This is a discussion post and I need to respond with a thoughtful answer in respond to her post. This is the post. Also please use whatever amount of references you need. Assessment of Emphysema Clinical symptoms of exacerbation of COPD/emphysema are dyspnea, tachypnea, use of accessory muscles, low o2 sats, ‘lip breathing’, barrel chest, cool, clammy, diaphoresis, prolonged expiration, hyperventilation (which causes hypercapnia) and cough. Pulmonary Function Test (PFT) Pulmonary function tests (PFT) are diagnostic tools to help in identifying abnormalities, probable causes, prognosis’, and treatments within the pulmonary system (Brashers, 2014). Charlene is having increased SOB and non-productive cough with low o2 sats. Patients’ with emphysema are known to have decreased forced expiratory volumes (FEV), forced vital capacity (FVC), increased functional residual capacity (FRC), residual volume (RV), and total lung capacity (TLC). FVC is defined at maximum amount of gas displaced from lungs during expiration. Patients with emphysema have decreased FVC due to the air trapping in distal portions of lungs (Brashers & Huether, 2014). These patients also have decreased FEV1 which is the amount of air flow during expiration in 1 second. According to the GOLD standards of COPD, this patient exhibits signs of a mild case of COPD (“COPD”, 2018). **PTF are influenced by race, gender, age, and height so it is somewhat difficult to interpret her results without having all the necessary values. Pathophysiology of Emphysema Emphysema is the abnormality of “permanent enlargement of gas-exchange airways accompanied by destruction of alveolar walls” (Brashers & Huether, 2014, p. 1269). There is a loss of elasticity and an imbalance between proteases and antiproteases, oxidative stress, and apoptosis (Brashers & Huether, 2014). An imbalance of these enzymes causes a decreased surface area within the lungs causing a disruption of gas exchange. The destruction within the alveolar walls causes air spaces to form called bullae and blebs. Due to decrease elasticity within the cells in the lungs, there is a deceased volume of air during expiration and air is trapped within the lungs, called air trapping (Brashers & Huether, 2014). Since there is a decrease in the diffuse capacity, which is the gas across the alveolocapillary membranes, hypoxia (low oxygenation) and hypercapnia (high Co2) are seen. Three Functions of the Brainstem (Respiratory Center) The brainstem is responsible for “transmitting impulses to the respiratory muscles which causes them to relax and contract” (Brashers, 2014, p. 1232). 1.) Neuroreceptors in the circulatory system and brainstem sense effectiveness of ventilation by monitoring pH in CSF and Pao2. 2.) Located in the medulla are dorsal respiratory group (DRG) are inspiratory nerve cells. The cells help regulate the diaphragm and inspiratory intercostal muscles by efferent impulses. DRG also receive signals from the peripheral chemoreceptors in the carotid and aortic bodies which measure and regulate the PaCo2 and Pao2. 3.) The ventral respiratory group (VRG) are located in the medulla, which control the inspiration and expiration phases of breathing. (Brashers, 2014). Oxyhemoglobin Dissociation Curve When hemoglobin and oxygen combine together it creates oxyhemoglobin (hbo2). The oxyhemoglobin dissociation curve is a curve on a graph that outlines the amount of hemoglobin that is oxygenated (vertical axis) versus the prevailing oxygen tension (horizontal axis). This graph helps better understand how blood carries and releases oxygen. Things that could shift the curve to the right would be low pH, hyperthermia, and hypercapnia. During this shift to the right, oxygen moves into the cells (Brashers, 2014). High pH, hypothermia, and hypocapnia are things that shift the curve to the left. Pathophysiology of Bronchitis There are two different types of bronchitis; acute and chronic. Acute bronchitis is usually caused by a virus. Symptoms are (non)productive cough, congestion, dyspnea, fevers, and generalized malaise. However, on a CXR there are no signs of pneumonia. Chronic bronchitis is defined as hypersecretion of mucus with constant productive cough lasting three months for two consecutive years (Brashers & Huether, 2014). In bronchitis, the airway is inflamed from cytokines releasing irritates; such as, neutrophils, macrophages, and lymphocytes, which causes bronchial edema and the number of mucous glands in the epithelium. This mucus cannot be cleared due to ciliary function being impaired. This causes muscle weakness and dyspnea (Brashers & Huether, 2014). References: Brashers, V.L. (2014). Chapter 34 Structure and Function of the Pulmonary System. In McCance, K. L., & Huether, S. E., The Pathophysiology: The Biologic Basis for Disease in Adults and Children (7th ed., pp. 1225-1247). Retrieved from VitalSource Bookshelf Brashers, V.L. & Huether, S.E. (2014). Chapter 35 Alterations of Pulmonary Function. In McCance, K. L., & Huether, S. E., The Pathophysiology: The Biologic Basis for Disease in Adults and Children (7th ed., pp. 1248-1289). Retrieved from VitalSource Bookshelf Pocket Guide to COPD Diagnosis, Management, and Prevention. (2018). Global Initiative for Chronic Obstructive Lung Disease, Inc., 1-44. Retrieved from https://goldcopd.org/wp-content/uploads/2018/02/WMS-GOLD-2018-Feb-Final-to-print-v2.pdf

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