand that smoking and air pollution will further damage their lungs. Patients need to make a special effort to avoid respiratory infections and to get yearly influenza vaccinations (Rich & McLaughlin, 2007; Shapiro et al., 2005).

At each stage of the disease, there are some characteristic medical therapies:

• Mild COPD is usually treated with short-acting bronchodilators, which are used as needed for dyspnea.
• Moderate COPD requires regular treatments with bronchodilators, sometimes with the addition of inhaled corticosteroids. At this stage, patients are often enrolled in a pulmonary rehabilitation program.
• Severe COPD typically requires two or more bronchodilators regularly. Inhaled corticosteroids are added to the regimen to prevent repeated acute exacerbations.
• Very severe COPD usually needs the addition of long-term oxygen therapy. Surgical treatments can be appropriate at this stage.

(Source: National Institutes of Health.)

Therapeutic Lifestyle Changes

Medications are the fundamental day-to-day tools for controlling the symptoms of COPD, but there are also five effective nonpharmaceutical techniques for treating COPD: patient education, smoking cessation, keeping airways clear, nutritional therapy, and pulmonary rehabilitation (Shapiro et al., 2005; Stulbarg & Adams, 2005).

PATIENT EDUCATION

Teach your COPD patients about their disease. Explain that the disease causes irreversible and progressive problems. Warn patients that they will have episodes in which the symptoms—difficulty breathing, wheezing, productive cough, and tiredness—get worse for days or even weeks.

Assure patients that you will help them by ordering medications that make breathing easier. Tell them there are several things that they themselves can do to slow the progression of the disease and to lessen the number of acute exacerbations. The most important thing is to stop smoking: although smoking has already damaged their lungs, continued smoking will increase the damage and will make their COPD worsen more quickly.

Explain to patients the importance of staying active. In addition, give them practical suggestions that will help them to cope with the inevitable limitations posed by COPD. For example, tell them:

• Don’t push yourself. Slow the speed at which you do things, and stop and rest when you are tired.
• Pace your activities and plan strenuous activities for times when you have the most energy. For example, you will feel best soon after you take your bronchodilator medicines. On the other hand, wait an hour after meals before you do activities.
• Sit on a chair or stool in the shower—don’t stand. Likewise, sit while you shave, comb your hair, and brush your teeth.
• Don’t use products that are hard on the lungs, such as hair sprays, spray-on deodorants, or strong perfumes.
• Use the exhaust fan in your kitchen to make it less likely that you will breathe smoke and cooking vapors.
• Wear slip-on shoes so you don’t have to bend over to tie laces.
• Make sure your occupation does not require more physical exercise than you can actually do. Consider setting smaller goals at work and allow more time to finish tasks.
• Find out how to get a daily air pollution report, and don’t go outside on days with moderate or severe pollution.
• Ask people not to smoke in your home or work area.

SMOKING CESSATION

In the United States, smoking is the major cause of COPD (CDC, 2009b). Americans start smoking in their teenage years: 90% of adult smokers began smoking before the age of 18. More than 1/4 of high school students and 1 in 10 middle school students smoke (Ranney et al., 2006).

Most patients with COPD have a long smoking history, and many will still be smoking when they are under medical care. Currently, the only way to change the course of COPD is for the patient to stop smoking. No matter how old they are and no matter how long they have been smoking, COPD patients will benefit from quitting. Workplace and public smoking bans help, and they have been shown to reduce both the use of tobacco and second-hand smoke exposure (Goodfellow & Waugh, 2009).

COPD is an insidious disease; it develops long before its effects cause people to seek medical care. The disease has become irreversibly destructive by the time that it is diagnosed, so treatment should be aggressive from the beginning. From day one, strongly urge your patients to stop smoking.

Quitting can be difficult. The nicotine in tobacco smoke is powerfully addictive. In addition, the rituals of smoking fill basic psychological needs. Therefore, when doctors merely tell patients to stop smoking, their patients succeed over the long-term only 5% of the time.

Smoking cessation programs significantly improve the odds. Long-term success rates of greater than 20% to 40% can be achieved by comprehensive programs that include behavioral therapy and medications.

Counseling Patients

Although simply advising smokers to quit is rarely effective, healthcare professionals often forget to offer help along with their advice (CDC, 2007). Many patients are not eager to quit smoking, so healthcare workers are encouraged to use a step-by-step approach, as outlined in the box below.

THE FIVE A’S FOR COUNSELING SMOKERS

Healthcare workers should use five steps—the five A’s—when counseling their patients who smoke. Taking even one step is constructive.

1. Ask. Ask the patient if they smoke.
2. Advise. Strongly advise quitting.
3. Assess. Ask the patient whether they are ready to quit.
4. Assist. Help to formulate a workable smoking cessation plan, including medications and regular interactions with a counselor.
5. Arrange. Take steps to put the plan into action: organize the necessary medications, counseling, and follow-up visits.

Begin by saying to your patients, “COPD cannot be cured, but if you continue smoking, the disease will worsen much more quickly. Have you thought about quitting smoking?” Regardless of the answer, follow it with the offer, “When you’re ready to stop smoking, I’ll be happy to work with you to set up as effective a program as possible.”

Successful smoking intervention programs begin by asking the patient to set a specific quitting date. The programs then maintain continued contact with the patient to provide medication, counseling, support, advice, and a modicum of social pressure. For specific recommendations, The report “Treating Tobacco Use and Dependence: Clinical Practice Guidelines” from the U.S. Surgeon General’s website offers specific recommendations (see “Resources” at the end of the course).

Pharmacologic Therapy

The pharmacologic aspect of smoking cessation programs attempts to ease the effects of nicotine withdrawal. Smokers who need their first cigarette within a half-hour of getting up in the morning are likely to be highly addicted to nicotine. When these people stop smoking, they become anxious, irritable, easily angered, easily tired, and depressed. Their sleep is disrupted. They have difficulty concentrating. These withdrawal effects are common during the first 2 to 3 weeks after quitting (Goodfellow & Waugh, 2009).

PHARMACOLOGIC THERAPY FOR SMOKING CESSATION

• Nicotine replacements. To lessen withdrawal symptoms, nicotine can be taken without smoking. Nicotine replacements are available as gum, lozenges, transdermal patches, inhalers, and nasal sprays. These should be used on a regular schedule and PRN (as needed for cigarette cravings) for about two weeks, and then the doses should be tapered. Nicotine patches are marketed as Habitrol and NicoDerm CQ; nicotine gum includes Nicorette.
• Antidepressants. One antidepressant, bupropion SR (sustained-release) or Zyban, is approved by the FDA to help patients for whom nicotine replacement therapy has not worked.
• Nicotine agonists. In 2006, varenicline (Chantix), a nicotine agonist, was approved by the FDA for anti-smoking therapy. Varenicline binds to nicotine receptors and prevents nicotine from activating the receptors while producing a smaller stimulant effect thaicotine.

Sources: Goodfellow & Waugh, 2009; Kamangar et al., 2009.

CHANTIX AND ZYBAN HAVE FDA WARNINGS

On July 1, 2009, the U.S. Food and Drug Administration (FDA) announced that it is requiring manufacturers to put a Boxed Warning on the prescribing information for the smoking cessation drugs Chantix (varenicline) and Zyban (bupropion). The warning will highlight the risk of serious mental health events including changes in behavior, depressed mood, hostility, and suicidal thoughts when taking these drugs.

“The risk of serious adverse events while taking these products must be weighed against the significant health benefits of quitting smoking,” says Janet Woodcock, M.D., director of FDA’s Center for Drug Evaluation and Research. “Smoking is the leading cause of preventable disease, disability, and death in the United States and we know these products are effective aids in helping people quit.”

Source: FDA, 2009.

KEEPING AIRWAYS CLEAR

COPD patients with significant chronic bronchitis must keep their airways clear. They should be encouraged to cough up sputum, and they should not get in the habit of using cough suppressants or sedatives. Postural drainage can help patients who cannot clear their secretions by coughing (Stulbarg & Adams, 2005).

Most people’s lungs secrete extra mucus in response to inhaled irritants. To avoid stimulating excess secretions, COPD patients need to stay out of smoke-filled rooms, and they should stay indoors during air pollution alerts. Home air conditioners and air filters are effective at keeping indoor air clear of particulates.

NUTRITIONAL THERAPY

The symptoms of COPD improve when overweight patients lose weight. Some COPD patients, however, have the opposite problem: they have become thin and malnourished. In part, this cachexia results from the high energy cost of breathing with COPD. In addition, the chronic inflammatory state underlying COPD tends to put the body’s metabolism into a catabolic state. To help them maintain a healthy body weight, thin COPD patients should be given dietary counseling that includes specific recommendations for meals that are nutritionally balanced and that contain sufficient calories to make up for the work of breathing (Stulbarg & Adams, 2005; Wise, 2007; ADA, 2009). (For more information, see “Resources” at the end of the course.)

PULMONARY REHABILITATION

Pulmonary rehabilitation is the term for a group of techniques used to improve patients’ conditioning and to ease their exercising difficulties. Pulmonary rehabilitation is done as outpatient therapy. Some rehabilitation programs continue for an extended time, but most run for a few weeks and then give patients individualized instructions for continuing at home. Education sessions are important parts of rehabilitation programs; in these sessions, patients and their families learn details about COPD and its treatment (Chesnutt et al., 2010).

2008 ACCP/AACVPR GUIDELINES FOR PULMONARY REHABILITATION

The updated American College of Chest Physicians/American Association of Cardiovascular and Pulmonary Rehabilitation guidelines on pulmonary rehabilitation (PR) for patients with COPD includes these key statements:

Appropriate PR lessens dyspnea and improves the quality of life

Required elements of PR include:

• Education on self-care and on prevention and management of acute exacerbations
• A regular, individually tailored exercise program
• Target muscles: muscles of ambulation and upper-body muscles (specific training of breathing muscles is not essential)
• Types of training:
• Both low- and high-intensity aerobic training (for lower limbs, high-intensity training is most beneficial)
• Endurance training of upper extremities
• Strength training to increase muscle mass and strength
• Length of program: minimum of 6–12 weeks
• Oxygen: supplemental oxygen should be used for patients with severe hypoxemia on exercise

Source: Ries, 2008.

Physical inactivity is the greatest source of the muscle weakness that plagues COPD patients. Although people with COPD have irreversible breathing difficulties, exercise training can significantly increase a patient’s strength and endurance and reduce their fatigability. These improvements result from increased muscle size (specifically, cross-sectional area), increased blood flow to muscles, increased oxidative enzyme capacity, and reduction of lactic acid production during exercise (Man et al., 2009).

Typical Programs

Pulmonary rehabilitation programs are tailored to the needs of each individual. Typically, the programs include graded aerobic exercises, such as regular sessions of walking or stationary bicycling three times weekly. The walking exercise program, for example, might begin with slow treadmill walking for only a few minutes. Gradually, the length and speed of the walking is increased over 4 to 6 weeks. The goal would be for the patient to walk for 20 to 30 minutes without needing to stop because of shortness of breath. At that point, the patient would be assigned a maintenance exercise program to be done at home.

Rehabilitation sessions also include:

• Exercises for reconditioning the upper body and exercises aimed at strengthening respiratory muscles.
• Breathing instruction that teaches patients how to slow their rate of breathing by pursing their lips. Also, instruction on how to rest the upper respiratory muscles by using abdominal breathing instead of chest breathing.

Comprehensive pulmonary rehabilitation improves the quality of patients’ lives. However, only one aspect of it—individually tailored exercise training—has been shown to reverse the muscle deconditioning caused by COPD (Man et al., 2009). Exercise training does not improve lung functioning, but it can reduce COPD symptoms and increase the amount of exercise that the patients can do without being stopped by dyspnea. It can also reduce the number of hospitalizations for acute exacerbations (Stulbarg & Adams, 2005).

Neuromuscular Stimulation

Some COPD patients have such poor lung function or such weak musculature that they cannot take part in the usual aerobic exercise training programs. Small studies suggest that electrical stimulation of the patients’ lower limbs can improve their muscle strength and exercise tolerance. This has worked even for bedridden patients. Neuromuscular stimulation routines are safe and inexpensive, and they can be done at home (Man et al., 2009).

Medications

The medicines currently available for COPD do not significantly change the progressive decline in lung function that is caused by the disease (Gross, 2008). Instead, drug therapy is used to reduce the extent to which dyspnea restricts a patient’s activities. Most COPD drugs work by keeping airways as wide open as possible (Hall & Ahmed, 2007). Medications (bronchodilators) used to reduce airflow obstruction are not typically given to asymptomatic COPD patients (Qaseem et al., 2009). Restrepo (2009) presents a detailed discussion of the management of stable COPD using inhaled medications.

COMMONLY PRESCRIBED COPD MEDICINES
Sources: Gold, 2009; Kamangar et al., 2009; and Restrepo, 2009.
Bronchodilators
Anticholinergic	Short-acting	ipratropium (Atrovent)
	Long-acting	tiotropium (Spiriva)
Beta-agonist	Short-acting	albuterol (Accuneb, ProAir, Proventil, Ventolin, VoSpire) fenoterol (Berotec) levalbuterol (Xopenex) metaproterenol ( Alupent) pirbuterol (Maxair) salbutamol (albuterol) terbutaline (Brethaire, Brethine)
	Long-acting	arformoterol (Brovana) formoterol (Oxis, Foradil) salmeterol (Serevent)
Premixed Combination Inhalers		ipratropium & albuterol (DuoNeb, Combivent) ipratropium & fenoterol (DuoVent)
Phosphodiesterase Inhibitor		theophylline (Aminophylline, Theo-24, Slo-bid, Theo-Dur)
Anti-Inflammatory Agents
Corticosteroids		beclomethasone (Beclovent, Qvar) budesonide (Pulmicort) fluticasone (Flovent) prednisone (Sterapred) triamcinolone (Azmacort)
Premixed Combination Inhalers (long-acting)		formoterol & budesonide (Symbicort) salmeterol & fluticasone (Advair)

BRONCHODILATORS

Bronchodilators are the workhorses of the COPD medications. Although spirometry shows that bronchodilators only modestly reduce airway obstruction in most COPD patients, regular doses of bronchodilators relieve dyspnea sufficiently for COPD patients to increase their levels of activity.

