By C F Donner; N Ambrosino; Roger Goldstein
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Maltais F. Simard A. Simard J et 01. Oxidative capacity of the bdween dyspnea, diaphragm and sternomastoid recruitment during skeletal muscle and lactic acid kinetics during exercise in normal inspiratory resistance breathing in normal subjects. Chest 1990; subjects and in patients with COPO. Am J RespirCdtCore Med 98:298-302. 65. Cohen C, Zagelbaum G, Gross 0 et al. Clinical manifestations of inspiratory muscle fatigue. A m ) Med 1982; 73: 308-16. 66. Martinez F, Montes de Oca M, Whyte R et aJ.
Lung inflation hinders rib cage anatomy and respiratory muscle function. All of this results in increased work of breathing, decreased reserve and dyspnoea. In addition, COPD has important associated peripheral muscle dysfunction,which, coupled with the respiratory events, promotes a sedentary lifestyle and ever-increasing functional limitation. Pulmonary rehabilitation reverses many of the consequences of these pathophysiological problems and thereby improves overall outcome with little impacl on airflow limitation.
The interaction between the central drive (con troller output) and the final output (ventilation) is complex and involves many components (45, 46). This complexity renders it very difficult to ascribe dyspnoea to a dysfunction in any individual portion of the system. The ventilatory control can be assessed at different levels. The simplest is the minute ven tilation (VE), which reflects the final effectiveness of the venti latory drive. , the tidal volume (VT) represented by the volume of air inhaled in a breath and the respiratory frequency.