Respiratory muscle function in asthma.
Asthma increases the load on the ventilatory pump by causing simultaneous increases in airway resistance, lung volume, and minute ventilation. The inspiratory muscles bear the majority of this load, whereas expiratory muscle recruitment is relatively minor. Respiratory muscle strength and endurance appear to be normal in stable asthmatics. During acute attacks, airway closure and expiratory airflow limitation result in a dynamic increase in end-expiratory lung volume. In turn, hyperinflation compromises the function of inspiratory muscles, especially that of the diaphragm, by reducing their force-generating capacity (muscle shortening) and impairing their mechanical advantage on the chest wall. Thus, exacerbations of asthma cause an acute increase in mechanical load together with decreased ventilatory capacity, thereby predisposing to inspiratory muscle fatigue and precipitating hypercapnic respiratory failure in severe cases. Management of ventilatory failure in asthma consists of mechanical unloading of the inspiratory muscles by positive pressure ventilation together with pharmacotherapy (anti-inflammatory and bronchodilating agents) to improve airway function. The strategy of mechanical ventilation is aimed at minimizing dynamic hyperinflation, which increases inspiratory muscle load as well as promotes barotrauma.
Hill
A R
AR
Department of Medicine, State University of New York Health Science Center, Brooklyn 11203.
D000305:Adrenal Cortex Hormones / Q000009:adverse effects; D001249:Asthma / Q000503:physiopathology*; D006801:Humans; D011175:Positive-Pressure Respiration; D012121:Respiration, Artificial; D015656:Respiratory Mechanics; D012132:Respiratory Muscles / Q000187:drug effects / Q000503:physiopathology*; D013806:Theophylline / Q000627:therapeutic use; D014109:Total Lung Capacity
D000305:Adrenal Cortex Hormones; D013806:Theophylline