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Comprehensive care plan for a 65-year-old woman with emphysema

Last reviewed: January 28, 2014 ~24 min read
Abstract

Researchers and clinicians are becoming more aware that patients with progressive, chronic lung diseases may be suffering from multiple conditions, including asthma, COPD, emphysema, chronic bronchitis, pneumonia, and lung cancer. The diagnostic tests that can discriminate between the different diseases are available and effective, but more research needs to be done into the best treatment approaches. This report examines the pathophysiology, signs and symptoms, diagnostic tests, and treatment recommendations for patients suffering from what has been called ‘overlap syndrome.’

Essay 4,687 words

Chronic Lung Disease Care Planning

Respiratory Care

A Case Study in Chronic Lung Disease Care Planning

A Case Study in Chronic Lung Disease Care Planning

A 65-year-old Caucasian woman is the subject of this case study. Symptoms include a dry nocturnal cough lasting two weeks, mild morning sore throat, and anorexia. The cough is worse when lying down and all symptoms have worsened over the past two days. Chest X-ray (CXR) revealed hyperinflation of lungs, increased AP diameter, and evidence of emphysema. Physical examination revealed prehypertension, body mass index (BMI) of 30.2 (obese), normal sinus rhythm, tachypnea, SpO2 at 98%, and leukocytosis with a left shift. Patient self-efficacy is low and she remains resistant to further diagnostic testing, possibly due to depression and/or cost concerns, despite reporting feeling better after a course of antibiotic therapy and inhaler use. The relevant patient history includes childhood asthma and life-long heavy smoking. One older sister developed osteoporosis and the other breast cancer as seniors. The signs and symptoms of primary concern are dyspnea, leukocytosis, fever, tachypnea, prehypertension, obesity, emphysema, asthma, depression/anxiety, and low patient self-efficacy.

Having been a widow for 20 years and living on a $40,000 annual pension the patient does not have the financial resources to cover expensive diagnostic testing. Prescription medications are often not covered by her insurance plan, which forces her to rely heavily on free samples. Two middle-aged healthy daughters visit once a month, but a desire to grow closer has not been acted upon. Her desire to spend more time with daughters may be related to a perception of declining self-efficacy, social isolation, and chronic depression. Regular church attendance has fostered connections with a few community residents, but the patient spends most of her time alone. Although she attends an occasional church function, she has remained ignorant of the many other services offered in her community. The primary socioeconomic concerns are social isolation, medical costs, and moderate estrangement from family members.

Despite personal awareness of the benefits of a healthy lifestyle, the patient fails to get any exercise due to shortness of breath. The patient has been smoking a pack of cigarettes a day for the past 40 years and reports eating a healthy diet. She is knowledgeable about the benefits of a healthy lifestyle; however, the main personal efficacy concerns are her resistance to diagnostic testing, continued smoking, sedentary lifestyle, obesity, and possible nutritional concerns.

Given the above assessment of the patient's medical issues, history, and socioeconomic concerns, an individualized patient care plan will be created. Special attention will be paid to pathophysiology, diagnostic testing, treatment recommendations, and the role and scope of integrated disease management.

Epidemiology of Common Pulmonary Diseases in Older Adults

Lung diseases, such as pneumonia, COPD, asthma, lung cancer, and fibrosis, are common ailments among aging adults (Akgun, Crothers, & Pisani, 2012). In smokers, the primary pulmonary concerns are emphysema, chronic bronchitis, and COPD. Most of these are relevant to the patient under consideration here. If the patient under consideration here has pneumonia it is probably community acquired, since the patient has not been hospitalized recently. In older U.S. adults an estimated 350,000 to 620,000 individuals are hospitalized each year due to community acquired pneumonia, with an incidence of 14 in 1,000. By comparison, over 10% of adults over the age of 65 have been diagnosed with COPD. The COPD incident rate for men over 55-years of age is equal to pneumonia, but it is half that for women. Asthma is also common, estimated to afflict between 4% and 8% of adults over the age of 65. Unfortunately, opportunities for effective treatment are missed because asthma is frequently misdiagnosed as COPD in older adults. The incidence of lung cancer peaks between the ages of 75 and 79, with most diagnoses occurring after the age of 60. Recent estimates suggest the incidence for men and women who are 65-years and older, between the years 2005 and 2009, was 4.2-5.5 and 2.9-3.2 per 1,000 residents, respectively (Henley et al., 2014). Other smoking related diseases, such as emphysema and chronic bronchitis, affect an estimated 5-6% and 6-7% of the U.S. population over the age of 65, respectively (Schiller, Lucas, & Peregoy, 2012, p. 152).