Bronchodilators work by relaxing the muscles in the walls of the lung’s airways; this widens the airways and allows air to move through them more easily. Short- and fast-acting bronchodilators are used as “rescue” medicines to relieve sudden bouts of dyspnea and coughing. Long-acting bronchodilators are used in daily, regularly scheduled drug regimens (Gross, 2008; Qaseem et al., 2009).

Airway muscles are smooth muscles, which are controlled by the autonomic nervous system. The autonomic nervous system has two divisions: parasympathetic and sympathetic. The major parasympathetic neurotransmitter is acetylcholine. The major sympathetic neurotransmitter is norepinephrine. Stimulation of the parasympathetic division of the autonomic nervous system tightens airway muscles and narrows the airways, while stimulation of the sympathetic division of the autonomic nervous system relaxes airway muscles and widens the airways. Bronchodilators are available to work at either parasympathetic receptors or sympathetic receptors.

All symptomatic patients are prescribed a short-acting bronchodilator that they can use to recover from a bout of suddenly worsening dyspnea (Restrepo, 2009). Either short-acting parasympathetic or short-acting sympathetic bronchodilators can be used as fast-relief medications.

Parasympathetic Bronchodilators

The parasympathetic bronchodilators are anticholinergic drugs, which relax airway muscles by blocking the effect of acetylcholine. The classic anticholinergic drug is atropine, but atropine has unwanted side effects because it gets through the blood-brain barrier and into the central nervous system (CNS). The anticholinergic drugs used for COPD do not get into the CNS, and their side effects are in the periphery, causing, for example, pupillary dilation, blurred vision, and dry mouth (Hall & Ahmed, 2007).

The most commonly prescribed short-acting anticholinergic bronchodilator is ipratropium (Atrovent). Ipratropium is relatively inexpensive and widely available. It is usually administered via a metered-dose inhaler (MDI), although there are other formulations. It can be used as a PRN medication; it takes effect in 15 to 30 minutes, has its peak action in 1 to 2 hours, and lasts 4 to 6 hours.

Traditionally, ipratropium has also been used as the main anticholinergic in long-term drug regimens. However, recent studies show that tiotropium (Spiriva) is a more effective drug (Qaseem et al., 2007; Gross, 2008). Tiotropium is a longer-acting anticholinergic bronchodilator. It is more expensive than ipratropium, but a typical dose lasts an entire day. Tiotropium is helpful when used alone and is even more effective in combination with a long-acting beta agonist (Gross, 2008). Tiotropium is inhaled as a powder via a dry powder inhaler (DPI).

Sympathetic Bronchodilators: Beta2 Adrenergic Agonists

One class of sympathetic bronchodilators, the beta2 agonists, acts by mimicking the effect of norepinephrine on airway muscles. Beta2 agonists stimulate the beta2-adrenergic neuroreceptors and cause smooth muscles to relax; this widens airways. Muscle tremors and heart palpitations are the most common side effects of beta2 agonists, but when the medicines are inhaled (as opposed to taken in oral formulations), the side effects are usually mild.

WHAT ARE BETA2 ADRENERGIC AGONISTS?

When the sympathetic nervous system is activated, we get a “fight or flight” response—the heart beats faster and harder, the lungs’ airways widen, sugar is released into the bloodstream, and peripheral blood vessels narrow, sending more blood to central organs and muscles. To produce this response, epinephrine and norepinephrine are secreted by sympathetic nerve endings, and the neurotransmitters then activate adrenergic receptors.

Adrenergic agonists are chemicals like epinephrine and norepinephrine that can cause sympathetic responses. There are two main types of adrenergic receptors, alpha and beta. Lung airways have mainly beta2 receptors, while the heart has mainly beta1 receptors. To limit the side effects on other organs, COPD is treated using beta2 agonists, such as albuterol.

Source: Westfall & Westfall, 2006.

The short-acting beta2 agonists, which include albuterol (Accuneb, ProAir, Proventil, and Ventolin) and metaproterenol (Alupent), are the most commonly prescribed sympathetic bronchodilators. These drugs are usually administered via either MDI or DPI. Short-acting beta2 agonists such as albuterol and metaproterenol take effect in 5 to 15 minutes and last for 2 to 4 hours.

Short-acting beta2 agonists are used as rescue medicines when a patient needs immediate relief from sudden episodes of increased dyspnea. A short-acting beta2 agonist can also be added to an anticholinergic drug as part of a regular drug regimen.

The long-acting beta2 agonist bronchodilators include formoterol (Foradil) and salmeterol (Serevent). These drugs are more expensive than albuterol or metaproterenol, but a typical dose lasts for at least 12 hours. Inhalation is the recommended route for administering the long-acting beta2 agonists.

Sympathetic Bronchodilators: Phosphodiesterase Inhibitors

Another class of sympathetic bronchodilators, the phosphodiesterase inhibitors, acts by stimulating the release of norepinephrine, which then relaxes smooth muscles in the airways of the lung. For COPD, the phosphodiesterase inhibitor theophylline (Elixophyllin, Theo-Dur) is used to dilate airways, stimulate the respiratory centers of the brain, and improve the function of respiratory muscles.

Theophylline is usually used as a systemic drug. It is taken orally and side effects are common; among them are sleeplessness and gastrointestinal upset, including nausea and vomiting. Occasionally, theophylline causes serious cardiac arrhythmias or seizures, especially when liver disease has decreased the body’s ability to metabolize the drug. Older people are more likely to get theophylline toxicity. Two newer phosphodiesterase inhibitors, cilomilast (Ariflo) and roflumilast (Daxas), appear to be safer than theophylline.

Bronchodilator Regimens

Patients vary in their response to bronchodilators, so the most effective drug regimens are those that have been individually tailored. Finding the right drug or set of drugs is empirical. When drug combinations are being tried, it is best to introduce the drugs one at a time to learn the patient’s response to that drug only.

For patients with with chronic stable COPD, short-acting bronchodilators will eventually be insufficient to control their symptoms. Currently, the long-acting anticholinergic drug tiotropium is usually recommended as the first drug to try in a regular daily medication regimen. It is taken once daily, it does not have the side effects of sympathetic drugs, and it is generally more effective than the comparable twice-daily beta agonists. Concurrently, a short-acting beta2 agonist, such as albuterol, is usually prescribed as a rescue drug.

If this initial regimen is insufficient, the short-acting beta2 agonist is added to the regularly schedule drug regimen rather than being used only when needed. The combination of ipratropium and albuterol is available commercially (DuoNeb) as an inhalant.

As COPD progresses, most patients do better with combinations of two or three bronchodilators. In American and Western European medicine, theophylline (or another phosphodiesterase inhibitor) is usually the last bronchodilator to be added.

If they are to be followed faithfully, drug regimens must be realistic. Bronchodilator therapy with 2 or 3 drugs is expensive. In addition, using inhalers can be physically difficult for some people, especially the elderly, and physicians may need to modify an optimal pharmacologic therapy to make it practical for a particular patient.

CORTICOSTEROIDS

Corticosteroids are two-edged swords. On the one hand, they are effective anti-inflammatory medicines and can be used to tone down the inflammatory response that underlies or exacerbates many diseases. On the other hand, the continued use of corticosteroids causes Cushing’s syndrome, glaucoma, cataracts, myopathy, ulcers, osteoporosis, hyperglycemia, poor wound healing, and the inability to overcome infections.

In stable COPD, the problems that come from the long-term use of oral (i.e., systemic) corticosteroids usually outweigh the drugs’ benefits. Inhaled steroids—such as fluticasone (Flovent), beclomethasone (Beclovent, Beconase), and budesonide (Pulmicort Turbuhaler)—have fewer adverse effects than oral formulations, and approximately 10% of people with COPD find that regularly inhaled steroids reduce their airway obstruction. For this population of patients, inhaled steroids can be a useful addition to the other regularly scheduled bronchodilators.

The regular use of inhaled corticosteroids is usually reserved for patients with severe COPD. In people with severe COPD, steroids will reduce the number of exacerbations and the rate of mortality. For people with severe COPD, inhaled corticosteroids are typically combined with a long-acting beta2 agonist in a regular treatment regimen (Hall & Ahmed, 2007). Regular use of inhaled corticosteroids for COPD does, however, increase a patient’s risk of developing pneumonia (Restrepo, 2009).

The usefulness of corticosteroid therapy cannot be predicted in advance for any one patient. At the moment, spirometrically testing a patient’s response to the medication is the only way to identify in advance those COPD patients who will be helped by adding inhaled steroids to their regular regimen of bronchodilators.

OTHER MEDICATIONS

COPD is a continually worsening condition. Researchers have been searching for additional medications that can slow the inevitable decrease in lung function suffered by COPD patients. Examples of ongoing investigations include:

• Studies show that mucolytic agents (e.g., carbocisteine) appear to be effective adjuncts to long-term drug regimens in place of inhaled corticosteroids (Hurst & Wedzicha, 2009).
• In some studies, the addition of erythromycin to the long-term drug regimen have reduced the frequency of acute exacerbations (Hurst & Wedzicha, 2009).
• Fast-onset, ultra-long-acting (>24 hrs.) inhaled beta2 agonists, such as indacaterol and carmoterol, are now in phase III clinical testing (Restrepo, 2009).
• Initial studies suggest that the regular oral administration of statins might lessen mortality and morbidity of COPD patients (Dobler et al., 2009).
• Oral n-acetylcysteine, which is used as an antidote for acetaminophen overdose, may prevent or reduce the frequency of acute exacerbations of COPD (Millea, 2009).

VACCINATIONS

As protection against serious respiratory illnesses, people with COPD should get an influenza vaccination each year. During outbreaks of strains of flu not covered by the annual vaccination, people with COPD should probably receive prophylactic antiviral treatment such as amantadine (Symmetrel), rimantadine (Flumadine), oseltamivir (Tamiflu), or zanamivir (Relenza). Pneumococcal vaccinations are also recommended (Hall & Ahmed, 2007).

Oxygen Therapy

Supplemental oxygen improves levels of blood oxygenation and reduces the rate at which patients need to breathe. For people with COPD, supplemental oxygen also slows the rate at which muscles fatigue. These effects make it easier for patients to breathe more deeply and to exercise for longer periods. For patients with advanced COPD, supplemental oxygen reduces mortality rates.

Oxygen therapy is expensive and involves special equipment. Therefore, when people with COPD can maintain a blood oxygenation level of PaO₂ >55–60 mm Hg (an oxygenation saturation of more than ~89%), supplemental oxygen therapy is not routinely prescribed (Rich & McLaughlin, 2007; Chesnutt et al., 2010).

CONTINUOUS OXYGEN

Eventually, however, supplemental oxygen will be necessary. For some COPD patients, oxygen is needed to participate in regular exercise programs. For other patients, oxygen is needed to carry out the typical activities of daily living.

If they live long enough, all patients with COPD lose sufficient lung function that they will be hypoxemic at rest, even on an optimal regimen of regular bronchodilator treatments. For these people, continuous oxygen therapy can prolong their lives and reduce hospitalizations. When a patient’s blood PaO₂ <55–60 mm Hg (an oxygen saturation of less than ~85–89%) at rest, it is recommended that supplemental oxygen should be given continuously—which means, in practical terms, more than 19 hours per day (Qaseem et al., 2007).

Low-flow (2–3 liter/min) oxygen inhaled through nasal cannulas is usually sufficient to raise a COPD patient’s blood PaO₂ to 65–80 mm Hg (an oxygen saturation of 89–94%). In addition to increasing survival rates by about 50%, this level of supplemental oxygen lowers the person’s hematocrit toward a normal range, makes sleep easier, and improves exercise tolerance.

Home oxygen therapy is also recommended for COPD patients with heart failure, pulmonary hypertension, or erythrocytosis (i.e., a hematocrit >56%), even when their PaO₂ is >55 mm Hg. Some patients who maintain a higher level of arterial oxygen during the day drop to a PaO₂ <55 mm Hg when they sleep; for people whose hemoglobin desaturates at night, nocturnal oxygen therapy is helpful.

HOME OXYGEN DELIVERY SYSTEMS

Home oxygen can be purchased as liquid O₂ or as compressed gas; it can also be “manufactured” directly by home oxygen concentrators. The cost of continuous home oxygen therapy can be $500 or more per month; in many cases, Medicare will cover 80% of the cost.

Patients usually breathe supplemental oxygen via a continuous flow nasal cannula. Devices that “conserve oxygen”—reservoir cannulas, demand pulse delivery devices, transtracheal oxygen delivery—are especially efficient because they provide all the supplemental oxygen early in each inhalation. Some patients who have trouble keeping low blood-levels of carbon dioxide can be fitted with face masks from machines that deliver supplemental oxygen at continuous positive-pressure; these systems provide noninvasive positive-pressure ventilation (NIPPV) (Kamangar et al., 2009).

A home system is usually adjusted to deliver 2 to 3 liters of oxygen per minute, and in most cases this will maintain a patient’s oxygen saturation at >89%. For patients who continue to have dyspnea at night, the flow rate is raised by 1 liter/min during sleep.

One goal of oxygen therapy is to allow patients to remain active. Inside the home, long tubes can connect the nasal cannulas to stationary oxygen delivery units so patients that can move around. For more freedom and to go outdoors, patients can carry portable tanks of compressed oxygen or liquid oxygen.

HAZARDS

• Medical. There is a small risk that too high a concentration of inspired oxygen will suppress the respiratory drive of COPD patients. Long-term low-flow oxygen therapy is probably safest when the amount of oxygen delivered gives the patient a PaO₂ of 60–65 mm Hg, which is toward the low end of the acceptable range of inspired oxygen (Kamangar et al., 2009).
• Physical. Concentrated oxygen is flammable and poses a fire hazard. Patients and their families cannot smoke or use open flames near the oxygen equipment.

AIR TRAVEL

Commercial planes maintain an internal air pressure equivalent to 5,000–8,000 feet above sea level. For those COPD patients whose resting arterial blood oxygen concentration is low (PaO₂ <69 mm Hg) even at sea level, the cabin concentration of oxygen will usually not be high enough to avoid hypoxemia. Airlines can provide supplemental oxygen, and some airlines will allow patients to bring small oxygen delivery systems with them, although patients must make arrangements with the airline in advance.

