Chronic obstructive pulmonary disease (COPD) is a serious respiratory disorder that is quite common and dangerous because of the patients rather than its revelations. Coughing and breezing difficulties are not paid attention to by those people, who smoke much or work in some hazardous conditions. However, these complaints can be the first symptoms of COPD. The same as with any other disease, it is important to accurately and promptly diagnose a patient and prescribe them a treatment course. R.S. case study reveals a typical clinical manifestation of COPD, assesses the patient’s risk of cardiovascular disease, and allows for a conclusion that a patient’s treatment is reasonable.
A single case of COPD clinical presentation, possible consequences and a prescribed variant of treatment for R. S. may be helpful for generalizing similar symptoms and developing most effective treatment for such patients. Nowadays, there exists a dilemma in the diagnosis assessment of COPD. It is defined as both a state characterized with an airflow limitation and “a complex syndrome with numerous pulmonary and extrapulmonary componentes” (Han et al., 2010, p. 599). The clinical findings that R. S. may have as a consequence of his COPD include: (a) barrel-chest appearance; (b) diminished breath sounds; (c) coughing with sputum; (d) wheezing (depending on the degree of bronchoconstriction); and (e) crackles and bronchial breath sounds exceeding the respiration line length (RLL). The patient may also have some form of cyanosis conditioned by polycythemia, but in order to confirm this supposition, the results of a hemoglobin test are needed. The manifestations like “decreased fat-free mass, impaired systemic muscle function, osteoporosis, anemia, depression, pulmonary hypertension, corpulmonale, left-sided heart failure” become systematic (Mosenifar, 2015, para. 4), and R. S. may reveal some of them due to his long COPD and smoking history.
As it was mentioned in the introduction, smoking is a risk factor for the COPD development. Those people, who are exposure to many toxins from the environment, may also develop emphysema, when “the lung tissue loses its elasticity, the alveoli become distended with trapped air, and the walls of the alveoli are destroyed” (Mistovich, Karren & Hafen, 2013, p. 451). Though the revelations of emphysema are similar to the signs of other respiratory diseases, the consequences of R.S.’s state differ from the manifestations of emphysematous COPD. These differences lie in the fact that R.S. shows minimal anxiety and breathing difficulties, as well as coughing with much sputum. Emphysema patients, as a rule, have serious breathing difficulties, little sputum, while coughing, and having prolonged exhalation. A physician may expect more diminished breath sound in emphysematous COPD, but more wheezing and coarse crackles in R.S.’s case (Mistovich, Karren, Hafen, 2013). An “A-to-E” test is a typical verification of emphysema. While pronouncing prolonged “EEEE” many times, emphysema patients will turn this sound into “AAAA” in the lung areas, where the air is significantly trapped. This sound substitution does not take place with the COPD patients.
Undoubtedly, laboratory tests add much accuracy to the clinical diagnosis. R.S.’s results verify that this patient has acidosis that may be classified as partially compensated. He has moderate hypoxemia and mild polycythemia, which was mentioned above. The fact that his pH is acidotic confirms that even if there is some compensation, it is not complete. The PaCO2 conforms to the acidosis state and demonstrates its respiratory nature. The level of bicarbonate proves that it is a respiratory disorder and not a mixed state. Therefore, R.S. has a partially compensated respiratory acidosis. The patient’s PaO2 value is an indicator of moderate hypoxemia. It is possible to calculate the total arterial oxygen content only having the value of the hemoglobin level. However, the state of polycythemia proves that this content is most likely normal. R.S. has a secondary polycythemia not related to any gene modification (National Heart, Lung, and Blood Institute [NHLBI], 2011). “Secondary polycythemia isn’t related to the JAK2 gene. Long-term exposure to low oxygen levels causes secondary polycythemia” (NHLBI, 2011, para. 3). R.S.’s state developed due to chronic hypoxemia. The defined incomplete compensation and polycythemia prove that this is an acute problem originated from a chronic disorder. It takes some months for polycythemia to develop and the kidneys need several days to completely compensate the determined acidosis. Therefore, R.S. has passed all necessary tests, apart from a hemoglobin index, to characterize his state.
