Ventilatory inefficiency: a key physiopathological mechanism increasing dyspnea and reducing exercise capacity in chronic obstructive pulmonary disease

摘要

Lin et al. (1), remembers an essential principle of physiology, which states that one objective of alveolar ventilation is to clear CO2 production (VCO2), maintain an adequate arterial CO2 pressure (PaCO2), and control acid-base balance. The central PCO2 set point regulated by the respiratory centers, govern the ventilatory response to depurate CO2. In absence of fixed acids, the disproportionate increment in minute ventilation (VE) for VCO2, indicates inefficiency of ventilation (VI). This mechanism exists particularly in chronic obstructive pulmonary disease (COPD) (1-5), where VI raise subrogated to physiological dead space (VDphys/VT), due to waisted ventilation and the need to control the PaCO2. In consequence, the VE/VCO2 ratio also increase. As example, a normal individual in moderate exercise requires 20–25 L of ventilation to clear 1 L of CO2, and patient with COPD frequently overpass 35 L.