Pathophysiology, Symptoms & Signs, and Diagnostic Criteria of Chronic Lung Diseases

Most patients with chronic pulmonary disease will present with cough and dyspnea, but the presenting symptoms for older adults can sometimes be atypical, especially patients with chronic comorbid conditions (Akgun, Crothers, & Pisani, 2012). In older adults, community acquired pneumonia (CAP) typically causes tachypnea, delirium, and failure to thrive, rather than the cardinal signs and symptoms of fever, cough, and purulent sputum. For this reason, a diagnosis of pneumonia in older adults is frequently delayed. Streptococcus pneumoniae is the most frequent pathogen found to be causing CAP (Garau & Calbo, 2008). Some of the other pathogens that can cause CAP in patients with lung disease include Haemophilis influenzae and Moraxella catarrhalis. Antibiotic therapy to rid the patient of the offending pathogen(s) is typically done empirically, most often with a ? lactam and macrolide combination (Drancourt, Gaydos, Summersgill, & Raoult, 2013). The reason for empiric antibiotic therapy is because the reliability and turnaround times of laboratory tests has been historically low and slow, respectively. Recent advancements in point-of-care testing have generated several rapid diagnostic tests that can provide some information is as little as 1 to 3 hours, but these tests are not universally available, nor comprehensive.

The main diagnostic indicators of a pulmonary infection are fever and leukocytosis (Mouton et al., 2001). In older adults (? 65-years) thermoregulatory responses can be poor; therefore, an increase in body temperature of 2° F. Or more should be cause for concern. If the temperature reaches 101° F. Or higher, a severe, life-threatening infection may be present and immediate hospitalization required. The patient considered here has a fever of 101° F, leukocytosis (> 11x10-9/L), and tachypnea, but does not have chest pains, hypoxemia, tachycardia, productive cough, or radiologic findings consistent with pneumonia (Albert, 2010); however, older adults often present with only a cough and a definitive diagnosis is obtained in only a minority of patients (Mouton et al., 2001). Given the serious condition of this patient, blood cultures should be performed, in addition to culturing sputum and conducting any rapid diagnostic tests that may be available. These tests must be performed to check for the presence of antibiotic-resistant strains. The patient under consideration here has most of the symptoms associated with CAP, including tachypnea, dyspnea, failure to thrive, malaise, fever, cough, and leukocytosis, which is enough to justify beginning empiric antibiotic therapy despite an unproductive cough and negative CXR. The risk of pneumonia-associated mortality is so great in adults over the age of 65, especially those with preexisting lung disease, that antibiotic therapy should be administered immediately for this patient.

Many of the same symptoms are found in patients with COPD, with chronic cough being the best predictor for smokers (Akgun, Crothers, & Pisani, 2012). The main presenting symptoms are cough, chronic sputum production, wheeze, and dyspnea. The experience of dyspnea can be so frightening in older adults with severe COPD that depression and anxiety are common. A definitive diagnosis of COPD is based on the presence of an airway obstruction, which can occur in a number of chronic airway diseases and conditions, including asthma, chronic bronchitis, and emphysema (Nakawah, Hawkins, & Barbandi, 2013). The obstruction can be caused by inflammation, bronchospasms, mucosal edema, mucus plugs, and smooth muscle hypertrophy and hyperplasia.

