Manifestations of COPD are associated with episodes of moderate-severe respiratory impairment due to obstruction of airflow, which is greater on expiration than inspiration, resulting in increased work of breathing but decreased effectiveness. Pt’s chest X-ray showed cardiomegaly with mild vascular congestion and retrocardiac atelectasis.
In patients that have moderately severe COPD, their drive to breathe becomes oxygen because their body retains too much carbon dioxide. This will increase the risk of patients developing hypercapnia and requiring supplemental oxygen therapy. An increase in arterial carbon dioxide leads to an increase depth and rate of respiration. Over time, COPD patients will have high arterial levels of carbon dioxide and low levels of oxygen. The central chemoreceptors become less sensitive to these changes, consequently the stimulus to breathe is now managed by the peripheral chemoreceptors located in the carotid bodies and the aortic arch. These receptors are stimulated by low arterial levels of oxygen, and leads to hypercapnia. Thus, if supplemental oxygen is required, small changes to the rate of administration can have significant effects in those who have a hypoxic drive to breathe.
(Porth, 2011)
GERD
Gastroesophageal reflux is the backward flow of stomach contents into the esophagus without associated vomiting. It is caused by relaxation of the lower esophageal sphincter. Normal LES pressure is 10-30 mmHg and is under muscular, hormonal and neural control. In patients with GERD, the pressure is less than 10 mmHg. The decreased pressure is what allows the reflux stomach contents. Mucosal damage and erosion can result form this disease because the esophageal mucosa does not have the same protective lining mechanism as the stomach. This disease becomes chronic when the esophagus is exposed to gastric contents for a prolonged period, and an inflammatory process is initiated. The normal squamous epithelial cells are replaced with columnar epithelium,