Case Study of a Patient with Chronic Obstructive Pulmonary Disease

The presented case is of a patient named R.S. who has a smoking history of many years, which can be directly tied to his development of chronic bronchitis, a chronic obstructive pulmonary disease (COPD) specified as Type B. It is estimated that in 90% of chronic bronchitis or “blue bloaters”, cigarette smoking is the major cause. Chronic bronchitis involves persistent and irreversible airway obstruction, due to the constant inflammation of the bronchial mucosa, leading to hypertrophy and hyperplasia of bronchial glands. The latter exposes the individual to higher risks of bacterial infections; often colonization of organisms such as Streptococcus or Staphyloccocus pneumoniae can be exhibited. This is due to the lost or impaired function of mucociliary clearance action which results from the replacement of certain sections of ciliated columnar epithelium by squamous cells in the bronchi. (Copstead &Banasik, 546-547)

R.S.’s clinical findings as a consequence of his chronic bronchitis are likely to include: being overweight, experiencing shortness of breath on exertion, producing excessive amount of sputum, having a chronic productive cough, as well as edema and hypervolemia just to name a few. (Copstead & Banasik, 548) Some of these signs and symptoms would be different if R.S. had emphysematous COPD. In emphysema (or “pink puffers”), there is weight loss, the cough is absent or negligible, and edema is not present. While central cyanosis and jugular vein distention are present in late chronic bronchitis, these pathologic manifestations are absent in emphysema. . (Copstead & Banasik, 549)

Additionally, some of the general diagnostic and pulmonary function tests are distinct in emphysema in comparison to chronic bronchitis. In the case of R.S. the arterial blood gas (ABG) values are the following: pH=7.32, PaCO2= 60mm Hg, PaO2= 50 mm Hg, HCO3- = 80mEq/L. R.S.’s laboratory findings are indicative of chronic bronchitis, where the pH and PaO2 are decreased, whereas PaCO2 and HCO3- are increased, when compare to normal indices. Based on the arterial blood gas evaluation, the physician can deduce that the increased carbon dioxide is due to the airway obstruction displayed by the hypoventilation. Furthermore the excessive mucus production in chronic bronchitis hinders proper oxygenation leading to the hypoxia. On the other hand, in emphysema the arterial blood gas values would include a low to normal PaCO2 and only a slight decrease in PaO2 which tend to occur in the later disease stages.

R.S. has been using the recommended treatment for his condition, which inlcude inhaled short-acting Beta-2 agonist and Theophylline, a bronchodilator, to control his respiratory disease.