The manner in which a subject breathes has a great bearing on the amount of aerosolized drug deposited in the airways and the pattern of distribution of the drug in the pulmonary tree, i.e., central versus peripheral airways. Minute volume influences the amount of drug delivered to the airway lumen. Ventilatory frequency, tidal volume, and lung volume determine the residence time of an aerosol in the airways  and thereby dictate the duration during which the airways are exposed to drug. The distribution of aerosolized agent can be controlled by the pattern of breathing. For example, rapid, shallow breathing results in a deposition in the central airways, whereas slow, deep breathing results in peripheral airway deposition . Under conditions of moderate-to-severe airway obstruction, as might occur during asthmatic bronchospasm, functional residual capacity and ventilation rate tend to increase while tidal volume tends to decrease. As such, the bronchospasm-induced changes in ventilatory parameters are envisaged as modifying the deposition of the aerosol and, therefore, its therapeutic activity. Fortuitously, the rapid, shallow breathing promotes deposition in the central airways that, in general, are the sites of bronchoconstric-tion. However, the increases in ventilatory rate, airways resistance, and apparent lung stiffness result in an increase in the work of breathing, particularly during inspiration  and may lead to fatigue of ventilatory muscles. Under these conditions, the capacity of a severely compromised patient to inhale an aerosol effectively may be limited. These subjects would require more rigorous (e.g., intravenous) therapy.
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If you suffer with asthma, you will no doubt be familiar with the uncomfortable sensations as your bronchial tubes begin to narrow and your muscles around them start to tighten. A sticky mucus known as phlegm begins to produce and increase within your bronchial tubes and you begin to wheeze, cough and struggle to breathe.