A human model of chronic obstructive pulmonary disease

Abstract

Expiratory flow-limitation (EFL) during exercise enforces slowing of the velocity of shortening of expiratory muscles, which according to the muscles' force velocity characteristics will increase the force (measured as pressure) that they develop. It has been suggested that high expiratory pressures might have adverse circulatory effects. To investigate this further we have studied normal subjects during incremental or constant workload exercise with a Starling resistor in the expiratory line which limited flow to ∼1 Vs. We found that this intervention: 1) caused a marked increase in expiratory pressures; 2) limited maximal exercise workload (W m a x ) to 67% of control W m a x ; 3) led to intolerable dyspnea, attributable largely to expiratory muscle recruitment; 4) caused CO 2 retention not entirely explicable by a reduction in minute ventilation, thus implicating an increased alveolar dead space; 5) shifted blood from trunk to extremities, possibly accounting for the increased dead space and hypercapnia; 6) decreased cardiac output by 10% and systemic O 2 delivery by 15%. EFL during exercise reproduces the main clinical features of COPD, namely, exercise intolerance, prominent dyspnea and carbon dioxide retention and produces a condition similar to acute cor pulmonale. Thus it is a human model of how COPD leads to impairment of ventilatory pump function that is safe and repeatable. The results suggest that patients with COPD who recruit expiratory muscles excessively may limit exercise by decreasing systemic O 2 delivery.