Surgery for COPD

Surgery is risky in people with severe COPD. Postoperatively, many normal patients temporarily have reduced lung volumes, rapid shallow breathing, and an impaired ability to take in oxygen and expel carbon dioxide. These routine postoperative problems add additional stress to the already compromised respiratory systems of patients with COPD. One result is that patients with severe COPD develop postoperative pneumonia 13 times more often than patients with normal lung function. (Preoperative antibiotics can reduce the high rate of postoperative pneumonia.)

Nonetheless, the lack of alternative treatments for severe COPD has led to the development of three surgical procedures that attempt to improve and prolong the lives of COPD patients. The techniques are lung transplantation, lung volume reduction surgery, and bullectomy (Gold, 2005a).

LUNG TRANSPLANTATION

People with severe COPD are the most common recipients of lung transplants. Candidates for lung transplantation are patients with severe COPD who have exhausted medical therapies and have life expectancies of ≤2 years. (The BODE Index is usually used to estimate a COPD patient’s life expectancy [Kamangar et al., 2009]. See box.) Typically, patients should also be younger than 65 years. Three-quarters of COPD patients who receive lung transplants live for ≥2 years after the operation, and many of the survivors have substantially improved abilities to exercise.

BODE INDEX

The BODE Index uses four measurements to assign COPD patients to one of four groups, each with a different estimated survival rate. The measurements are:

1. Body mass index (BMI)
2. Degree of airflow obstruction (FEV1)
3. Amount of dyspnea (MMRC dyspnea scale)
4. Exercise capacity (distance walked in 6 minutes)

Four years after a BODE assessment is made, estimated survival rates are approximately:

• 82% for group 1
• 68% for group 2
• 57% for group 3
• 18% for group 4

Source: Celli et al., 2004.

LUNG VOLUME REDUCTION

As noted earlier, the lungs of an emphysematous patient become hyperinflated with air spaces that contribute little to gas exchange. The widened chest caused by hyperinflated lungs is difficult for the patient to expand farther when attempting to inhale. By removing lung tissue that contains dead air space, surgery can sometimes reduce the patient’s work of breathing.

In lung volume reduction surgery, 20% to 30% of the lung volume is removed from both sides of the chest. As a result, survivors can usually exercise more than they could before the surgery. Those patients who have mainly upper-lung emphysema also have an increased lifespan after this surgery. For other COPD patients, however, longevity is not increased and it may even be shortened.

The major postoperative complication of lung volume reduction surgery is continuing air leakage from the lungs into the chest. Operative mortality rates are from 4% to 10% in hospitals providing the procedure.

BULLECTOMY

In some cases, individual large empty air spaces (bullae) can be surgically removed. Typical bullae in a patient with emphysema are a few centimeters in diameter. Occasionally, however, bullae can be huge, taking up as much as a third of the chest space. These giant bullae squeeze the healthier lung tissue and compress the adjacent blood vessels. By removing giant bullae, the remaining lung tissue can reexpand, and some of the circulation will be restored. As with lung volume reduction surgery, a major postsurgical complication of bullectomy is persistent air leakage.

ACUTE EXACERBATION OF COPD

Patients with COPD have little or no ventilatory reserve, and a further compromise of their respiratory system can send them into hypoxemia. The normal wear and tear of daily life puts respiratory compromises in everyone’s path periodically. People with COPD respond poorly to these respiratory problems and often experience an increase in dyspnea, cough, and sputum production. Such episodes of suddenly worsening symptoms are called “acute exacerbations” (Hurst & Wedzicha, 2009).

Causes of Acute Exacerbations

Acute exacerbations of COPD can be brought on by a variety of factors. Infections, especially respiratory infections from colds to pneumonias, are common triggers. Acute exacerbations occur more often in the winter, the season with the most viral infections. Increases in air pollution can also trigger an acute exacerbation.

Acute exacerbations can be triggered by other medical conditions, especially when these conditions impinge on the cardiovascular or respiratory systems. Pneumothorax, pulmonary emboli, congestive heart failure, heart arrhythmias, chest trauma, lung atelectasis, and pleural effusions will all worsen a patient’s COPD.

Inappropriate drugs can also trigger an acute exacerbation of COPD. For example, beta-blockers and cholinergic drugs prescribed for other reasons can produce bronchospasms, or sedatives can reduce a person’s respiratory drive, which may bring on hypoxemia in COPD patients (Braithwaite & Perina, 2009).

At the same time, however, many acute exacerbations cannot be easily explained. No cause can be identified in approximately one-third of the episodes of suddenly worsening COPD (Punturieri et al., 2009).

Signs and Symptoms of an Acute Exacerbation

During an acute exacerbation, patients become more breathless than usual. They have chest tightness, they may begin to wheeze or to cough, and they can find it difficult to talk. In addition, their airways can become clogged with sputum, which may be yellowish or greenish and filled with white cells.

A sudden decrease in the ability to breath efficiently makes patients tachycardic and sweaty, and their percent of oxygenated hemoglobin (measured by pulse oximetry) decreases. In serious cases, patients become hypercapnic because they cannot get rid of sufficient carbon dioxide, making them acidotic and lethargic.

Treatment of an Acute Exacerbation

A patient’s regularly scheduled medications will not reverse an acute exacerbation; instead, extra “rescue” medicines—typically, short-acting bronchodilators—are needed. To prevent ventilatory decompensation from worsening, further medical assistance, including hospitalization, can be needed to treat an acute exacerbation and its cause.

Unlike attacks of asthma, which can usually be reversed quickly, acute exacerbations of COPD improve slowly even when the patient gets prompt medical help. On average, it will take a week for a person to recover from an exacerbation of COPD, and recovery from 1 out of 4 acute exacerbations takes more than a month. For patients with severe COPD, an acute exacerbation can even be fatal.

RESCUE MEDICATIONS

As a first step in counteracting the sudden worsening of their lung functions, patients are usually advised to take a predetermined “rescue dose” of a short-acting bronchodilator. Typically, it is a beta2 agonist (albuterol, pirbuterol, or terbutaline), ipratropium, or the combination of albuterol and ipratropium. Patients should be advised to always keep their quick relief inhaler with them (Hurst & Wedzicha, 2009).

EMERGENCY EVALUATION

When a sudden worsening of the ability to breathe is not improved by rescue therapy, the patient needs to be seen quickly by a doctor. Besides COPD, the patient could be experiencing a medical emergency such as pneumothorax, pulmonary embolism, anaphylaxis, airway obstruction, or myocardial infarction.

Anyone with the sudden onset of severe dyspnea should be evaluated as a medical emergency. First, it must be ascertained that the patient has a clear airway. The patient should then be checked for trauma, bleeding, shock, cardiac failure, and the inability to move air autonomously into and out of the lungs. Any of these problems require immediate treatment.

At the same time, an intravenous (IV) line should be established and a cardiac monitor connected. If the patient’s pulse oximetry shows an oxygen saturation of <98%, supplemental oxygen should be given. Blood chemistries, blood gases, and chest x-rays (both PA and lateral) should be obtained. The cardiac status should be assessed with an ECG. The possibility of a pulmonary embolus should always be considered when there is a sudden increase in dyspnea and hypoxia (Gold, 2009).

The patient should be medically stabilized. Patients with a serious instability or decompensation are admitted to an intensive care unit and the workup continues there. Mental confusion, cyanosis, lethargy, extreme muscle fatigue, worsening hypoxemia, respiratory acidosis, or the need for mechanical ventilation are all conditions best treated in intensive care (Gold, 2009).

MEDICAL MANAGEMENT

For patients experiencing an acute exacerbation of COPD, the immediate goals are to maintain an adequate level of blood oxygen and an appropriate blood pH in the patient.

For some COPD patients, their exacerbation will be sufficiently mild that bronchodilators, steroids, and oxygen will lead to a rapid improvement. If no treatable trigger is found for this episode, the patients can often be sent home and followed outside the hospital.

Other patients’ lung functioning will have deteriorated sufficiently that the persoeeds to be supported in a hospital. COPD leads to chronic respiratory failure, and acute exacerbations can lead to the superposition of acute respiratory failure. The result has been called “acute-on-chronic respiratory failure.” In acute-on-chronic respiratory failure, patients have increasing dyspnea and may eventually develop an altered mental state or even respiratory arrest. Acute-on-chronic respiratory failure typically produces an acidosis, with pH <7.35 (normal is pH = 7.38–7.44) (Goldring & Wedzicha, 2008).

For acute-on-chronic respiratory failure patients, hospital therapy includes bronchodilator treatments, systemic steroids, controlled oxygen, and often, intravenous antibiotics. Wheecessary, steps must be taken to maintain the patient’s ventilation and circulation. Supplemental oxygen is given to keep blood oxygenation levels of 88–92%. Meanwhile, attempts are made to identify and reverse the precipitating factors; if a specific infection has not been identified, antibiotics are sometimes given prophylactically (Goldring & Wedzicha, 2008).

ANTIBIOTICS FOR ACUTE EXACERBATIONS OF COPD

Respiratory infections are frequent causes of acute exacerbations of COPD. When an acute exacerbation includes signs of infection (e.g., fever, elevated white blood-cell count, purulent sputum, or a suggestive chest x-ray), the empirical administration of antibiotics is usually recommended. Likely microbes include Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Pseudomonas aeruginosa, and appropriate antibiotics include:

• cefuroxime (Zinacef)
• azithromycin (Zithromax)
• clarithromycin (Biaxin)

Source: Kamangar et al., 2009.

The patient’s blood gases and blood chemistries should be watched, and supplemental oxygen given to maintain the PaO₂ >60 mm Hg (oxygen saturation >~89%). In severe cases, noninvasive positive pressure mechanical ventilation (also called noninvasive ventilatory support or NIVS) with a facemask or nasal cannulas will often improve gas exchange without having to intubate the patient. Noninvasive ventilation leads to fewer secondary pneumonias and is easier to wean than endotracheal intubation (Goldring & Wedzicha, 2008).

Recovery from an acute exacerbation can take weeks to months. For those COPD patients who need to be hospitalized during an acute exacerbation, there is a 10% mortality rate.

END-STAGE CARE

The American Thoracic Society recommends that COPD patients be given a balance of palliative and restorative care from the very outset of the patient’s symptoms (Lanken et al., 2008). This means that maintaining and, when possible, improving a patient’s quality of life should always be a prime motivator of therapy.

Early palliative care also means that patients and their families should be encouraged to consider end-of-life options early in the disease process, before the patient becomes mentally compromised or the family becomes emotionally worn out. Decisions that patients and their families will face include whether to participate in drug trials, what type of ventilation to use and for how long, whether to consider lung transplantation, whether to take advantage of hospice, and what type of end-of-life palliation is desired (Lanken et al., 2008).

Severe difficulty in breathing is an uncomfortable and upsetting problem to both patients and their families. Near the end of a COPD patient’s life, dyspnea must be eased (Lanken et al., 2008).

Although patients with chronic lung disease are normally encouraged to exercise to maintain their state of fitness, there comes a time when a different approach is required and the focus shifts from prolongation of life to relief of distress. When dyspnea with exertion is extreme, it may be more appropriate to restrict activity and to focus on modifying treatments such as oxygen, opiates, and anxiolytics. Palliative treatment may include partial ventilatory support or, under rare circumstances, a tracheostomy with mechanical ventilation. Such dramatic steps to relieve dyspnea must be taken with full understanding of the ramifications and complications. Some patients may choose a morphine drip to allow a comfortable death, whereas others might choose an aggressive approach focused on prolongation of life as well as relief of discomfort. It is up to the healthcare provider to help the individual patient understand these choices (Stulbarg & Adams, 2005).

PROGNOSIS

COPD develops quietly. Early in their disease, patients have measurable declines in their lung function before they develop symptoms. The first symptoms are usually an intermittent cough and some shortness of breath during exercise. Patients often dismiss these as temporary lung irritations or as a lack of physical conditioning.

After many years, the cough becomes chronic or the spells of breathlessness become more frequent. Typically, this is the stage at which people first seek medical help. As time progresses, even with bronchodilator therapy, the patient’s lung function continues to gradually decline. Occasional episodes of debilitating exacerbations become more frequent. Patients admitted to intensive care units with acute exacerbations of COPD have a mortality rate of >20%, and when the patient is older than 65 years, the mortality rate doubles. Forty percent of the COPD deaths in an ICU are from pulmonary emboli.

Eventually, dyspnea limits a COPD patient to only minimal activity. Patients are continually fatigued, they lose weight, and at some point they succumb to a respiratory illness, pulmonary embolism, heart failure, acute respiratory failure, or lung cancer. When the patient’s FEV1 has dropped to <0.75 liters/sec (very severe COPD), there is a 30% chance that they will die within a year and a 95% chance that they will die within 10 years (Roizen & Fleisher, 2009).

ANSWERS TO TELEPHONE QUESTIONS

Health professionals who advise patients over the telephone should know straightforward answers to basic questions. Here are a few important questions and answers about COPD and smoking.

About COPD

What Is COPD?

The full name for COPD is “chronic obstructive pulmonary disease.” This disease is caused by inflammation of the lungs from many years of breathing in cigarette smoke or other types of pollution. The airways in the lungs become narrowed, and in some people, the airways become clogged with mucus. These problems make it harder and harder to move air into and out of your lungs.

A person with COPD frequently feels short of breath. COPD makes normal breathing tiring, and it can make it so difficult to breathe that exercise becomes too tiring to do. COPD continues to worsen over time, especially if the person is still smoking.

What causes COPD?

Smoking is the most common cause of COPD. Cigarette, cigar, and pipe tobacco can all cause COPD when the smoke is inhaled. Other kinds of air pollution can be just as bad as smoke if the pollution is inhaled for many years.

Anyone can get COPD from smoking, although it usually takes many years of smoking for the disease to be noticeable. A small number of people have an inherited genetic defect called alpha1-antitrypsin deficiency that makes them more likely to get the disease after only a few years of smoking or sometimes without having ever smoked at all.

Is COPD contagious?

No.

Do children inherit COPD?

Most types of COPD are not inherited. COPD is usually caused by cigarette smoking. Teach childreot to smoke will protect them from getting COPD.

A small number of people inherit a genetic defect called alpha1-antitrypsin deficiency, which makes them unusually susceptible to developing COPD. When these people get COPD, it is the emphysema type of COPD, and it usually shows up early, in people younger than 40 years old. If you think you may have this problem, your doctor can test you to find out.

Can COPD be cured?

There is no cure for COPD, and it is a major cause of illness and death.

