**2. Mechanisms of AECOPD**

An acute exacerbation among COPD patients often stimulated by dyspnea (Shortness of breathe) that related with respiratory bacteria or viruses infection (which may coexist), environmental pollutants, or unknown factors. Most of respiratory infection can trigger AECOPD that is pneumonia. During exacerbation happened, there is increased hyperinflation and gas trapping, it resulted to reduced expiratory flow, so effect to dyspnea increased. Airflow limitation and air trapping are the cause of dyspnea and more dyspnea is the one symptom of AECOPD. The pathophysiology of COPD involves an inflammation, fibrosis, and luminal exudates in small airways. It is contributed to gas trapping during expiration and effected to decrease FEV1 and FEV1/forced vital capacity (FVC) ratio especially more severe disease. Hyperinflation increases end expiratory lung volume (EELV) and reduces inspiratory capacity (IC) such that functional residual capacity increase, particularly during exercise (dynamic hyperinflation), resulted in mechanical disadvantage (inspiratory muscle dysfunction), neuromechanical uncoupling (increased dyspnea), cardiovascular effects and worsening of gas exchange. Moreover, the increasing of ventilator drive and tachypnea stimulate the worsening of expiratory flow limitation and dynamic hyperinflation each other [5, 6].
