Anna E. Marshall MSN Portfolio



Anna MarshallNU 507 Case Study 3 - AsthmaEmmanuel and his mother live in an urban community housing complex. The building is worn down and dirty from the urban dust, cockroaches, and mold. Emmanuel is 5 years of age and has suffered from asthma for the past 2 years. One evening his mother poured him some milk and put him to bed. Shortly afterward, Emmanuel woke up wheezing and coughing. As he gasped for air, he became more and more anxious. His mother ran for his inhaler, but he was too upset and restless to use it. Emmanuel’s skin became moist with sweat, and as he began to tire, his wheezing became quieter. His mother called 911 and waited anxiously for the ambulance to arrive.Emmanuel uses a corticosteroid inhaler for the management of his asthma. What is the mechanism of action for this drug? How is its action different from the β2-agonist inhalants?The mechanism of action of a corticosteroid inhaler includes anti-inflammatory effects to help open airways and make breathing easier. Corticosteroid inhalers are also referred to as ‘maintenance’ or ‘long-term control’ inhalers because, when used daily, they can help achieve and maintain control of persistent asthma symptoms. Corticosteroid inhalers, considered the most effective anti-inflammatory agents for use in long-term treatment of asthma, work directly by causing a reduction in markers of airway inflammation in airway tissues and airway secretions (eosinophils, mast cells, activated lymphocytes, macrophages, cytokines, inflammatory mediators) thereby decreasing the intensity of airway hyperresponsiveness. caused by asthma. In addition to relieving the inflammation within the airway passages by preventing and decreasing the swelling in the lungs and airways, and decreasing mucus production, they work over time to make airways less sensitive to asthma triggers. They do not provide immediate, or rescue effects in the event of an asthma attack; in this way, they are different from the short-acting inhaled β2-agonists. The β2-agonist inhalants are not useful long-term, and do not treat the inflammation, but rather provide quick (usually within 30 minutes) relief by relaxing the tightened bronchial smooth muscle around the airways. This allows them to open up for easier breathing and prompt relief of an asthma attack.?Why does someone with severe asthma become physically fatigued during a prolonged attack? Address the physiologic events that occur during an attack to explain your answer.The increased work of breathing during a severe asthma attack requires more energy and further increases oxygen demands causing physical fatigue. During an asthma attack, the airways narrow because of bronchospasm, edema of the bronchial mucosa, and mucus plugging. Progressive obstruction causes the expiration to become prolonged, and both the amount of air that can be forcibly expired in a second and the peak expiratory flow rate are decreased. During a prolonged attack, air becomes trapped behind the occluded, narrowed airways, causing hyperinflation of the lungs. With hyperinflation of the lungs, there is an increase in the residual volume, along with a decrease in the inspiratory reserve capacity and forced vital capacity, and the person is forced to breathe close to his or her functional residual capacity (Porth & Matfin, p. 712). Physical fatigue results as increased work of breathing means that more energy is needed to overcome the tension present in the lungs, and accessory muscles are needed to maintain the ventilation and gas exchange. Air is trapped in the alveoli and inspiration is occurring at higher residual lung volumes, making the cough less effective. Hypoxemia and hypercapnia also contribute to fatigue as the condition progresses and the effectiveness of alveolar ventilation declines, and ventilation does not match perfusion. ?One of the complications of respiratory fatigue is the development of hypercapnia. How does the body compensate for an increase in CO2? What are the effects of hypercapnia?on the central nervous system?Hypercapnia, increased levels of carbon dioxide (CO2) in the bloodstream, and hypoxemia, decreased levels of oxygen in the bloodstream are seen as an asthmatic episode progresses and respiratory fatigue sets in. Usually the body attempts to compensate for an increase in CO2 by increasing the CO2 elimination by the lungs, but persons with respiratory diseases may be unable to eliminate the excess CO2. Since CO2 readily crosses the blood-brain barrier, its effects on the central nervous system are mostly because of changes in the pH of brain fluids. Elevated levels of CO2 produce vasodilation of cerebral blood vessels causing headache, blurred vision, irritability, muscle twitching, and psychological disturbances. Increase in CSF pressure and papilledema can result if the condition is severe and prolonged, and if the level rises to extreme levels, there will be impaired consciousness, ranging from lethargy to coma, and maybe even paralysis of the extremities and respiratory depression. (Porth & Matfin, p. 822-3). ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download