Grimes, Manning, Patel and Via (2007) emphasize that COPD is the fourth leading cause of death in the USA. The authors state that this disease can be preventable and easily treated. There exist numerous schemes and courses for treating patients with different degree of COPD severity. The medical drugs most commonly used include inhaled anticholinergics, corticosteroids, long-acting ?2 agonist or mucolytics. According to the article created by Grimes et al. (2007), “treatment with theophylline may cause a small improvement in FEV1 [forced expiratory volume 1-second]; however, it is poorly tolerated, requires monitoring, and does not improve patient-oriented outcomes such as breathlessness” (p. 1146). The trial demonstrated that the combination of these two drugs is much more efficient than any of them prescribed alone. At the same time, the experiment proved that a ?2 agonist was superior than theophylline, when combined, “showed the lack of benefit with theophylline in quality of life and in exacerbation occurrence” (Grimes et al., 2007, p. 1146). Theophylline gives serious gastrointestinal side effects and brings more risks than benefits (Grimes et al., 2007).
At first glance, there are no significant reasons for prescribing R.S. a combined treatment with theophylline and a ?2 agonist. In order to determine why this direction of treatment was chosen for R.S. regardless of all the complications, it is important to consider the material created by Barnes (2006). The author believes that although newly invented and more progressive medicine has substituted theophylline, the drug will most likely regain its popularity. The results of the latest experiments demonstrate that the criticized medication has a strong anti-inflammatory power: “theophylline may have a unique effect in the treatment of COPD by restoring reduced HDAC [histone deacetylase] activity to normal levels, thus suppressing inflammation but also potentially making the patients responsive to corticosteroids” (Barnes, 2006, p. 744). Therefore, if R.S.’s physician have taken Barnes’ s (2007) opinion as a foundation for his prescription, there would be a strong rationale in treating the patient with an anti-inflammatory drug and ?2 agonist that has proved its effectiveness in all possible medical combinations.
One of the most common symptomatic features of COPD is a cardiovascular disease. “A number of population studies have shown that airflow limitation as measured by FEV1 or FEV1/FVC ratio is a predictor of cardiovascular risk” (MacLay & MacNee, 2013, p. 798). The mechanism that is responsible for a cardiovascular disease of the COPD patients is unknown. However, medical scholars have developed a theory about the effects which the state may have on a heart function. They confirm that it is impossible to reveal a direct correlation between COPD alone and a cardiovascular disorder. The patients, who were heavy-smokers and diagnosed with COPD, like R. S., revealed carotid intimal medial thickness an evidence of atherosclerosis. A systematic inflammation, stemming from R. S.’s treatment with theophylline, greatly increases the risk of rheumatoid arthritis, which in its turn, stimulates the development of a cardiovascular disease. These cellular mechanisms are complex and can be represented in a chain. The vascular endothelium injury, which makes it more permeable – lipoproteins, entering the intima – modified lipoproteins, systematic oxidative stress and inflammation provoke cytokine production and increase the expression of cell adhesion molecules, such on the vascular endothelium – circulating leukocytes attach to damaged endothelial surface – these leukocytes penetrate into the vascular intima and promote foam cells development. As a result, vascular smooth musclecells migrate from the media into the intima and give birth to the extracellular matrix, which accumulates in the plaque and forms fibro fatty lesions. This process results in vessel wall fibrosis and consequent smooth muscle cell death (MacLay and MacNee, 2013). Hence, R.S. is at risk of his cardiovascular function to be seriously disturbed. Fabbri, Luppi, Beghe and Rabe (2008) write about chronic comorbidities caused by COPD. A cardiovascular problem is one of them. The authors agree with MacLay and MacNee (2013) about the factors leading to the development of cardiovascular problems and state that “in addition to smoking, the other major risk factor for cardiovascular and other chronic comorbid conditions is obesity” (Fabbri et al., 2008, p. 205). This state is associated with the presence of inflammatory markers and elevated concentrations of cytokines (Fabbri et al., 2008). Therefore, scholars and medical specialists still research a connection between the effects of COPD and a cardiovascular disease, but they have already determined that smoking, obesity and constant inflammation seriously affect the patients’ cardiovascular function.
Taking everything into consideration, it is difficult to underestimate the severity of COPD. The analyzed case of R. S. is a reasonable foundation for researching the basic indices, symptoms and complications of the patient. He has mostly likely applied to the physician not at once. Thus, he has some side effects developed and health risks determined. At the same time, the results of his medical tests and his physician’s progressive and well-thought-out approach to treatment may improve R.S.’s quality of life. The most important for him now is to follow the doctor’s prescriptions and lead a healthy lifestyle without smoking.
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