What is a good way to get trustworthy information about COPD?

The American Lung Association has a COPD Center online that is full of useful information. Another good source is the COPD website of the National Heart, Lung, and Blood Institute.

COPD Diagnosis and Treatment

How do I know if I have COPD?

The signs and symptoms of COPD are different for each person, but common symptoms are cough, coughing up mucus, shortness of breath, wheezing, and chest tightness. COPD usually occurs in people who are at least 40 years old and who have smoked for many years. To make the diagnosis, a doctor will give you a physical exam and a set of breathing tests.

What is spirometry?

Spirometry measures how much air you breathe and how quickly you can get air into and out of your lungs. The tests are easy and painless. You breathe forcefully into a tube, and the machine at the other end measures how much air you are moving. Spirometry can detect COPD even before you have many symptoms.

I have COPD—so what do I do to fix it?

COPD cannot be cured, but it can be treated to make your life more comfortable. See your doctor and get set up with a treatment plan tailored specifically for you. Meanwhile, quitting smoking is the single most important thing you can do to slow the progress of the disease.

I have COPD. What should I do if I am having more trouble than usual catching my breath or if I am coughing more than usual?

If you have a set of rescue medicines that you have been told to take, then go ahead and use them. Then call your doctor right away.

I have COPD. What do I do when I’m getting sick, like with a fever or a cold?

Call your doctor right away.

How often do I have to get flu shots for my COPD?

Flu (influenza) can cause serious problems in people with COPD, and flu shots can reduce your chances of getting the flu. You should get a flu shot every year. In addition, you should have a pneumococcal vaccination, usually every five years.

I have COPD. How do I know when I need emergency help?

People with chronic obstructive pulmonary disease (COPD) will have episodes called “acute exacerbations.” During these times, you will have a much harder time catching your breath. You may also have chest tightness, more coughing, a change in your sputum, or a fever. It is important to call your doctor if you have any of those signs or symptoms. Specifically, you should get emergency help or advice if:

• You have taken your rescue medicines and you still feel as if you can’t breathe
• You find that it is suddenly hard to talk or to walk
• You are coughing up more mucus and it is yellow, green, or brown
• You develop a fever
• You get unusual chest pain or chest tightness
• Your heart is beating very quickly or irregularly for more than a few minutes
• Your lips or fingernails are gray or blue
• Your breathing is fast and hard, even after you have used your medicines
• Your mind is getting cloudy or you are getting tired and sleepy at the wrong time

Because it is likely that you will have an acute exacerbation at some time, be prepared. Plaow and have these things easily available:

• Your rescue medicines for sudden spells of difficult breathing
• Phone numbers of your doctor and of people who can take you to your doctor or to a nearby emergency room
• Directions to your doctor’s office and to a nearby emergency room
• A list of the medicines that you usually take

I have COPD. Can I still use my fireplace at home?

Unless it is the only way for you to heat your home, you should not burn wood or kerosene in your home. It is important to keep the air in your house clean. Keep your windows closed and stay indoors when there is a lot of pollution or dust outside. When you cook, keep smoke and cooking vapors out of the air with an exhaust fan or open a window or a door. Don’t let anyone smoke in your house. Avoid using any aerosol (spray) products. Don’t use strong perfumes. When your house is being painted or is being sprayed for insects, stay away from the house for as long as possible until the fumes settle.

What can be done for my COPD?

Treatment for COPD helps prevent complications, prolong life, and improve a person’s quality of life. Quitting smoking, staying away from people who are smoking, and avoiding exposure to other lung irritants are the most important ways to reduce your risk of developing COPD or to slow the progress of the disease if you have it.

Treatment for COPD includes medicines such as bronchodilators, steroids, flu shots, and pneumococcal vaccine to avoid or to reduce further complications.

As the symptoms of COPD get worse over time, a person may have more difficulty walking and exercising. You should talk to your doctor about exercise programs. Ask whether you will benefit from a pulmonary rehab program—a coordinated program of exercise, physical therapy, disease management training, advice on diet, and counseling.

Oxygen treatment and surgery (to remove part of a lung or even to transplant a lung) may be recommended for patients with severe COPD.

Exactly what is pulmonary rehab?

Pulmonary rehabilitation (“pulmonary rehab”) is a program that includes regular exercise, training in how to manage your disease, and practical advice, all of which help you to stay active and to remain able to carry out your day-to-day activities. After some medical breathing evaluations, you meet with a pulmonary rehab team and make a plan that is best for your disease and your lifestyle. Usually, there are meetings, exercise classes, suggestions for long-term improvements in your lifestyle, and an advisor whom you can always contact for advice.

About Smoking

Why should I quit smoking?

People who stop smoking live longer. If you quit smoking before you’re 35, you will live about six years longer. Even if you quit at age 55, you can still add two years to your life.

By quitting smoking, you reduce your chances of getting lung disease, heart disease, and cancer. You will feel better and healthier. Smoking injures your senses of taste and smell, and quitting smoking will even make food taste better.

Frankly, I like to smoke, and I know people who have lived a long time even though they were smokers. Why should I go through the agony of stopping something I enjoy? Besides, I may not even be able to quit.

Cigarettes are legal addictive drugs, and they are easier to buy and less expensive than illegal drugs—but smoking is gambling, with bad odds. As a smoker, you have a 1 in 3 chance of dying earlier than you would if you quit. When you do die, it will most likely be of heart disease, stroke, cancer, or COPD. Smoking is responsible for about 1 out of every 5 deaths in the United States, and almost a half million Americans die each year from diseases caused by smoking.

What’s more, your smoking hurts the people around you. Just breathing in another person’s smoke can cause lung problems in children and can cause cancer and heart disease in adults. Pregnant women and new mothers and fathers can protect their baby’s health by stopping smoking now.

Sure, it’s tough to quit smoking. Staying healthy and protecting the health of the people around you is difficult. But don’t hide behind the excuse that you can’t stop smoking. Studies suggest that everyone can quit smoking.

What is the first thing I need to do once I’ve decided to quit?

You should set a quit date. Then make an appointment to see a doctor before the quit date. Your doctor will help you devise a plan that will make quitting easier. There are a variety of anti-smoking medicines, and a doctor can suggest the best one for you.

Also, plan to join a support group or a stop-smoking program. The American Lung Association has an online stop-smoking program called “Freedom from Smoking Online.” Another helpful organization is Nicotine Anonymous, which runs 12-step programs with group support. Information can be found at http://www.nicotine-anonymous.org.

Here are some other general tips:

• Pick a good time to quit, a time when you won’t be under a lot of stress.
• Face the fact that it may not be easy and that you may have uncomfortable symptoms for a few weeks. You may get headaches or be sleepy or dizzy. You may become irritable or nervous. You will probably have cravings for a cigarette.
• Add some extra exercise to your quitting program. Walking, for example, is a great stress reducer.
• Tell your friends and family you are trying to quit smoking. Get their help to distract you, to keep up your spirits, and to be there when you need to complain.

What medicines should I take when I’m trying to stop smoking?

Nicotine is an addictive drug. For many people, nicotine replacements help to keep withdrawal symptoms to a minimum. Nicotine replacements come as patches, gums, lozenges, and an inhaler. Get your doctor to advise you when choosing which to take. Your doctor can also prescribe a new nicotine-free tablet called Chantix, which reduces withdrawal symptoms. Some people get help from an antidepressant called bupropion, which is also a prescription medicine.

Will I gain weight if I quit smoking?

Many smokers gain weight when they quit, but it is usually less than 10 pounds. Eat a healthy diet, stay active, and try not to let weight gain distract you from your main goal—quitting smoking. Some of the medications that help you quit may also help to delay weight gain. Remember, smoking will hurt your health much more than a few extra pounds of weight.

Aren’t nicotine replacement products just as bad as smoking?

No, nicotine replacements do not have all the tars and poisonous gases that are found in cigarettes. Furthermore, these medicines give you less nicotine than a smoker gets from cigarettes. Nicotine replacement products (patches, gums, lozenges, or inhalers) should not be used by pregnant or nursing women. People with other medical conditions should check with their doctor before using any nicotine replacement product. It is important that smokers quit smoking completely before starting to use nicotine replacements.

RESOURCES

COPD

American Thoracic Society
http://www.thoracic.org/sections/copd/

American Lung Association
http://www.lungusa.org/

GOLD Guidelines At-A-Glance Desk Reference
http://www.goldcopd.com/GuidelinesResources.asp?l1=2&l2=0

National Heart, Lung, and Blood Institute
http://www.nhlbi.nih.gov/health/public/lung/copd/

National Lung Health Education Program
http://www.nlhep.org/resources-medical.html

Alpha1-antitrypsin Deficiency Information
http://www.alpha1.org
http://www.alphanet.org
http://www.alphaone.org
http://www.alpha1advocacy.org

Smoking

Helping Smokers Quit: A Guide for Clinicians
http://www.ahrq.gov/clinic/tobacco/clinhlpsmksqt.htm

SmokeFree Website
http://www.smokefree.gov/

Treating Tobacco Use and Dependence: Clinical Practice Guideline
http://www.surgeongeneral.gov/tobacco/

Freedom From Smoking® Online (American Lung Association’s online smoking cessation program)
http://www.lungusa.org/

Nicotine Anonymous (A 12-step program with group support)
http://www.nicotine-anonymous.org

Nutrition and Diet Information

Cleveland Clinic Nutritional Guidelines for People with COPD
http://my.clevelandclinic.org/disorders/Chronic_Obstructive_Pulmonary_Disease_
copd/hic_Nutritional_Guidelines_for_People_with_COPD.aspx.

PNEUMONIA

Pneumonia is an inflammation of the lung parenchyma associated with alveolar edema and congestion that impair gas exchange. Primary pneumonia is caused by the client’s inhaling or aspirating a pathogen. Secondary pneumonia ensues from lung damage caused by the spread of bacteria from an infection elsewhere in the body. Likely causes include various infectious agents (bacterial, viral, or fungal), chemical irritants (including gastric reflux/aspiration, smoke inhalation), and radiation therapy. 

Pneumonia may be community acquired (including during the first 2 days of hospitalization) or nosocomial (hospital acquired occurring 48 hours or longer after admission). Viral pneumonia accounts for approximately half of all cases of community-acquired pneumonia with common causative organisms including respiratory syncytial virus (RSV) and influenza. Bacterial pneumonias are divided into typical and atypical types. Gram-positive Streptococcus pneumoniae Haemophilus, and Staphylococcus are the most common bacterial causes. The most common causes of fungal pneumonia are Pneumocystis carinii and cytomegalovirus, often occurring in immunocompromised persons. Nosocomial pneumonias are often caused by different pathogens, including Staphylococcus aureus and Klebsiella. Other atypical pneumonias can be caused by Mycoplasma, Mycobacterium tuberculosis, Coxiella burnetii, Chlamydia, Legionella, and others.

 

Severe pneumonia is life threatening, (sixth leading cause of death in the United States), especially for the elderly, for very young children, and for persons with asthma, cystic fibrosis, or other chronic respiratory conditions; smokers; immunocompromised persons; and those with heart disease or poorly controlled diabetes.

This plan of care deals primarily with typical bacterial pneumonias.

Care Setting

Most clients are treated as outpatients in community settings; however, persons at higher risk (e.g., age >65, persons with other chronic conditions such as COPD, diabetes, cancer, congestive heart failure) are treated in the hospital, as are those already hospitalized for other reasons and have developed nosocomial pneumonia.

Related Concerns

AIDS

Chronic obstructive pulmonary disease (COPD) and asthma

Psychosocial aspects of care

Sepsis/septicemia

Surgical intervention

Client Assessment Database

Activity/Rest

May report: Fatigue, weakness

Insomnia

Prolonged immobility/bed rest

May exhibit: Lethargy

Decreased tolerance to activity

Circulation

May report: History of recent/chronic heart failure (HF)

May exhibit: Tachycardia

Flushed appearance, pallor, central cyanosis

Ego Integrity

May report: Multiple stressors, financial concerns

Food/Fluid

May report: Loss of appetite, nausea/vomiting

May be receiving intestinal/gastric feedings

May exhibit: Distended abdomen

Hyperactive bowel sounds

Dry skin with poor turgor

Cachectic appearance (malnutrition)

Neurosensory

May report: Frontal headache (influenza)

May exhibit: Changes in mentation (confusion, somnolence) or behavior (irritability, restlessness, lethargy)

Pain/Discomfort

May report: Headache

Chest pain (pleuritic) aggravated by cough, substernal chest pain (influenza)

Myalgia, arthralgia, abdominal pain

May exhibit: Splinting/guarding over affected area (client commonly lies on affected side to restrict movement)

Respiration

May report: History of recurrent/chronic URIs, tuberculosis, COPD, cigarette smoking

Progressive dyspnea

Cough: Dry hacking (initially) progressing to productive cough

Presence of tracheostomy/endotracheal (ET) tube

May exhibit: Tachypnea, shallow grunting respirations, use of accessory muscles, nasal flaring

Sputum: Scanty or copious; pink, rusty, or purulent (green, yellow, or white)

Percussion: Dull over consolidated areas

Fremitus: Tactile and vocal, gradually increases with consolidation

Pleural friction rub

Breath sounds: Diminished or absent over involved area or bronchial breath sounds over area(s) of consolidation, coarse inspiratory crackles

Color: Pallor or cyanosis of lips/nail beds

Safety

May report: Recurrent chills

History of altered immune system (i.e., systemic lupus erythematosus [SLE], AIDS, active malignancies, neurologic disease, heart failure, diabetes, steroid or chemotherapy use), institutionalization, general debilitation

Fever (e.g., 102°F–104°F/39°C–40°C)

May exhibit: Diaphoresis

Shaking

Rash may be noted in cases of rubeola or varicella

Teaching/Learning

May report: History of recent surgery, chronic alcohol use, intravenous (IV) drug therapy or abuse, immunosuppressive therapy

Use of herbal supplements (e.g., garlic, ginkgo, licorice, onion, tumeric, horehound, marshmallow, mullein, wild cherry bark, astragalus, echinacea, elderberry, goldenseal, Oregon graperoot)

Discharge plan

considerations: Assistance with self-care, homemaker tasks

Oxygen may be needed, especially if recovery is prolonged or other predisposing condition exists

Refer to section at end of plan for postdischarge considerations.

