Acute severe asthma is a chronic lung disease that causes the narrowing and the inflammation of the small airways, especially, the bronchi and the bronchioles. Individuals with severe acute asthma, like Jackson Smith, have severe clinical manifestations like, a respiratory rate above 25 breaths/minute, heart rate higher than 110 beats/minute, is inability to complete sentences in one breath, has oxygen saturated level below 92%, hypotension, dyspnoea, coughing, wheezing, chest tightness, vriable airflow obstruction and airway hyperresponsiveness (Hazeldine, 2013). An asthma attack occurs when an individual gets exposed to the trigger in which it binds to an immunoglobin E hormone (IgE) present on the surface of mucosal mast cells. The cross-linking of these IgE molecules triggers degranulation of the mast cells, releasing mediators such as histamine, leukotrienes, prostaglandin D2, platelet-activating factor, and certain cytokines. The vasoactive effects of these cytokines include vasodilation and increased capillary permeability. This causes an increase in blood flow to the area, inflammatory cells and chemicals move through the cells into the interstitial tissue (Perkin and Ledoux, 2013). The chemotactic factors, which are chemicals that attract inflammatory cells to the site of inflammation, are produced that result in bronchial infiltration by white blood cells like neutrophils, eosinophils, and lymphocytes. Eosinophils release a variety of chemicals that contribute to inflammation and tissue damage. The resulting inflammatory process produces bronchial smooth muscle spasm, vascular congestion, oedema formation, production of thick mucus, impaired mucociliary function, thickening of airway walls and increased bronchial hyperresponsiveness (Mcdonald and Penola, 2015). The constriction of the airway muscles narrows the lumen of the airways affecting airflow resistant resulting in Jackson to experience chest tightness and difficulty breathing. The bronchi and bronchioles contain mucosa lining which has goblet cells which produce mucus to filter bacteria and other irritants, however, when asthma trigger is inhaled the goblet cells produce an excessive amount of mucus and cause the airways to become more inflamed in the airways when the asthma trigger is inhaled (Mcdonald and Penola, 2015). These result in further decrease in the airflow due to excessive mucous secretion and severely inflamed mucosal lining causing Jackson to cough, wheeze during expiratory and air trapping in the air sacs (alveoli) (Mcdonald and Penola, 2015). Dimished breathing leads to air trapping and hyperinflation distal to obstructions that accumulate the work of breathing. Intrapleural and alveolar gas pressures rise and cause decreased perfusions of the alveoli. These alterations lead to ventilation-perfusion mismatch which induces hypoxemia to 90% in Jackson’s blood. As the obstruction becomes more severe, the number of alveoli being adequately ventilated and perfused decreases. The chemotactic factors that attract inflammatory cells to the site of inflammation are produced for bronchial infiltration by the white blood cells, in particular, neutrophils, eosinophils, and lymphocytes. Eosinophils release a variety of chemicals that contribute to inflammation and tissue damage causing inflammatory process to produce bronchial smooth muscle spasm, vascular congestion, oedema formation, production of thick mucus, impaired mucociliary function, thickening of airway walls and increased bronchial hyperresponsiveness (Mcdonald and Penola, 2015). The constriction of the airway muscles narrows the lumen of the airways affecting airflow resistant resulting in Jackson to experience chest tightness and difficulty breathing. The bronchi and bronchioles contain mucosa lining which has goblet cells which produce mucus to filter bacteria and other irritants, however, when asthma trigger is inhaled the goblet cells produce an excessive amount of mucus and cause the airways to become more inflamed in the airways when the asthma trigger is inhaled (Mcdonald and Penola, 2015). These result in further decrease in the airflow due to excessive mucous secretion and severely inflamed mucosal lining causing Jackson to cough, wheeze during expiratory and air trapping in the air sacs (alveoli) (Mcdonald and Penola, 2015). Impaired exhalation causes air trapping and hyperinflation distal to obstructions and increases the work of breathing. Intrapleural and alveolar gas pressures rise and cause decreased perfusions of the alveoli. These changes lead to uneven ventilation-perfusion relationships causing hypoxemia to 90% in Jackson’s blood. As the obstruction becomes more severe, the number of alveoli being adequately ventilated and perfused decreases. Air trapping continues worsening and the work of breathing increases further, leading to hypoventilation (decreased tidal volume), carbon dioxide retention which increases partial pressure of carbon dioxide (PCO2) levels in the blood to 50mmHg resulting in respiratory acidosis (Perkin and Ledoux, 2013). As inefficient oxygen is present in the blood, the body’s response will be to inhale more breaths in a shorter period of time in order to provide enough oxygen to the body as it needs to function properly. This means that Jackson will exhibit an increase in the respiratory rate to 32 breaths per minute classified above the normal adult range. An abnormal increase in respiratory rate inadvertently causes the heart to pump blood faster to deliver oxygen to the body resulting in Jackson to have an increased pulse rate of 132 beats per minute and a blood pressure reading of 150/85mmHg. These results indicate Jackson has tachycardia and is categorized as a stage 1 hypertension (National Asthma Council Australia, 2017).