Differentiating asthma patients from those with COPD can be difficult, often leading to a misdiagnosis (Akgun, Crothers, & Pisani, 2012). A defining feature of COPD and asthma is a reduction in forced expiratory volume in the first second (FEV1) below normal limits (GICOPD, 2013, p. 7); however, total lung capacity (TLC) and carbon monoxide diffusing capacity (DLCO/VA) will be normal or above normal in asthma, whereas patients with COPD will have an elevated TLC and reduced DLCO/VA (Pelligrino et al., 2005). In addition, asthmatics will typically have a greater bronchodilator response compared to COPD patients, although COPD patients may experience some improvement due to the inflammatory component of their disease. A differential diagnosis is important because asthma is more responsive to treatment (Snider, 1985), while COPD is a progressive disease that develops later in life and the obstruction only partly relieved by bronchodilator use (Nakawah, Hawkins, & Barbandi, 2013). The severity of COPD is graded based on FEV1 scores and symptomology (Albertson, Louie, & Chan, 2010). FEV1 scores of > 80%, 50-80%, 30-50%, and < 30% are Stage I, II, III, and IV, respectively. When exacerbations occur they become clinically significant when acute worsening of dyspnea, cough, and sputum volume/purulence happens over a relatively short period of time.

COPD patients are typically heavy smokers presenting with hyperinflated lungs, hypoxemia, and diffusion impairment (Akgun, Crothers, & Pisani, 2012). The patient considered here has hyperinflated lungs and is a heavy smoker (Wender et al., 2013), but is not hypoxemic based on pulse oximetry (Pretto, Roebuck, Beckert, & Hamilton, 2014). The absence of hypoxemia at rest, however, does not preclude a diagnosis of COPD since exercise may reveal impaired oxygen diffusion capacity (Andrianopoulos et al., 2014). The inflammation component in COPD is primarily neutrophilic and CD8 T cell driven, which is consistent with the patient's leukocytosis with a left shift. By comparison, asthma is primarily an inflammatory disease commonly associated with a type 2 T. helper responses and eosinophilia (Akgun, Crothers, & Pisani, 2012). In patients with combined asthma and COPD, smoking will induce neutrophilia and steroid resistance. For the patient under consideration here a diagnosis of COPD is supported by the CXR findings of bilateral hyperinflation, increased AP diameter, leukocytosis, and signs of emphysema ("Emphysema," n.d.). The absence of chronic sputum production argues against a diagnosis of COPD, but this symptom may be absent in older patients with severe disease (Snider, 1985). A lung function test revealing a below normal FEV1 and DLCO/VA for this patient would be sufficient confirmation for a diagnosis of COPD, but given the patient's resistance to lung function testing a less demanding 6-minute walk test for exercise-induced hypoxemia (? 88%) using pulse oximetry might be more feasible (Andrianopoulos et al., 2014).

Not so long ago COPD was defined in part by the inclusion of the terms 'emphysema' and 'chronic bronchitis,' but the most recent definition by the Global Initiative for Chronic Obstructive Lung Disease (GICOPD) has deemphasized the use of these terms (GICOPD, 2013, p. 1). From their perspective, emphysema represents the functional destruction of alveoli and is thus a pathological term, not a clinical one; therefore, the term 'emphysema' describes one of several structural abnormalities that help define COPD. In addition, the hallmark symptoms of chronic bronchitis is cough and sputum production, which can occur in COPD, but chronic bronchitis can also occur independent of COPD and therefore represents a distinct disease. With this distinction in mind, the pathophysiology of emphysema and chronic bronchitis will be reviewed next.

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The radiological findings unique to emphysema are bullae and a lack of vascularization in the peripheral third of the lung ("Emphysema," n.d.). The main pathogenic risk factor for emphysema is inhaled tobacco smoke (Snider, 1985) and the patient in this case study has been a heavy smoker for the past 40 years. Over time the pulmonary capillary bed and alveolar septa is destroyed by cigarette smoke, resulting in the loss of elastic lung tissue recoil, the trapping of air in the peripheral lungs, and hyperinflation (MacNee, 2005). The diagnostic indicators are decreased FEV1 / FVC ratio, elevated TLC, and low DLCO/VA (Pelligrino et al., 2005). A bronchodilator challenge will typically reveal little improvement, but this is less true in COPD patients. Typical radiologic findings are hyperinflation of the lungs, increased AP diameter, bullae, and reduced vascularization ("Emphysema," n.d.). The morphological changes are irreversible and in severe disease the loss of elastic recoil inhibits bronchial drainage (Snider, 1985). For this reason, the lower airways are susceptible to the development of chronic bronchitis and inflammation. A definitive diagnosis of emphysema will require a lung function test with bronchodilator challenge.

