The response of asthmatic airways to irritant stimuli is twofold: bronchoconstriction and airway inflammation. The inevitable mechanical consequence of bronchoconstriction is hyperinflation of the lungs, a phenomenon that produces characteristic clinical and radiologic signs. Hyperinflation helps to maintain airway patency at the expense of increased respiratory muscle work. Airway inflammation accounts in large part for the increased ventilatory drive of asthmatic patients, which results in alveolar hyperventilation and dyspnea. The resultant respiratory alkalosis further compromises tissue oxygen delivery both by cerebral vasoconstriction and by the leftward shift of the oxyhemoglobin dissociation curve. Optimal correction of hypoxia in the hyperventilating asthmatic patient requires delivery of oxygen at a high flow rate. Failure of patients with asthma to respond to simple bronchodilator therapy indicates the presence of continuing inflammatory activity and hence the need for anti-inflammatory therapy and frequency monitoring.