Exaggerated lower air response to an environment exposure is the one referred top as the Asthma exacerbations (Erskine, Notley, Wilson & Philpott , 2014). This infection mostly is caused by respiratory virus that causes airway inflammation. Currently, there are diverse methods used to respond to asthma but all aimed at reducing the day to day variability of asthma (Erskine, Notley, Wilson & Philpott , 2014). Pathophysiology of Acute Asthma and Chronic Asthma In acute asthma, the air inflammation indicates that heterogeneous inflammatory infiltrate with a mixture of neutrophils and eosinophils (Lonneke et al, 2012). This is actually very different from allergen induced asthma. This is the main reason why it is recorded that, the pathogenesis of acute asthma and that of chronic asthma are very different (Lonneke et al, 2012). In this case, there are increased numbers of neutrophils which are in the bronchoalveolar lavage fluid and endobronchial biopsy tissue. T cell activations are also present in the case of acute asthma (Erskine, Notley, Wilson & Philpott , 2014). This is indicated by T cell markers in peripheral blood and increases CD8 cells which have been activated in the tissue of fatal cases of asthma (Erskine, Notley, Wilson & Philpott , 2014). During asthma exacerbation there is marked hyperinflation which is as a result of air trapping from mucus plugging the airway. The airway remodeling also causes inflammation. This therefore means that, both the airway mucus cell hyperplasia and mucus secretion are relevant mechanisms of mucus plugging asthma. The inflammatory pattern is as a result of stimuli and consequent cytokine response pattern (Erskine, Notley, Wilson & Philpott , 2014). In chronic asthma, there is the presence of high dose inhaled corticosteroids which is solved by adding a long acting inhaled B2 adrenoceptor agonist (Patelet al, 2014). This means that, chronic asthma is as a result of susceptible airways which