Chronic cough and sputum production define chronic bronchitis and these symptoms are triggered by an inflammatory response to cigarette smoke (MacNee, 2005). The primary pulmonary structures affected are the central airway epithelium and mucus-producing glands, resulting in excess mucus production, reduced mucus clearance, and increased airway epithelium permeability. The role that excess mucus production plays in COPD is uncertain, but could represent a downstream event triggered by inflammatory cell protease secretion. Chronic bronchitis is defined as 3 or more months of cough and sputum production each year for two years in a row, in the absence of other diseases that can cause a cough (Albertson, Louie, & Chan, 2010). Chronic bronchitis is a common comorbid condition in COPD patients.

When chronic bronchitis exacerbations occur the most common symptoms are increased volume of sputum production, altered sputum color (darker), and worse dyspnea (Albertson, Louie, & Chan, 2010). When all three are present the disease severity is considered Type I, but when only two out of three are present the exacerbation is Type II. If only one symptom is present, in addition to wheezing, worse cough, fever, increased heart rate, or increased respiration rate, then disease severity is Type III. The exacerbation risk factors are age, malnutrition, cardiac disease, smoking, recent viral infections, chronic lung disease, and alcoholism. The main triggers for exacerbations are pathogens (80%), including bacteria, viruses, and atypical pathogens; however, tobacco smoke, poor patient self-efficacy/compliance, and congestive heart failure will also trigger exacerbations. Antibiotic therapy has been shown to be effective for reducing adverse outcomes for patients experiencing a chronic bronchitis exacerbation. The pathogen(s) responsible can sometimes be predicted by the baseline FEV1. Gram-positive cocci infections for example, especially by S. pneumoniae, tend to be associated with a minimal change in FEV1, whereas H. influenzae and M. catarrhalis are most often found in patients with a greater reduction in FEV1. A still greater reduction in FEV1 can be caused by enterobacteria species and Pseudomonas. The patient under consideration here would be classified as experiencing a Type III chronic bronchitis exacerbation because of the worsening dyspnea, fever, and tachypnea, but a definitive diagnosis of the pathogen(s) responsible will have to await sputum cultures.

Diagnosis

The history of heavy smoking, childhood asthma, dyspnea with physical activity, and signs of emphysema on CXR is consistent with a diagnosis of COPD. Although the chronic cough is only two weeks old, sputum production is absent, and the patient is not hypoxemic, the dyspnea, wheeze, and radiological findings support a preliminary diagnosis of COPD. The absence of sputum does occur in patients with severe lung disease due to impaired airway clearance (Snider, 1985) and hypoxemia may only be evident with physical activity (Andrianopoulos et al., 2014). A definitive diagnosis of COPD should be obtained with a lung function test, if the patient is willing. A lung function test would also help differentiate between asthma and COPD. In addition, a 6-minute walk test with pulse oximetry could be used to evaluate the patient for exercise-induced hypoxemia (Andrianopoulos et al., 2014).

The most immediate concern is the fever and absence of sputum production. The fever, together with leukocytosis, supports a diagnosis of lower airway infection; however, the absence of CXR signs for pneumonia is more consistent with a diagnosis of chronic bronchitis with an acute exacerbation due to infection. The recurrent exacerbations in the patient's history also support this diagnosis. The severity of the acute exacerbation of chronic bronchitis is Type III based on worsening dyspnea, wheezing, fever, tachypnea, and tachycardia. Given the likely diagnosis of COPD, the absence of sputum production is worrying because it may be a symptom of impaired airway clearance.

To summarize, a preliminary diagnosis of COPD and emphysema seems appropriate pending a lung function test, together with a diagnosis of acute exacerbation of chronic bronchitis due to an airway infection. Asthma could also be a contributing factor and the findings of a bronchodilator challenge could be definitive.

Diagnostic Tests

Sputum, pharyngeal swabs, blood, and urine should be collected for culture and other diagnostics tests used to detect and characterize common airway pathogens. A lung function test with bronchodilator challenge should be performed, if the patient is willing and capable. FEV1, FVC, TLC, FRC, RV, and DLCOA should be determined. A lung biopsy may be indicated depending on the lung function test results. The patient should also be encouraged to take a 6-minute walk test for exercise-induced hypoxemia. Arterial blood gases should be analyzed for hypoxemia and pH, since hyperventilation tends to increase pH. In light of the patient's obesity and sedentary lifestyle a metabolic panel should be run to check for metabolic syndrome. Sedentariness and metabolic syndrome has been associated with systemic inflammation, which could be contributing to pulmonary inflammation (Yawn, 2012).