Diagnostic Studies

Chest x-ray: Identifies structural distribution (e.g., lobar, bronchial), may also reveal multiple abscesses/infiltrates, empyema (staphylococcus); scattered or localized infiltration (bacterial); or diffuse/extensive nodular infiltrates (more often viral). In Mycoplasma pneumonia, chest x-ray may be clear.

 

Fiberoptic bronchoscopy: : May be both diagnostic (qualitative cultures) and therapeutic (reexpansion of lung segment).

ABGs/pulse oximetry: : Abnormalities may be present, depending on extent of lung involvement and underlying lung disease. Pulse oximetry Gram stain/cultures: : Sputum collection; needle aspiration of empyema, pleural, and transtracheal or transthoracic fluids; lung biopsies and blood cultures may be done to recover causative organism. More than one type of organism may be present; common bacteria include Diplococcus pneumoniae, Staphylococcus aureus, α-hemolytic streptococcus, Haemophilus influenzae, and cytomegalovirus (CMV). Note: Sputum cultures may not identify all offending organisms. Blood cultures may show transient bacteremia.

CBC: :  Leukocytosis with a left shift usually present in bacterial pneumonia, although a low white blood cell (WBC) count may be present in viral infection, immunosuppressed conditions such as AIDS, and overwhelming bacterial pneumonia.

Erythrocyte sedimentation rate (ESR): : Elevated.

Serologic studies, e.g., viral or Legionella titers, cold agglutinins: : Assist in differential diagnosis of specific organism.

Pulmonary function studies: : Volumes may be decreased (congestion and alveolar collapse); airway pressure may be increased and compliance decreased. Shunting is present (hypoxemia).

Electrolytes: : Sodium and chloride levels may be low.

Bilirubin: May be increased.

Percutaneous aspiration/open biopsy of lung tissues: : May reveal typical intranuclear and cytoplasmic inclusions (CMV), characteristic giant cells (rubeola).

Nursing Priorities

1. Maintain/improve respiratory function.

2. Prevent complications.

3. Support recuperative process.

4. Provide information about disease process/prognosis and treatment.

Discharge Goals

1. Ventilation and oxygenation adequate for individual needs.

2. Complications prevented/minimized.

3. Disease process/prognosis and therapeutic regimen understood.

4. Lifestyle changes identified/initiated to prevent recurrence.

5. Plan in place to meet needs after discharge.

NURSING DIAGNOSIS: ineffective Airway Clearance

May be related to

Tracheal bronchial inflammation, edema formation, increased sputum production

Pleuritic pain

Decreased energy, fatigue

Possibly evidenced by

Changes in rate, depth of respirations

Abnormal breath sounds, use of accessory muscles

Dyspnea, cyanosis

Cough, effective or ineffective; with/without sputum production

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:

Respiratory Status: Airway Patency (NOC)

Identify/demonstrate behaviors to achieve airway clearance.

Display patent airway with breath sounds clearing; absence of dyspnea, cyanosis.

ACTIONS/INTERVENTIONS Airway Management (NIC) Independent Assess rate/depth of respirations and chest movement. Monitor for signs of respiratory failure (e.g., cyanosis and severe tachypnea).     Auscultate lung fields, noting areas of decreased/absent airflow and adventitious breath sounds; e.g., crackles, wheezes.     Elevate head of bed, change position frequently.	RATIONALE     Tachypnea, shallow respirations, and asymmetric chest movement are frequently present because of discomfort of moving chest wall and/or fluid in lung. When pneumonia is severe, the client may require endotracheal intubation and mechanical ventilation to keep airways clear. Decreased airflow occurs in areas consolidated with fluid. Bronchial breath sounds (normal over bronchus) can also occur in consolidated areas. Crackles, rhonchi, and wheezes are heard on inspiration and/or expiration in response to fluid accumulation, thick secretions, and airway spasm/obstruction. Keeping the head elevated lowers diaphragm, promoting chest expansion, aeration of lung segments, and mobilization and expectoration of secretions to keep the airway clear.
Assist client with frequent deep-breathing exercises. Demonstrate/help client learn to perform activity; e.g., splinting chest and effective coughing while in upright position.     Suction as indicated (e.g., frequent or sustained cough, adventitious breath sounds, desaturation related to airway secretions).   Force fluids to at least 3000 mL/day (unless contraindicated, as in heart failure). Offer warm, rather than cold, fluids. Collaborative Assist with/monitor effects of nebulizer treatments and other respiratory physiotherapy; e.g., incentive spirometer, IPPB, percussion, postural drainage. Perform treatments between meals and limit fluids when appropriate.   Administer medications as indicated: mucolytics, expectorants, bronchodilators, analgesics.     Provide supplemental fluids; e.g., IV, humidified oxygen, and room humidification.     Monitor serial chest x-rays, ABGs, pulse oximetry readings. (Refer to ND: impaired Gas Exchange, following.)	Deep breathing facilitates maximum expansion of the lungs/smaller airways. Coughing is a natural self-cleaning mechanism, assisting the cilia to maintain patent airways. Splinting reduces chest discomfort, and an upright position favors deeper, more forceful cough effort. Note: Cough associated with pneumonias may last days to weeks or even months.   Stimulates cough or mechanically clears airway in client who is unable to do so because of ineffective cough or decreased level of consciousness.   Fluids (especially warm liquids) aid in mobilization and expectoration of secretions.   Facilitates liquefaction and removal of secretions. Postural drainage may not be effective in interstitial pneumonias or those causing alveolar exudate/destruction. Coordination of treatments/schedules and oral intake reduces likelihood of vomiting with coughing and expectorations. Aids in reduction of bronchospasm and mobilization of secretions. Analgesics are given to improve cough effort by reducing discomfort, but should be used cautiously because they can decrease cough effort/depress respirations.   Fluids are required to replace losses (including insensible) and aid in mobilization of secretions. Note: Some studies indicate that room humidification has been found to provide minimal benefit and is thought to increase the risk of transmitting infection. Follows progress and effects of disease process/therapeutic regimen, and facilitates necessary alterations in therapy.

NURSING DIAGNOSIS: impaired Gas Exchange

May be related to

Alveolar-capillary membrane changes (inflammatory effects)

Altered oxygen-carrying capacity of blood/release at cellular level (fever, shifting oxyhemoglobin curve)

Altered delivery of oxygen (hypoventilation)

Possibly evidenced by

Dyspnea, cyanosis

Tachycardia

Restlessness/changes in mentation

Hypoxia

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:

Respiratory Status: Gas Exchange (NOC)

Demonstrate improved ventilation and oxygenation of tissues by ABGs within client’s acceptable range and absence of symptoms of respiratory distress.

Participate in actions to maximize oxygenation.

ACTIONS/INTERVENTIONS Respiratory Monitoring (NIC) Independent Assess respiratory rate, depth, and ease.   Observe color of skin, mucous membranes, and nail beds, noting presence of peripheral cyanosis (nail beds) or central cyanosis (circumoral).   Assess mental status.   Monitor heart rate/rhythm. Monitor body temperature, as indicated. Assist with comfort measures to reduce fever and chills; e.g., addition/removal of bedcovers, comfortable room temperature, and tepid or cool water sponge bath. Maintain bed rest. Encourage use of relaxation techniques and diversional activities.

RATIONALE     Manifestations of respiratory distress are dependent on/and indicative of the degree of lung involvement and underlying general health status. Cyanosis of nail beds may represent vasoconstriction or the body’s response to fever/chills; however, cyanosis of earlobes, mucous membranes, and skin around the mouth (“warm membranes”) is indicative of systemic hypoxemia.   Restlessness, irritation, confusion, and somnolence may reflect hypoxemia/ decreased cerebral oxygenation. Tachycardia is usually present as a result of fever/dehydration but may represent a response to hypoxemia. High fever (common in bacterial pneumonia and influenza) greatly increases metabolic demands and oxygen consumption and alters cellular oxygenation.   Prevents overexhaustion and reduces oxygen consumption/demands to facilitate resolution of infection.

 

Elevate head and encourage frequent position changes, deep breathing, and effective coughing.   Assess level of anxiety. Encourage verbalization of concerns/feelings. Answer questions honestly. Visit frequently, arrange for SO/visitors to stay with client as indicated.   Observe for deterioration in condition, noting hypotension, copious amounts of pink/bloody sputum, pallor, cyanosis, change in level of consciousness, severe dyspnea, restlessness. Collaborative Monitor ABGs, pulse oximetry. Oxygen Therapy (NIC) Administer oxygen therapy by appropriate means; e.g., nasal prongs, mask, Venturi mask.     Prepare for/transfer to critical care setting if indicated.

These measures promote maximal inspiration, enhance expectoration of secretions to improve ventilation. (Refer to ND: ineffective Airway Clearance.)   Anxiety is a manifestation of psychologic concerns and physiologic responses to hypoxia. Providing reassurance and enhancing sense of security can reduce the psychologic component, thereby decreasing oxygen demand and adverse physiologic responses.   Shock and pulmonary edema are the most common causes of death in pneumonia and require immediate medical intervention.   Identifies problems (e.g., respiratory failure), follows progress of disease process or improvement; and facilitates alterations in pulmonary therapy.   The purpose of oxygen therapy is to maintain Pao2 above 60 mm Hg (or greater than 90% o2 saturation). Oxygen is administered by the method that provides appropriate delivery within the client’s tolerance. Intubation and mechanical ventilation may be required in the event of severe respiratory insufficiency. (Refer to CP: Ventilatory Assistance (Mechanical.)

NURSING DIAGNOSIS: Activity Intolerance

May be related to

Imbalance between oxygen supply and demand

General weakness

Exhaustion associated with interruption in usual sleep pattern because of discomfort, excessive coughing, and dyspnea

Possibly evidenced by

Verbal reports of weakness, fatigue, exhaustion

Exertional dyspnea, tachypnea

Tachycardia in response to activity

Development/worsening of pallor/cyanosis

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:

Activity Tolerance (NOC)

Report/demonstrate a measurable increase in tolerance to activity with absence of dyspnea and excessive fatigue, and vital signs within client’s acceptable range.

ACTIONS/INTERVENTIONS Energy Management (NIC) Independent Evaluate client’s response to activity. Note reports of dyspnea, increased weakness/fatigue, and changes in vital signs during and after activities. Provide a quiet environment and limit visitors during acute phase as indicated. Encourage use of stress management and diversional activities as appropriate. Explain importance of rest in treatment plan and necessity for balancing activities with rest.

RATIONALE     Establishes client’s capabilities/needs and facilitates choice of interventions. Reduces stress and excess stimulation, promoting rest.     Bed rest is maintained during acute phase to decrease metabolic demands, thus conserving energy for healing. Activity restrictions thereafter are determined by individual client response to activity and resolution of respiratory insufficiency.

 

Assist client to assume comfortable position for rest/sleep.   Assist with self-care activities as necessary. Provide for progressive increase in activities during recovery phase. and demand.

Client may be comfortable with head of bed elevated, sleeping in a chair, or leaning forward on overbed table with pillow support. Minimizes exhaustion and helps balance oxygen supply and demand.

NURSING DIAGNOSIS: acute Pain

May be related to

Inflammation of lung parenchyma

Cellular reactions to circulating toxins

Persistent coughing

Possibly evidenced by

Reports of pleuritic chest pain, headache, muscle/joint pain

Guarding of affected area

Distraction behaviors, restlessness

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:

Pain: Disruptive Effects (NOC)

Verbalize relief/control of pain.

Demonstrate relaxed manner, resting/sleeping and engaging in activity appropriately.

ACTIONS/INTERVENTIONS Pain Management (NIC) Independent Determine pain characteristics; e.g., sharp, constant, stabbing. Investigate changes in character/location/intensity of pain.       Monitor vital signs.         Provide comfort measures; e.g., back rubs, change of position, quiet music or conversation. Encourage use of relaxation/breathing exercises.		RATIONALE     Chest pain, usually present to some degree with pneumonia, may also herald the onset of complications of pneumonia, such as pericarditis and endocarditis. Changes in heart rate or BP may indicate that client is experiencing pain, especially when other reasons for changes in vital signs have been ruled out. Nonanalgesic measures administered with a gentle touch can lessen discomfort and augment therapeutic effects of analgesics. Client involvement in pain control measures promotes independence and enhances sense of well-being.
Offer frequent oral hygiene.     Instruct and assist client in chest splinting techniques during coughing episodes. (Refer to ND: ineffective Airway Clearance.) Collaborative Administer analgesics and antitussives as indicated.	Mouth breathing and oxygen therapy can irritate and dry out mucous membranes, potentiating general discomfort.   Aids in control of chest discomfort while enhancing effectiveness of cough effort.     These medications may be used to suppress nonproductive/paroxysmal cough or reduce excess mucus, thereby enhancing general comfort/rest.

NURSING DIAGNOSIS: risk for imbalanced Nutrition: less than body requirements

Risk factors may include

Increased metabolic needs secondary to fever and infectious process

Anorexia associated with bacterial toxins, the odor and taste of sputum, and certain aerosol treatments

Abdominal distention/gas associated with swallowing air during dyspneic episodes

Possibly evidenced by

[Not applicable; presence of signs and symptoms establishes an actual diagnosis.]

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:

Nutritional Status (NOC)

Demonstrate increased appetite.

Maintain/regain desired body weight.

ACTIONS/INTERVENTIONS Nutrition Therapy (NIC) Independent Identify factors that are contributing to nausea/vomiting; e.g., copious sputum, aerosol treatments, severe dyspnea, pain.

RATIONALE     Choice of interventions depends on the underlying cause of the problem.

 

Provide covered container for sputum and replace at frequent intervals. Assist with/encourage oral hygiene after emesis, after aerosol and postural drainage treatments, and before meals. Schedule respiratory treatments at least 1 hr before meals.   Auscultate for bowel sounds. Observe/palpate for abdominal distention.       Provide small, frequent meals, including dry foods (toast, crackers) and/or foods that are appealing to client. Evaluate general nutritional state, obtain baseline weight.

Eliminates noxious sights, tastes, smells from the client environment and can reduce nausea.     Reduces effects of nausea associated with these treatments.   Bowel sounds may be diminished/absent if the infectious process is severe/prolonged. Abdominal distention may occur as a result of air swallowing or reflect the influence of bacterial toxins on the gastrointestinal (GI) tract. These measures may enhance intake even though appetite may be slow to return.   Presence of chronic conditions (e.g., COPD or alcoholism) or financial limitations can contribute to malnutrition, lowered resistance to infection, and/or delayed response to therapy.

