The Physiological Consequences of Emphysema - Research Paper Example

The Physiological Consequences of Emphysema The Physiological Consequences of Emphysema Emphysema is a chronic ailment of the lungs that permanently damages the alveoli in the lungs leading to complications mainly in exhalation (Voikel, 2008). Studies suggest the condition is the fourth leading cause of death in the United States. The anatomy of the lungs undergoes certain permanent changes. The alveoli are small air sacs found in the lungs where the exchange of gasses occurs. The alveoli walls get inflammation, and they lose their ability to stretch and shrink as they do under normal conditions (Voikel, 2008). The inflammation damages the alveoli trapping air pockets in the injured areas. Trapped pockets of the air block airways leading to a difficulty in breathing. Emphysema is similar to another condition called the chronic obstructive pulmonary disease (COPD) that leads to a reduced airflow into the lungs. COPD is characterized by running out of breath, chronic cough, phlegm, and reduced ability to exhale. Emphysema gets worse with time, with the alveoli becoming larger while decreasing in number (Turino, 2006). As a result, the air sacs are destroyed as they change in structure. The condition greatly reduces the amount of air absorbed by the blood in the lungs. The major predisposing factor to the state includes smoking especially from the age of 35 years, air pollution, and exposure to allergens, genetics and other respiratory diseases such as asthma among other suspected causes. The expiratory flow limitation is chronic and permanent. The limitation results from the airway inflammation and parenchymal cells damage. Progressive airways obstruction which leads to more breathing difficulties. The condition worsens with the inflammation of the airway characterized by the mucosal airway edema and mucous impaction. Emphysema results in the destruction of elastin impairing the ability of the lung to recoil after inhalation. As a result causing the lungs defective expiratory pressure. The airways become weak and narrow and thus there is an increased resistance to airflow. Expiratory flow limitation occurs when the expiratory airflow during spontaneous tidal breathing represents the maximum possible flow rate at operating lung volume. The expiratory flow rate does not rely on the muscle effort but on the ability of the lung to produce enough pressure for adequate exhalation during the recoil tide. In the case of expiratory flow limitation, the lung does not generate enough pressure for sufficient additional due to the reduced surface area and high volume of the alveoli, and the damaged elastin. The emphysema condition affects people with old age. The relaxation volume of the lungs as determined by the equilibrium of forces between the inward elastic recoil in the lungs and the outward recoil pressure of the chest wall. Old age is related to the deterioration of the connective tissue due to the change in elastic properties of the parenchymal tissue of the alveoli. As a result, older people have a lower lung elastic recoil pressure. The equilibrium point of the respiratory system usually occurs when the net elastic recoil of the respiratory system is zero. At old age, the equilibrium occurs at a higher lung volume than in young people. It is a primary risk factor for emphysema condition in old people. The emphysema destruction consequence of the alveoli structure leads to the resetting of the systems relaxation volume to a higher volume in as state known as lung hyperinflation air spaces is more severe in people above 35 years of age. The resting lung volume is the residual capacity of the lungs achieved after a successful exhalation. The resting lung volume is higher in the case of emphysema. The end-expiratory lung volume in a relaxed breathing corresponds to the actual equilibrium volume of the system. In emphysema, the end-expiratory lung volume is maintained at a higher level. The condition in inflow-limited individuals shows a longer expiration rate than in healthy individual. This delayed mechanical exhalation rate occurs when expiration time is limited to compensate for extrusion of the excess volume in the alveoli. As a result, the end exhalation lung volume is higher than in healthy individuals. The condition ends up in air trapping. It is clear how the lung ends up not completely emptied. Exhalation flow limitation, breath time abnormalities, and breathing pattern determines the variability of the end exhalation lung volume. An acute exacerbation is a state the patients experiences an increased limitation of airflow. As a result, the constant is influenced. The patient experiences shortness of breath and thus there is a rise in the frequency of breathing. The acute exacerbations results to the increase in the end exhalation lung volume, leading to acute dynamic hyperinflation (Keller, 2003). The hyperinflation is a temporary condition where there is an increase in gas volume in the lungs or part of the lungs is higher than the predicted value. A clinician detects acute hyperinflation through physical examinations or radiographic techniques. The hyperinflation exhibits symptoms such as the inward motion of the lower lateral ribcage in the inhalation tide and an inward movement of the anterior abdominal wall during inhalation. The development of acute hyperinflation has been shown to begin with the residual lung volume increase resulting in an increased airway closure. In followed by the increase in the end exhalation lung volume to indicate the consequence of exhalation flow limitation and obstruction of the static processes (Turino, 2006). Finally, the total lung volume results as the lung compliance increases. The risk factors predisposing the acute exacerbations includes exercise, stress and anxiety among other causes. With a rise in the inhalation tidal volume, the time diminishes for exhalation leading a breathing frequency that is higher than the baseline value resulting to acute on the chronic situation. Reduced inhalation capacity can also demonstrate a hyperinflation. Impaired gas exchange due to loss of alveoli and blood capillaries damage at the gas exchange points. High-resolution computerized tomography shows that alveoli dilation is both regionally or homogenously throughout the two lungs. The destruction of the walls has been shown to cause a merging of alveoli spaces leading to larger air spaces, resulting high volume and small surface area in the lungs. The dilation of the alveoli causes many pathophysiological consequences such as lower diffusion capacity of the carbon dioxide as well as oxygen across the membranes. The emphysema leads to elevation of total lung capacity as in the case of hyperinflation. Low inhalation capacity leads to a smaller ratio between the operating tidal volume and the total lung capacity thus a lower pressure-volume ratio that in turn reduces the elastic loading potential. During an exercise, there is an increase in the elastic threshold of the inhalation muscles to reinforce the breathing negatively leading to weakness due to shortened diaphragm muscle fibers (Keller, 2003). Tidal volume fails to expand efficiently leading to a technical limitation in ventilation. It may result in carbon dioxide retention. The total lung capacity does not change. However, in emphysema patients, the inhalation capacity reduces leading to an increase in the end exhalation lung volume indicating a hyperinflation (Voikel, 2008). The condition of hyperinflation develops through over long time. The body adapts to the changes in the lung properties and functional defects. These adaptations enhance the lungs to respond to the weakening elastin functions in the alveoli. The sarcomere reduces in length. The sarcomere is a muscle in the lungs. The change in length enables it to generate more force at lower pressures and higher lung volumes. The lung also produces more fatigue resistant muscle fiber to take on the extra load of effort. As a result, the lung is supplied with more mitochondrial structures that supply the extra power needed for the extra work of supplying oxygen. There is also an elevated level of red blood cells in the blood to maintain the supply of oxygen to the body. These adaptations do not adequately cope with hyperinflation. In conclusion, emphysema leads to adverse physiological defects in the respiratory system. Exhalation flow limitation makes the body to launch adaptive mechanisms to compensate for the lower supply of oxygen into the lungs. Emphysema patients exhibit symptoms such as shortness of breath during a physically demanding activity. As a result, it affects the quality of life of the individual for the rest of their life. References Keller, C. (2003). Pathophysiology and classification of emphysema. Chest Surgery Clinics Of North America, 13(4), 589-613. doi:10.1016/s1052-3359(03)00092-9 Turino, G. (2006). Emphysema in COPD: consequences and causes. Thorax, 61(12), 1031-1036. doi:10.1136/thx.2006.066308 Voelkel, N. (2008). Chronic obstructive lung disease. Hamilton, Ont: Decker. Read More