Care Plan: Integrated Disease Management

Despite the patient's past resistance to diagnostic testing the symptoms were severe enough to cause her to seek medical help, which implies that the patient is probably very sick and anxious about her health. The worsening of a non-productive cough, morning sore throat, fever, and mild anorexia over the past two days should be cause for concern; however, psychogenic dyspnea and COPD exacerbations can occur secondary to generalized anxiety disorder and depression, respectively (Wahls, 2012). The patient has expressed concerns that she might have heart disease or cancer, which may be a sign of generalized anxiety disorder; however, the fever and leukocytosis supports a diagnosis of acute exacerbation of chronic bronchitis due to a lower airway infection.

The patient should be immediately admitted and empirically administered an antibiotic cocktail containing a macrolide and ? lactam to combat the suspected airway infection (Drancourt, Gaydos, Summersgill, & Raoult, 2013) and neutrophilic inflammation (Simpson, Phipps, & Gibson, 2009). Systemic glucocorticoids and a short-acting bronchodilator will also be administered to control the inflammation caused by the acute exacerbation (Nakawah, Hawkins, & Barbandi, 2013). Blood oxygen saturation levels will be monitored using pulse oximetry and if indicated oxygen administered.

The above steps are intended to stabilize the patient's health in the short-term, but there are significant barriers to effective long-term management of the suspected COPD, chronic bronchitis, and asthma. The patient's resistance to hospitalization and lung function testing precludes a more definitive diagnosis and individualized treatment plan (Yawn, 2012). The patient has revealed that she is on a fixed income and has basic medical coverage, yet is forced to rely on samples for prescription medication not covered by her insurance plan. The economic barriers are therefore significant and may be contributing to her resistance to being admitted and more comprehensive diagnostic testing.

The patient also feels socially isolated. She has two healthy daughters and two healthy sisters, who seem willing to be engaged in her life, but she has failed to reach out to them to express her need for greater intimacy. Depression could also be contributing to the patient's self-report of declining self-efficacy over the past 10 years. The socioeconomic barriers to effective long-term management of COPD, chronic bronchitis, and asthma are therefore medically underinsured, low fixed-income, depression/anxiety, and social isolation.

The patient will require an integrated disease management (IDM) approach to address the several treatment barriers that have been identified. Such an approach has proven to be effective for improving COPD patient quality of life, exercise tolerance, emotional state, and self-efficacy, in addition to reducing dyspnea severity, hospitalizations, and length of stays (Kruis, 2013). The IDM approach will involve coordination of care by nursing staff and involve a team consisting of pulmonologist, social worker, dietician, physical therapist, psychiatrist, and psychologist.

The social worker will begin working with the patient to address the economic barriers. The patient's economic needs will be identified and potential sources of assistance located, including those available through the patient's community and church. The patient's minister could be an important source of emotional and spiritual help for the patient, in addition to adding to the knowledge base of what resources are available in the community. The main focus of this assistance would be the identification of resources that can compensate for the shortcomings of the patient's medical coverage plan, thereby minimizing the patient's concerns about medical expenses. These fears could be contributing to her resistance for comprehensive diagnostic testing and inpatient treatment.

