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Running head: ACUTE AND CHRONIC ASTHMA1Acute and Chronic AsthmaHannah ReevesWalden UniversityAdvanced Pathophysiology Dr. FlemingJuly 8, 2018
ACUTE AND CHRONIC ASTHMAAcute and Chronic AsthmaAsthma is a respiratory alteration that affects approximately seven million children in the United States and has been identified as being one of the leading reasons for emergency room visits (Navandandan, Federico, & Mistry, 2016). Asthma exacerbations are characterized by airway obstruction secondary to inflammation of airway because of a hyper-response from the body’s immune system (Huether & McCance, 2017). Asthma cases can vary from mild to life-threatening. The purpose of this paper is to describe the pathophysiological mechanisms of chronic asthma and acute asthma exacerbations and outline my treatment plan for my selected patient factor.Pathophysiology of Acute and Chronic AsthmaAsthma is a chronic condition affecting the airways that are characterized by intermittent,recurrent exacerbations or flare-ups. According to Kew et al. (2013), an explicit clinical definition of asthma has not yet been determined. Research suggests that in all forms of asthma, chronic inflammation is catalyzed by bronchial hyper-responsiveness, that causes recurrent, intermittent periods of wheezing, breathlessness, cough, and chest tightness, that commonly occurs night and early in the morningAsthma ExacerbationDuring an acute exacerbation, the airways become inflamed and the bronchial tubes narrow, which causes breathing to become effortful. Airway obstruction from inflammation of the airway increases the amount of resistance to airflow and decreases flow rates, specifically expiratory flow. When expiration is impaired, air becomes trapped and causes hyperinflation distal to the obstruction, making breathing increasingly laborious. Hyperventilation is initiated by lung receptors that respond to increased lung volume and obstruction. Early in the attack, 2
ACUTE AND CHRONIC ASTHMAthere is hypoxemia without retention of CO2. As the exacerbation progresses, hypoxemia continues to drive hyperventilation as a compensatory mechanism, causing PACO2 to decrease and the pH to increase. If the attack continues, air trapping inside the lungs will become more problematic causing hyperexpansion of the thorax that will further compromise the respiratory muscles.