NURSING DIAGNOSIS: risk for deficient Fluid Volume

Risk factors may include

Excessive fluid loss (fever, profuse diaphoresis, mouth breathing/hyperventilation, vomiting)

Decreased oral intake

Possibly evidenced by

[Not applicable; presence of signs and symptoms establishes an actual diagnosis.]

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:

Demonstrate fluid balance evidenced by individually appropriate parameters; e.g., moist mucous membranes, good skin turgor, prompt capillary refill, stable vital signs.

ACTIONS/INTERVENTIONS Fluid Management (NIC) Independent Assess vital sign changes; e.g., increased temperature/prolonged fever, tachycardia, orthostatic hypotension.

RATIONALE     Elevated temperature/prolonged fever increases metabolic rate and fluid loss through evaporation. Orthostatic BP changes and increasing tachycardia may indicate systemic fluid deficit.

 

Assess skin turgor, moisture of mucous membranes (lips, tongue).   Note reports of nausea/vomiting. Monitor intake and output (I&O), noting color, character of urine. Calculate fluid balance. Be aware of insensible losses. Weigh as indicated. Force fluids to at least 3000 mL/day or as individually appropriate. Collaborative Administer medications as indicated; e.g., antipyretics, antiemetics. Provide supplemental IV fluids as necessary.

Indirect indicators of adequacy of fluid volume, although oral mucous membranes may be dry because of mouth breathing and supplemental oxygen. Presence of these symptoms reduces oral intake. Provides information about adequacy of fluid volume and replacement needs.   Meets basic fluid needs, reducing risk of dehydration. Useful in reducing fluid losses.   In the presence of reduced intake/excessive loss, use of parenteral route may correct/prevent deficiency.

 

NURSING DIAGNOSIS: deficient Knowledge [Learning Need] regarding condition, treatment, self-care, and discharge needs

May be related to

Lack of exposure

Misinterpretation of information

Altered recall

Possibly evidenced by

Requests for information; statement of misconception

Failure to improve/recurrence

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:

Knowledge: Illness Care (NOC)

Verbalize understanding of condition, disease process, and prognosis.

Verbalize understanding of therapeutic regimen.

Initiate necessary lifestyle changes.

Participate in treatment program.

ACTIONS/INTERVENTIONS Teaching: Disease Process (NIC) Independent Review normal lung function, pathology of condition. Discuss debilitating aspects of disease, length of convalescence, and recovery expectations. Identify self-care and homemaker needs/resources. Provide information in written and verbal form. Stress importance of continuing effective coughing/deep-breathing exercises. Emphasize necessity for continuing antibiotic therapy for prescribed period. Review importance of cessation of smoking. Outline steps to enhance general health and well-being; e.g., balanced rest and activity, well-rounded diet, program of aerobic exercise or strength training (particularly elderly individuals), avoidance of crowds during cold/flu season and persons with URIs. Stress importance of continuing medical follow-up and obtaining vaccinations/immunizations as appropriate. Identify signs/symptoms requiring notification of healthcare provider; e.g., increasing dyspnea, chest pain, prolonged fatigue, weight loss, fever/chills, persistence of productive cough, changes in mentation.

RATIONALE Promotes understanding of current situation and importance of cooperating with treatment regimen. Information can enhance coping and help reduce anxiety and excessive concern. Respiratory symptoms may be slow to resolve, and fatigue and weakness can persist for an extended period. These factors may be associated with depression and the need for various forms of support and assistance. Fatigue and depression can affect ability to assimilate information/follow medical regimen. During initial 6–8 weeks after discharge, client is at greatest risk for recurrence of pneumonia. Early discontinuation of antibiotics may result in failure to completely resolve infectious process. Smoking destroys tracheobronchial ciliary action, irritates bronchial mucosa, and inhibits alveolar macrophages, compromising body’s natural defense against infection. Increases natural defenses/immunity, limits exposure to pathogens. Recent research suggests elders with moderate physical limitations can significantly improve immunologic defenses through exercise that increase levels of salivary IgA (immunoglobulin that aids in blocking infectious agents entering through mucous membranes). May prevent recurrence of pneumonia and/or related complications. Prompt evaluation and timely intervention may prevent/minimize complications.

POTENTIAL CONSIDERATIONS following acute hospitalization (dependent on client’s age, physical condition/presence of complications, personal resources, and life responsibilities)

Fatigue—increased energy requirements to perform ADLs, discomfort, effects of antimicrobial therapy.

risk for Infection—inadequate secondary response (e.g., leukopenia, suppressed inflammatory response), chronic disease, malnutrition, current use of antibiotics.

ineffective Therapeutic Regimen Management—complexity of therapeutic regimen, economic difficulties, perceived seriousness/susceptibility.

CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) AND ASTHMA – Nursing management

Technorati Tags: CHRONIC,OBSTRUCTIVE,PULMONARY,DISEASE,COPD,ASTHMA,Nursing,management

All respiratory diseases characterized by chronic obstruction to airflow fall under the broad classification of COPD, also known as chronic airflow limitations (CAL). COPD is a condition of chronic dyspnea with expiratory airflow limitation that does not significantly fluctuate. Within that broad category, the primary cause of the obstruction may vary; examples include airway inflammation, mucous plugging, narrowed airway lumina, or airway destruction. The term COPD includes chronic bronchitis and emphysema. Although asthma also involves airway inflammation and periodic narrowing of the airway lumina (hyperreactivity), the condition is the result of individual response to a wide variety of stimuli/triggers and is therefore episodic in nature with fluctuations/exacerbations of symptoms. Because client response and therapy needs can be similar, asthma has been included in this plan of care.

Asthma: Sometimes called chronic reactive airway disease, asthma is a chronic inflammatory disorder characterized by episodic exacerbations of reversible inflammation and constriction of bronchial smooth muscle, hypersecretion of mucus, and edema. Precipitating factors include allergens (e.g., foods, animals, latex, plants, molds), emotional upheaval, air pollution, cold weather, exercise, chemicals, medications, and viral infections. The prevalence of asthma is rising, accounting for the sixth most common chronic disease in the United States.

Chronic bronchitis: Widespread inflammation of airways with narrowing or blocking of airways, increased production of mucous sputum (productive cough), and marked cyanosis.

Emphysema: Most severe form of COPD characterized by recurrent inflammation that damages and eventually destroys alveolar walls to create large blebs or bullae (air spaces) and collapsed bronchioles on expiration (air-trapping). Clinically, emphysema typically presents with nonproductive or minimally productive cough and progressive dyspnea.

Note: Chronic bronchitis and emphysema coexist in many clients and are most commonly seen in hospitalized COPD clients when acute exacerbations occur. Chronic bronchitis and emphysema are usually irreversible, although some effects can be mediated.

 

COPD, or chronic obstructive pulmonary (PULL-mun-ary) disease, is a progressive disease that makes . In chronic obstructive bronchitis, the lining of the . ->

 

COPD – Chronic Obstructive Pulmonary Disease – symptoms, causes, and .
Learn about COPD – Chronic Obstructive Pulmonary Disease which is primarily two related diseases – chronic bronchitis and emphysema. ->

Lung diseases – COPD – What is COPD? : Canadian Lung Association
The Canadian Lung Association – asthma, COPD, tuberculosis, sleep apnea, emphysema, . What is COPD? COPD stands for Chronic Obstructive Pulmonary Disease. . ->

Chronic Obstructive Pulmonary Disease (COPD) — familydoctor.org
Information about chronic obstructive pulmonary disease (COPD) from the . What is chronic obstructive pulmonary disease? What are the symptoms of COPD? . ->

Chronic Obstructive Pulmonary Disease, THE MERCK MANUAL OF HEALTH & AGING
Chronic Obstructive Pulmonary Disease. Chronic Obstructive Pulmonary Disease. Chronic obstructive pulmonary disease (COPD) is the collective name for two . ->

COPD – What is COPD – Chronic Obstructive Pulmonary Disease Emphysema
Chronic Obstructive Pulmonary Disease, otherwise known as COPD is a blanket term that covers both chronic bronchitis and emphysema. ->

Chronic obstructive pulmonary disease – Wikipedia, the free encyclopedia
People who have chronic obstructive pulmonary disease (COPD) usually have some . Next Article: Chronic Obstructive Pulmonary Disease (COPD) Topics. Overview . ->

Care Setting

Primarily community level; however, severe exacerbations may necessitate emergency and/or inpatient hospital stay.

Related Concerns

Heart failure: chronic

Pneumonia: microbial

Psychosocial aspects of care

Ventilatory assistance (mechanical

Surgical intervention

Client Assessment Database

Activity/Rest

May report: Fatigue, exhaustion, malaise

Inability to perform basic activities of daily living (ADLs) because of breathlessness

Inability to sleep, need to sleep sitting up

Dyspnea at rest or in response to activity or exercise

May exhibit: Fatigue

Restlessness, insomnia

General debilitation/loss of muscle mass

Circulation

May report: Swelling of lower extremities

May exhibit: Elevated blood pressure (BP)

Elevated heart rate/severe tachycardia, dysrhythmias

Distended neck veins (advanced disease)

Dependent edema, may not be related to heart disease

Faint heart sounds (due to increased anteroposterior [AP] chest diameter)

Skin color/mucous membranes may be pale or bluish/cyanotic, clubbing of nails and peripheral cyanosis, pallor (can indicate anemia)

Ego Integrity

May report: Increased stress factors

Changes in lifestyle

Feelings of hopelessness, loss of interest in life

May exhibit: Anxious, fearful, irritable behavior, emotional distress

Apathy, change in alertness, dull affect, withdrawal

Food/Fluid

May report: Nausea (side effect of medication/mucus production)

Poor appetite/anorexia (emphysema)

Inability to eat because of respiratory distress

Persistent weight loss, decreased muscle mass/subcutaneous fat (emphysema) or weight gain may reflect edema (bronchitis, prednisone use)

May exhibit: Poor skin turgor

Dependent edema

Diaphoresis

Abdominal palpation may reveal hepatomegaly (bronchitis)

Hygiene

May report: Decreased ability/increased need for assistance with ADLs

May exhibit: Poor hygiene

Respiration

May report: Variable levels of dyspnea, such as insidious and progressive onset (predominant symptom in emphysema), especially on exertion; seasonal or episodic occurrence of breathlessness (asthma); sensation of chest tightness, inability to breathe (asthma); chronic “air hunger”

Persistent cough with sputum production (gray, white, or yellow), which may be copious (chronic bronchitis); intermittent cough episodes, usually nonproductive in early stages, although they may become productive (emphysema); paroxysms of cough (asthma)

History of recurrent pneumonia, long-term exposure to chemical pollution/respiratory irritants (e.g., cigarette smoke), or occupational dust/fumes (e.g., cotton, hemp, asbestos, coal dust, sawdust)

Familial and hereditary factors; i.e., deficiency of α₁-antitrypsin (emphysema)

Use of oxygen at night or continuously

May exhibit: Respirations: Usually rapid, may be shallow; prolonged expiratory phase with grunting, pursed-lip breathing (emphysema)

Assumption of three-point (“tripod”) position for breathing (especially with acute exacerbation of chronic bronchitis)

Use of accessory muscles for respiration; e.g., elevated shoulder girdle, retraction of supraclavicular fossae, flaring of nares

Chest may appear hyperinflated with increased AP diameter (barrel-shaped), minimal diaphragmatic movement

Breath sounds may be faint with expiratory wheezes (emphysema); scattered, fine, or coarse moist crackles (bronchitis); rhonchi, wheezing throughout lung fields on expiration, and possibly during inspiration, progressing to diminished or absent breath sounds (asthma)

Percussion may reveal hyperresonance over lung fields (e.g., air-trapping with emphysema) or dullness over lung fields (e.g., consolidation, fluid, mucus)

Difficulty speaking sentences of more than four or five words at one time, loss of voice

Color: Pallor with cyanosis of lips, nail beds; overall duskiness; ruddy color (chronic bronchitis, “blue bloaters”); normal skin color despite abnormal gas exchange and rapid respiratory rate (moderate emphysema, known as “pink puffers”)

Clubbing of fingernails (not characteristic of emphysema and if present should alert clinician to another condition; e.g., pulmonary fibrosis, cystic fibrosis, lung cancer or asbestosis)

Safety

May report: History of allergic reactions or sensitivity to substances/environmental factors

Recent/recurrent infections

Flushing/perspiration (asthma)

Sexuality

May report: Decreased libido

Social Interaction

May report: Dependent relationship(s)

Insufficient support from/to partner/significant other (SO), lack of support systems

Prolonged disease or disability progression

May exhibit: Inability to converse/maintain voice because of respiratory distress

Limited physical mobility

Neglectful relationships with other family members

Inability to perform/inattention to employment responsibilities, absenteeism/confirmed disability

Teaching/Learning

May report: Use/misuse of respiratory drugs

Use of herbal supplements (e.g., astragalus, coleus, echinacea, elderberry, elencampe, ephedra, garlic, ginkgo, horehound, licorice, marshmallow, mullein, onion, tumeric, goldenseal, Oregon graperoot, wild cherry bark, peppermint, hyssop)

Smoking/difficulty stopping smoking, chronic exposure to second-hand smoke, smoking substances other than tobacco

Regular use of alcohol

Failure to improve over long period of time

Discharge plan

considerations: Changes in medication/therapeutic treatments, use of supplemental oxygen, ventilator support; end-of-life issues

Refer to section at end of plan for postdischarge considerations.

Diagnostic Studies

Chest x-ray: May reveal hyperinflation of lungs with increased anterior-posterior (AP) diameter, flattened diaphragm, increased retrosternal air space, decreased vascular markings/bullae (emphysema), increased bronchovascular markings (bronchitis), normal findings during periods of remission (asthma).

Pulmonary function tests: Spirometry is an established method of measuring lung function, recommended for diagnosis and management of persons with COPD, those at risk of COPD, and follow-up of persons with documented COPD to determine cause of dyspnea, whether functional abnormality is obstructive or restrictive, to estimate degree of dysfunction and to evaluate effects of therapy; e.g., bronchodilators. Exercise pulmonary function studies may also be done to evaluate activity tolerance in those with known pulmonary impairment/progression of disease.

