Gas Exchange Efficiency in Congestive Heart Failure II

It has become increasingly apparent that congestive heart failure (CHF) affects not only the cardiovascular system, but every organ system involved with oxygen transport, including the respiratory system, skeletal muscles, and the hormonal and neural feedback control systems for breathing, cardiac output, blood pressure, blood volume, and distribution of blood flow. One segment of this transport system cannot be isolated from the rest. The ventilatory response to exercise in patients with CHF is augmented despite normal arterial O2 saturation and a normal or low end-tidal Pco2.1 2 3 4 5 6 The augmented ventilatory response is measured as a steep slope of the increase in ventilation with respect to CO2 output (ΔVe/ΔVco2) or as a high Ve/Vco2 ratio at peak exercise. The source of this ventilatory augmentation has been controversial, but its pathophysiological significance is clear. A high slope at submaximal exercise or a high Ve/Vco2 ratio at peak exercise is a powerful index of poor prognosis in patients with CHF.4 7 As indicated by Ponikowski et al8 in the current issue of Circulation , this prognostic power is retained in patients with CHF, even when the maximal O2 uptake (Vo2 max) is near the normal range.A high Ve/Vco2 ratio has 2 possible sources: (1) increased ventilation, which is required to overcome a large dead space to maintain a normal arterial CO2 tension (Paco2), or (2) increased central drive to ventilation, which drives the Paco2 below what is normally expected. Ponikowski et al8 present convincing evidence that the augmented ventilatory response to exercise in CHF is significantly correlated with other markers of abnormal cardiorespiratory reflex control (ie, …