A feature of heart failure patients is exercise-induced hyperventilation, due to several causes including alteration of lung mechanics and gas diffusion, increased ventilation relative to CO2 production, elevated dead space ventilation, and overactive metaboreceptor and chemoreceptor reflexes.1
It is a well-established physiological concept that chemical ventilatory control depends and responds to afferent input, that is, arterial partial pressure of carbon dioxide (PaCO2) and of oxygen (PaO2), from the peripheral and central chemoreceptors to maintain PaCO2 and PaO2 within a specific and narrow range. However, this PaO2/PaCO2/pH-dependent regulation of ventilation seems too simplistic in several pathophysiological conditions including heart failure.