Tidal volume (V_T): Decreased V_T may indicate restrictive disease.

Minute volume (MV): Decreased MV may indicate pulmonary edema; increased MV can occur with acidosis, increased CO₂, decreased Pao₂ ,and low compliance states.

Forced expiratory volume over 1 second (FEV₁): Reduced FEV₁ not only is the standard way of assessing the clinical course and degree of reversibility in response to therapy but also is an important predictor of prognosis. Measurements done pre and postbronchodilator help to distinguish obstructive disease (COPD) from restrictive disease (asthma).

Total lung capacity (TLC), functional residual capacity (FRC), and residual volume (RV): May be increased, indicating air-trapping. In obstructive lung disease, the RV will make up the greater portion of the TLC.

Thoracic gas volume (TCV): Increased TCV indicates air-trapping such as might occur with COPD. Body plethysmography may be used to measure pressure and flow or volume changes (e.g., TCV, airway resistance, and conductance).

Maximal voluntary ventilation (MVV), also known as maximum breathing capacity: Decreased in obstructive disease and normal or decreased in restrictive disease.

DLCO: Assesses diffusion in lungs. Carbon monoxide is used to measure gas diffusion across the alveocapillary membrane. Because carbon monoxide combines with hemoglobin 200 times more easily than oxygen, it easily affects the alveoli and small airways where gas exchange occurs. Emphysema is the only obstructive disease that causes diffusion dysfunction.

Arterial blood gases (ABGs): Determines degree and severity of disease process, e.g., most often Pao₂ is decreased, and Paco₂ is normal or increased in chronic bronchitis and emphysema, but is often decreased in asthma; pH normal or acidotic, mild respiratory alkalosis secondary to hyperventilation (moderate emphysema or asthma).

Pulse Oximetry: A continuous noninvasive study of arterial blood oxygen diffusion and saturation using a clip or probe attached to a sensor site (usually fingertip or earlobe). The percentage expressed is the ratio of oxygen to hemoglobin. Abnormally low levels (Peak Expiratory Flow (PEFor PEFR): Noninvasive meter used by client to monitor disease status by assessing speed at which air is forced out of lungs after deep inhalation.

Bronchogram: Can show cylindrical dilation of bronchi on inspiration, bronchial collapse on forced expiration (emphysema), enlarged mucous ducts (bronchitis).

Lung scan: Perfusion scanning can confirm vascular obstruction such as pulmonary or septic emboli. Ventilation studies may be done to differentiate between the various pulmonary diseases, such as PE, atelectasis, obstruction, tumors and COPD. COPD is characterized by a mismatch of perfusion and ventilation (i.e., areas of abnormal ventilation in area of perfusion defect).

Complete blood count (CBC) and differential: Increased hemoglobin (advanced emphysema), increased eosinophils (asthma). WBCs can be elevated in severe respiratory infection.

Blood chemistry: α₁-Antitrypsin is measured to verify deficiency and diagnosis of primary emphysema.

Sputum culture: Determines presence of infection, identifies pathogen.

Cytologic examination: Rules out underlying malignancy or allergic disorder.

Electrocardiogram (ECG): Right axis deviation, peaked P waves (severe asthma); atrial dysrhythmias (bronchitis), tall, peaked P waves in leads II, III, AVF (bronchitis, emphysema); vertical QRS axis (emphysema).

Exercise ECG, Stress test: May be done for evaluation of hypoxemia and/or desaturation in the presence of dyspnea, known pulmonary disease, abnormal diagnostic tests (e.g., diffusing capacity). Helps in assessing degree of pulmonary dysfunction, evaluating effectiveness of bronchodilator therapy, planning/evaluating exercise program.

Nursing Priorities

1. Maintain airway patency.

2. Assist with measures to facilitate gas exchange.

3. Enhance nutritional intake.

4. Prevent complications, slow progression of condition.

5. Provide information about disease process/prognosis and treatment regimen.

Discharge Goals

1. Ventilation/oxygenation adequate to meet self-care needs.

2. Nutritional intake meeting caloric needs.

3. Infection treated/prevented.

4. Disease process/prognosis and therapeutic regimen understood.

5. Plan in place to meet needs after discharge.

NURSING DIAGNOSIS

NURSING DIAGNOSIS: ineffective Airway Clearance

May be related to

Bronchospasm

Increased production of secretions, retained secretions, thick, viscous secretions

Decreased energy/fatigue

Possibly evidenced by

Statement of difficulty breathing

Changes in depth/rate of respirations, use of accessory muscles

Abnormal breath sounds; e.g., wheezes, rhonchi, crackles

Cough (persistent), with/without sputum production

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:

Respiratory Status: Airway Patency (NOC)

Maintain patent airway with breath sounds clear/clearing.

Demonstrate behaviors to improve airway clearance; e.g., cough effectively and expectorate secretions.

ACTIONS/INTERVENTIONS

RATIONALE

Airway Management (NIC) Independent Auscultate breath sounds. Note adventitious breath sounds; e.g., wheezes, crackles, rhonchi.       Assess/monitor respiratory rate. Note inspiratory/expiratory ratio.       Note presence/degree of dyspnea; e.g., reports of “air hunger,” restlessness, anxiety, respiratory distress, use of accessory muscles. Use 0–10 scale or American Thoracic Society’s “Grade of Breathlessness Scale” to rate breathing difficulty. Ascertain precipitating factors when possible. Differentiate acute episode from exacerbation of chronic dyspnea. Assist client to assume position of comfort; e.g., elevate head of bed, have client lean on overbed table or sit on edge of bed.       Keep environmental pollution to a minimum (e.g., dust, smoke, and feather pillows), according to individual situation. Encourage/assist with abdominal or pursed-lip breathing exercises.   Observe characteristics of cough; e.g., persistent, hacking, moist. Assist with measures to improve effectiveness of cough effort.   Increase fluid intake to 3000 mL/day within cardiac tolerance. Provide warm/tepid liquids. Recommend intake of fluids between instead of during meals

Some degree of bronchospasm is present with obstructions in airway and may/may not be manifested in adventitious breath sounds; e.g., scattered, moist crackles (bronchitis); faint sounds, with expiratory wheezes (emphysema); or absent breath sounds (severe asthma).   Tachypnea is usually present to some degree and may be pronounced on admission or during stress/concurrent acute infectious process. Respirations may be shallow and rapid, with prolonged expiration in comparison to inspiration.   Respiratory dysfunction is variable depending on the underlying process; e.g., infection, allergic reaction, and the stage of chronicity in a client with established COPD. Note: Using a 0–10 scale to rate dyspnea aids in quantifying and tracking changes in respiratory distress. Rapid onset of acute dyspnea may reflect pulmonary embolus.       Elevation of the head of the bed facilitates respiratory function by use of gravity; however, client in severe distress will seek the position that most eases breathing. Supporting arms/legs with table, pillows, and so on helps reduce muscle fatigue and can aid chest expansion.   Precipitators of allergic type of respiratory reactions that can trigger/exacerbate onset of acute episode.   Provides client with some means to cope with/control dyspnea and reduce air- trapping. Cough can be persistent but ineffective, especially if client is elderly, acutely ill, or debilitated. Coughing is most effective in an upright or in a head-down position after chest percussion.   Hydration helps decrease the viscosity of secretions, facilitating expectoration. Using warm liquids may decrease bronchospasm. Fluids during meals can increase gastric distention and pressure on the diaphragm

 

Collaborative Administer medications as indicated: β-Agonists: epinephrine (Adrenalin, AsthmaNefrin, Primatene, Sus-Phrine); albuterol (Proventil, Velmax,Ventolin, AccuNeb, Airet); formoterol (Foradil); levalbuterol (Xopenex); metaproterenol (Alupent): pirbuterol (Maxair): salmeterol, terbutaline (Brethine); salmeterol (Serevent);       Bronchodilators; e.g., anticholinergic agents: ipratropium (Atrovent);         Leukotriene antagonists: montelukast (Singulair); zafirlukast (Accolate); zileuton (Zyflo);       Anti-inflammatories: oral, IV, and inhaled steroids; e.g., prednisone (Cordrol, Deltasone, Pred-Pak, Liquid Pred), methylprednisolone (Medrol), dexamethasone (Decadron), beclomethasone (Beclovent, Vanceril), budesonide (Pulmacort), fluticasone (Flovent), triamcinolone (Azmacort);   Antimicrobials;

Inhaled β2-adrenergic agonists are first-line therapies for rapid symptomatic improvement of bronchoconstriction. These medications relax smooth muscles and reduce local congestion, reducing airway spasm, wheezing, and mucus production. Medications may be oral, injected, or inhaled. Inhalation by metered- dose inhaler (MDI) with a spacer is recommended, but medications may be nebulized in the event client has severe coughing or is too dyspneic to retain a puff effectively.   Inhaled anticholinergic agents are now considered the first-line drugs for clients with stable COPD because studies indicate they have a longer duration of action with less toxicity potential, whereas still providing the effective relief of the β-agonists. Some of these medications are available in combinations; e.g., Albuterol and Atrovent are available as Combivent. Reduce leukotriene activity to limit inflammatory response. In mild to moderate asthma, reduces need for inhaled β2-agonists and systemic corticosteroids. Not effective in acute exacerbations because there is no bronchodilator effect. Note: This drug class is not recommended for clients with COPD because of insufficient testing. Decrease local airway inflammation and edema by inhibiting effects of histamine and other mediators, to reduce severity and frequency of airway spasm, respiratory inflammation, and dyspnea. Studies have shown benefits of systemic steroids in the management of COPD exacerbations. Inhaled steroids may serve as a systemic steroid-sparing agent. Various antimicrobials may be indicated for control of bacterial exacerbations of COPD; e.g., pneumonia. Refer to CP, Pneumonia, microbial, page 000.)

 

Methylxanthine derivatives; e.g., aminophylline, oxtriphylline (Choledyl), theophylline (Bronkodyl, Theo-Dur, Elixophyllin, Slo-Bid, Slo-Phyllin);           Analgesics, cough suppressants, or antitussives; e.g., codeine, dextromethorphan products (Benylin DM, Comtrex, Novahistine);   Artificial surfactant; e.g., colfosceril palmitate (Exosurf).   Provide supplemental humidification; e.g., ultrasonic nebulizer, aerosol room humidifier.   Assist with respiratory treatments; e.g., spirometry, chest physiotherapy.       Monitor/graph serial ABGs, pulse oximetry, chest x-ray.

Decrease mucosal edema and smooth muscle spasm (bronchospasm) by indirectly increasing cyclic adenosine monophosphate (AMP). May also reduce muscle fatigue/respiratory failure by increasing diaphragmatic contractility. Use of theophylline may be of little or no benefit in the presence of adequate β-agonist regimen; however, it may sustain bronchodilation because effect of β-agonist diminishes between doses. Note: Theophylline products are used with less frequency now and are shied away from in older clients because of their potentially adverse cardiovascular effects. Persistent, exhausting cough may need to be suppressed to conserve energy and permit client to rest. Note: Regular use of antitussives is not recommended in COPD since cough can have a significant protective effect. Research suggests aerosol administration may enhance expectoration of sputum, improve pulmonary function, and reduce lung volumes (air trapping). Humidity helps reduce viscosity of secretions, facilitating expectoration, and may reduce/prevent formation of thick mucous plugs in bronchioles. Breathing exercises help enhance diffusion; aerosol/nebulizer medications can reduce bronchospasm and stimulate expectoration. Postural drainage and percussion enhance removal of excessive/sticky secretions and improve ventilation of bottom lung segments. Note: Chest physiotherapy may aggravate bronchospasm in asthmatics. Establishes baseline for monitoring progression/regression of disease process and complications. Note: Pulse oximetry readings detect changes in saturation as they are happening, helping to identify trends possibly before client is symptomatic. However, studies have shown that the accuracy of pulse oximetry may be questioned if client has severe peripheral vasoconstriction.

 

NURSING DIAGNOSIS: impaired Gas Exchange

May be related to

Altered oxygen supply (obstruction of airways by secretions, bronchospasm, air trapping) Alveoli destruction

Possibly evidenced by

Dyspnea

Confusion, restlessness

Inability to move secretions

Abnormal ABG values (hypoxia and hypercapnia)

Changes in vital signs

Reduced tolerance for activity

DESIRED OUTCOMES/EVALUATION CRITERIA—-CLIENT WILL:

Respiratory Status: Gas Exchange (NOC)

Demonstrate improved ventilation and adequate oxygenation of tissues by ABGs within client’s normal range and be free of symptoms of respiratory distress.Participate in treatment regimen within level of ability/situation.

INTERVENTIONS

RATIONALE

Acid/Base Management (NIC) Independent Assess respiratory rate, depth. Note use of accessory muscles, pursed-lip breathing, and inability to speak/converse. Elevate head of bed, assist client to assume position to ease work of breathing. Include periods of time in prone position as tolerated. Encourage deep-slow or pursed-lip breathing as individually needed/ tolerated. Assess/routinely monitor skin and mucous membrane color.   Encourage expectoration of sputum; suction when indicated.     Auscultate breath sounds, noting areas of decreased airflow and/or adventitious sounds.     Palpate for fremitus.     Monitor level of consciousness/mental status. Investigate changes.     Evaluate level of activity tolerance. Provide calm, quiet environment. Limit client’s activity or encourage bed/chair rest during acute phase. Have client resume activity gradually and increase as individually tolerated.     Evaluate sleep patterns, note reports of difficulties and whether client feels well rested. Provide quiet environment, group care/monitoring activities to allow periods of uninterrupted sleep. Limit stimulants; e.g., caffeine. Encourage position of comfort.   Monitor vital signs and cardiac rhythm

Useful in evaluating the degree of respiratory distress and/or chronicity of the disease process. Oxygen delivery may be improved by upright position and breathing exercises to decrease airway collapse, dyspnea, and work of breathing. Note: Recent research supports use of prone position to increase Pao2. Cyanosis may be peripheral (noted iail beds) or central (noted around lips/or earlobes). Duskiness and central cyanosis indicate advanced hypoxemia. Thick, tenacious, copious secretions are a major source of impaired gas exchange in small airways. Deep suctioning may be required when cough is ineffective for expectoration of secretions. Breath sounds may be faint because of decreased airflow or areas of consolidation. Presence of wheezes may indicate bronchospasm/retained secretions. Scattered moist crackles may indicate interstitial fluid/cardiac decompensation.   Decrease of vibratory tremors suggests fluid collection or air trapping.   Restlessness and anxiety are common manifestations of hypoxia. Worsening ABGs accompanied by confusion/somnolence are indicative of cerebral dysfunction due to hypoxemia. During severe/acute/refractory respiratory distress, client may be totally unable to perform basic self-care activities because of hypoxemia and dyspnea. Rest interspersed with care activities remains an important part of treatment regimen. An exercise program is aimed at improving aerobic capacity and functional performance, increasing endurance and strength without causing severe dyspnea and can enhance sense of well-being.   Multiple external stimuli and presence of dyspnea and/or hypoxemia may prevent relaxation and inhibit sleep.     Tachycardia, dysrhythmias, and changes in blood pressure (BP) can reflect effect of systemic hypoxemia on cardiac function.