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References
22 sources cited in this paper
  • Akgun, K. M., Crothers, K., & Pisani, M. (2012). Epidemiology and management of common pulmonary diseases in older persons. Journal of Gerontology: Biological Sciences, 67A(3), 276-91.
  • Albert, R. H. (2010). Diagnosis and treatment of acute bronchitis. American Family Physician, 82(11), 1345-50.
  • Albertson, T. E., Louie, S., & Chan, A. L. (2010). The diagnosis and treatment of elderly patients with acute exacerbation of chronic obstructive pulmonary disease and chronic bronchitis. Journal of the American Geriatrics Society, 58(3), 570-9.
  • Andrianopoulos, V., Franssen, F. M. E., Peeters, J. P. I., Ubachs, T. J. A., Bukari, H., Groenen, M. et al. (2014). Exercise-induced oxygen desaturation in COPD patients without resting hypoxemia. Respiratory Physiology & Neurobiology, 190, 40-46.
  • Drancourt, M., Gaydos, C. A., Summersgill, J. T., & Raoult, D. (2013). Point-of-care testing for community-acquired pneumonia. Lancet, 13, 647-9.
  • Emphysema. (n.d.). Retrieved from http://www.meddean.luc.edu/lumen/MedEd/Radio/curriculum/Mechanisms/emphysema4.htm.
  • Garau, J. & Calbo, E. (2008). Community-acquired pneumonia. Lancet, 371(9611), 455-458.
  • GICOPD. (2013). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease (updated 2013). Retrieved from: http://www.goldcopd.org/uploads/users/files/GOLD_Report_2013_Feb20.pdf.
  • Henley, J. S., Richards, T. B., Underwood, M. J., Sunderam, C. R., Plescia, M., McAfee, T. A. et al. (2014). Lung cancer incidence trends among men and women – United States, 2005-2009. Morbidity and Mortality Weekly Report, 63(1), 1-5.
  • Kruis, A. L., Smidt, N., Assendelft, W. J. J., Gussekloo, J., Boland, M. R. S., Rutten-van Molken, M. et al. (2013). Integrated disease management interventions for patients with chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews, 10, CD009437, doi: 10.1002/14651858.CD009437.pub2.
  • MacNee, W. (2005). Pathogenesis of chronic obstructive pulmonary disease. Proceedings of the American Thoracic Society, 2(4), 258-66.
  • Mouton, C. P., Bazulda, O. V., Pierce, B., & Espino, D. V. (2001). Common infections in older adults. American Family Physician, 63(2), 257-68.
  • Nakawah, M. O., Hawkins, C., & Barbandi, F. (2013). Asthma, chronic obstructive pulmonary disease (COPD), and the overlap syndrome. Journal of the American Board of Family Medicine, 26(4), 470-7.
  • Pelligrino, R., Viegi, G., Brusasco, V., Crapo, R. O., Burgos, R., Casaburi, A. et al. (2005). Interpretive strategies for lung function tests. European Respiratory Journal, 26(5), 948-68.
  • Pretto, J. J., Roebuck, T., Beckert, L., & Hamilton, G. (2014). Clinical use of pulse oximetry: Official guidelines from the Thoracic Society of Australia and New Zealand. Respirology, 19(1), 38-46.
  • Schiller, J. S., Lucas, J. W., & Peregoy, J. A. (2012). Summary Health Statistics for U.S. Adults: National Health Interview Survey, 2011. Series 10, No. 256. Washington, D.D.: U.S. Government Printing Office. Retrieved from http://www.cdc.gov/nchs/data/series/sr_10/sr10_256.pdf.
  • Simpson, J. L., Phipps, S., & Gibson, P. G. (2009). Inflammatory mechanisms of obstructive airway diseases with neutrophilic bronchitis. Pharmacology & Therapeutics, 124(1), 86-95.
  • Sniderl, G. L. (1985). Distinguishing among asthma, chronic bronchitis, and emphysema. Chest, 87(1), 35S-39S.
  • Thomsen, M., Ingebrigtsen, T. S., Marott, J. L., Dahl, M., Lange, P., Vestbo, J. et al. (2013). Inflammatory biomarkers and exacerbations in chronic obstructive pulmonary disease. Journal of the American Medical Association, 309(22), 2353-61.
  • Wahls, S. A. (2012). Causes and evaluation of chronic dyspnea. American Family Physician, 86(2), 173-80.
  • Wender, R., Fontham, E. T., Barrea E. Jr., Colditz, G. A., Church, T. R., Ettinger, D. S. et al. (2013). American Cancer Society lung cancer screening guidelines. CA: A Cancer Journal for Clinicians, 63(2), 107-17.
  • Yawn, B. P. (2012). Is ‘GOLD’ standard for the management of COPD in clinical practice? Drugs in Context, article no. 212243, doi: 107573/dic.212243.
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PaperDue. (2014). Comprehensive care plan for a 65-year-old woman with emphysema. PaperDue. https://www.paperdue.com/essay/respiratory-care-plan-181571

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