 

Collaborative Monitor/graph serial ABGs and pulse oximetry.       Administer supplemental oxygen judiciously, using appropriate delivery method (e.g., cannula, mask, mechanical ventilator) and titrate as indicated by ABG results and client tolerance.   Administer antianxiety, sedative, or narcotic agents (e.g., morphine) with caution.     Assist with noninvasive (or nasal intermittent) positive-pressure ventilation (NIPPV) or intubation, institution/maintenance of mechanical ventilation; transfer to critical care area depending on client directives.     Prepare for additional referrals/interventions; e.g., pulmonary specialist, pulmonary rehabilitation program, surgical intervention, as appropriate.

PaCO2 usually elevated (bronchitis, emphysema), and PaO2 is generally decreased, so that hypoxia is present in a greater or lesser degree. Note: A “normal” or increased PaCO2 signals impending respiratory failure for asthmatics.   Used to correct/prevent worsening of hypoxemia, improve survival, and quality of life. Supplemental oxygen can be provided during exacerbations only, or as a long-term therapy.   May be used to reduce dyspnea by controlling anxiety and restlessness, which increases oxygen consumption/demand, exacerbating dyspnea. Must be monitored closely because depressive effect may lead to respiratory failure. Development of/impending respiratory failure requires prompt life-saving measures. Note: NIPPV provides ventilatory support by means of positive pressure typically through a nasal mask. It may be useful in the home setting as well to treat chronic respiratory failure or limit acute exacerbations in clients who are able to maintain spontaneous respiratory effort. May be indicated to confirm diagnosis and optimize appropriate treatment. A multidisciplinary approach including education. Exercise training may be helpful in improving client function and quality of life. Screened candidates (those with severe dyspnea/end-stage emphysema with FEV1 (forced expiratory volume in 1 second) less than 35% of the predicted value despite maximal medical therapy, with the ability to complete preoperative pulmonary rehabilitation programs) may benefit from lung volume reduction surgery (LVRS) in which hyperinflated giant bullae/cysts are removed; e.g., those occupying at least one-third of the involved lobe, or areas of lung tissue with small cystic disease. In the absence of fibrosis, this procedure removes ineffective lung tissue, allowing for better lung expansion and elastic recoil, enhanced blood flow to healthy tissues (correction of ventilation-perfusion mismatch), improved respiratory muscle efficiency, and increased venous return to the right ventricle.

 

NURSING DIAGNOSIS: imbalanced Nutrition: less than body requirements

May be related to

Dyspnea, sputum production

Medication side effects; anorexia, nausea/vomiting

Fatigue

Possibly evidenced by

Weight loss, loss of muscle mass, poor muscle tone

Reported altered taste sensation, aversion to eating, lack of interest in food

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:

Nutritional Status (NOC)

Display progressive weight gain toward goal as appropriate.

Demonstrate behaviors/lifestyle changes to regain and/or maintain appropriate weight.

INTERVENTIONS Nutrition Therapy (NIC) Independent Assess dietary habits, recent food intake. Note degree of difficulty with eating. Evaluate weight and body size (mass).           Auscultate bowel sounds.     Give frequent oral care, remove expectorated secretions promptly, provide specific container for disposal of secretions and tissues. Encourage a rest period of 1 hr before and after meals. Provide frequent small feedings. Avoid gas-producing foods and carbonated beverages.   Avoid very hot or very cold foods.

RATIONALE     Client in acute respiratory distress is often anorectic because of dyspnea, sputum production, and medication effects. In addition, many COPD clients habitually eat poorly even though respiratory insufficiency creates a hypermetabolic state with increased caloric needs. As a result, client often is admitted with some degree of malnutrition. People who have emphysema are often thin with wasted musculature. Diminished/hypoactive bowel sounds may reflect decreased gastric motility and constipation (common complication) related to limited fluid intake, poor food choices, decreased activity, and hypoxemia. Noxious tastes, smells, and sights are prime deterrents to appetite and can produce nausea and vomiting with increased respiratory difficulty. Helps reduce fatigue during mealtime, and provides opportunity to increase total caloric intake. Can produce abdominal distention, which hampers abdominal breathing and diaphragmatic movement and can increase dyspnea. Extremes in temperature can precipitate/aggravate coughing spasms.

NURSING DIAGNOSIS: deficient Knowledge [Learning Need] regarding condition, treatment, self-care, and discharge needs

May be related to

Lack of information/unfamiliarity with information resources

Information misinterpretation

Lack of recall/cognitive limitation

Possibly evidenced by

Request for information

Statement of concerns/misconception

Inaccurate follow-through of instructions

Development of preventable complications

DESIRED OUTCOMES/EVALUATION CRITERIA—CLIENT WILL:

Knowledge: Illness Care (NOC)

Verbalize understanding of condition/disease process and treatment.

Identify relationship of current signs/symptoms to the disease process and correlate these with causative factors.

Initiate necessary lifestyle changes and participate in treatment regimen

INTERVENTIONS Teaching: Disease Process (NIC) Independent Explain/reinforce explanations of individual disease process, including factors that lead to exacerbation episodes. Encourage client/significant other (SO) to ask questions. Discuss self-management plan:   Avoidance of triggers, and education regarding zones as appropriate;           Review breathing exercises, coughing effectively, and general conditioning exercises;           Regular oral care/dental hygiene;   Importance of avoiding people with active respiratory infections. Stress need for routine influenza/pneumococcal vaccinations;       Identify individual environmental factors that may trigger or aggravate condition; e.g., excessively dry air, wind, environmental temperature extremes, pollen, tobacco smoke, aerosol sprays, air pollution. Encourage client/SO to explore ways to control these factors in and around the home and work setting.	RATIONALE     Understanding decreases anxiety and can lead to improved participation in treatment plan.       Avoiding triggers (e.g., known allergens, environmental temperature extremes, chemical products and fumes) is important in the self-management of asthma and in the prevention of acute exacerbations. Zones may be divided into green (peak expiratory flow rate [PEFR] 80%–100% and no breathing difficulty), yellow (PEFR 50%–80% of baseline and some difficulty breathing with wheezing and coughing), and red (PEFR<50% baseline and does not respond to inhaled bronchodilators). Pursed-lip and abdominal/diaphragmatic breathing exercises strengthen muscles of respiration, help minimize collapse of small airways, and provide the individual with means to control dyspnea. General paced conditioning exercises (carried out regularly and perhaps timed with activity soon after taking medication or breathing treatments) can increase activity tolerance, muscle strength, and sense of well-being/quality of life. Decreases bacterial growth in the mouth, which can lead to pulmonary infections. Decreases exposure to and incidence of acquired acute upper respiratory diseases (URIs).         These can induce/aggravate bronchial irritation, leading to increased secretion production and airway blockage.
Review the harmful effects of smoking, and strongly advise cessation of smoking by client and/or SO. Provide information regarding smoking cessation recourses (e.g., QUITLINES, support groups, nicotine substitutes). Provide information about benefits of regular exercise while addressing individual activity limitations.         Discuss importance of regular medical follow-up care, when to notify healthcare professional of changes in condition, and periodic spirometry testing, chest x-rays, sputum cultures. Review oxygen requirements/dosage for client who is discharged on supplemental oxygen. Discuss safe use of oxygen and refer to supplier as indicated. Instruct client/SO in use of NIPPV as appropriate. Problem solve possible side effects and identify adverse signs/symptoms; e.g., increased dyspnea, fatigue, daytime drowsiness, or headaches on awakening. Instruct asthmatic client in use of peak flow meter as appropriate.   Provide information/encourage participation in support groups; e.g., American Lung Association, public health department.     Refer for evaluation of home care if indicated. Provide a detailed plan of care and baseline physical assessment to home care nurse as needed on discharge from acute care. Assist client/SO in making arrangements for access to emergency assistance (e.g., buddy system for getting help quickly, special phone numbers, “panic button”). Facilitate discussion about healthcare directives, end-of-life wishes as indicated.		Cessation of smoking may slow/halt progression of COPD. Even when client wants to stop smoking, support groups and medical monitoring may be needed. Note: Research studies suggest that “side-stream” or “second-hand” smoke can be as detrimental as actually smoking. Having this knowledge can enable client/SO to make informed choices/decisions to reduce client’s dyspnea, maximize functional level, perform most desired activities, and prevent complications. This may include alternating activities with rest periods to prevent fatigue, learning ways to conserve energy during activities (e.g., pulling instead of pushing, sitting instead of standing while performing tasks; use of pursed-lip breathing, side-lying position, and possible need for supplemental oxygen during sexual activity).   Monitoring disease process allows for alterations in therapeutic regimen to meet changing needs and may help prevent complications. Reduces risk of misuse (too little/too much) and resultant complications. Promotes environmental/physical safety.   NIPPV may be used at night/periodically during day to decrease CO2 level, improve quality of sleep, and enhance functional level during the day. Signs of increasing CO2 level indicate need for more aggressive therapy. Peak flow level can drop before client exhibits any signs/symptoms of asthma during the “first time” after exposure to a trigger. Regular use of the peak flow meter may reduce the severity of the attack because of earlier intervention. These clients and their SOs may experience anxiety, depression, and other reactions as they deal with a chronic disease that has an impact on their desired lifestyle. Support groups and/or home visits may be desired or needed to provide assistance, emotional support, and respite care. Provides for continuity of care. May help reduce frequency of rehospitalization.   Client with chronic respiratory condition should have access to prompt assistance wheeeded. This is both necessary and psychologically comforting for self-management. Although many clients have an interest in discussing living wills, their wishes may be unspoken. In client with severe pulmonary disease, it is helpful to discuss specific treatment preferences (e.g., aggressive treatment, home care only, hospitalization for comfort care, full life support). It is useful also to discuss the goals of care (e.g., functional independence or continuation of life support in an extended care nursing facility).

 

Teaching: Disease Process (NIC) Discuss respiratory medications, side effects, drug interactions, adverse reactions.     Demonstrate correct technique for using a MDI, such as how to hold it, pausing 2–5 min between puffs, cleaning the inhaler. Devise system for recording prescribed intermittent drug/inhaler usage.   Discuss use of herbals, especially when client is on multiple respiratory medications.       Recommend avoidance of sedative antianxiety agents unless specifically prescribed/approved by physician treating respiratory condition.

Frequently these clients are simultaneously on several respiratory drugs that have similar side effects and potential drug interactions. It is important that client understand the difference betweeuisance side effects (medication continued) and untoward or adverse side effects (medication possibly discontinued/dosage changed). Proper administration of drug enhances delivery and effectiveness.   Reduces risk of improper use/overdosage of prn medications, especially during acute exacerbations, when cognition may be impaired. Many interactions can occur between herbals and medications used to treat respiratory disorders. Although most herbals do not have dangerous side effects, effects can be dangerous or lethal if combined with other substances or when taken in larger doses (e.g., ephedra should only be used in very small doses and for a short time; ecchinacea can alter the actions of a variety of drugs, and is not recommended for persons with HIV infection, multiple sclerosis (MS), and other auto immune disorders). Although client may be nervous and feel the need for sedatives, these can depress respiratory drive and protective cough mechanisms. Note: These drugs may be used prophylactically when client is unable to avoid situations known to increase stress/trigger respiratory response.

 

POTENTIAL CONSIDERATIONS following acute hospitalization (dependent on client’s age, physical condition/presence of complications, personal resources, and life responsibilities)

Self-Care Deficit, specify—intolerance to activity, decreased strength/endurance, depression, severe anxiety.

ineffective Home Maintenance—intolerance to activity, inadequate support system, insufficient finances, unfamiliarity with neighborhood resources.

risk for Infection—decreased ciliary action, stasis of secretions, tissue destruction, increased environmental exposure, chronic disease process, malnutrition.

 

 

References British Thoracic Society (2006) Clinical Component for the Home Oxygen Service in England and Waleswww.brit-thoracic.org.uk/Portals/0/Clinical Information/Home Oxygen Service/clinical adultoxygenjan06.pdf Buckman, R. (1992) How to Break Bad News: A Guide for Healthcare Professionals. Baltimore, MD: John Hopkins University Press. Duck, A. (2007a) Interstitial lung disease 1: diagnosis and investigation. Nursing Times; 103: 43, 28–29. Duck, A. (2007b) Interstitial lung disease 2: management strategies. Nursing Times; 103: 44, 26–27. Duck, A. (2006) Cost-effectiveness and efficacy in long-term oxygen therapy. Nursing Times;102: 7, 46. Ellershaw, J., Wilkinson, S. (2003) Care of the Dying. A Pathway to Excellence. Oxford: Oxford University Press. Fallowfield, L. et al (1995) No news is not good news: information preferences of patients with cancer. Psycho-oncology; 4: 3, 197–202. Hicks, S. et al (2007) Ambulatory oxygen in idiopathic pulmonary fibrosis: of what benefit? Thorax; 62: 12 (Supplement 111), A1–A168. Johnston, I. et al (2006) Connecting for Health – Do Once and Share Interstitial Lung Diseasenwww.informatics.nhs.uk/cgi-bin/library.cgi?action=detail&id=2704&dir_publisher_varid=2 Miller, J. (2000) Coping with Chronic Illness: Overcoming Powerlessness (2nd edn). Philadelphia, PA: F.A. Davis Company. Stewart, M. et al (2001) Group support for couples coping with a cardiac condition. Journal of Advanced Nursing; 33: 2, 190–199. Wells, A., du Bois, R. (1994) Prediction of disease progression in idiopathic pulmonary fibrosis. European Respiratory Journal; 7: 4, 637–639.