Isocapnic augmented exercise ventilation in congestive heart failure: effect of apparent (real‐feel) metabolic CO2 load in respiratory chemosensing

Abstract

CO2 breathing introduces an airway CO2 load that clogs the mechanism of pulmonary CO2 elimination, inevitably causing hypercapnia when the inspired PCO2 is high enough to prohibit isocapnia regardless of the ventilation level. The control law (Comroe's law) evidencing such self‐imposed permissive hypercapnia has been dubbed “CO2 tolerance curve” (rather than CO2 response curve) by Fenn and Craig (1963). By contrast, muscular exercise introduces a metabolic CO2 load that is readily countered with proportionate increase in ventilation without CO2 retention. Isocapnia from rest to exercise is maintained by the controller with the exercise ventilatory response being well adjusted for corresponding decrease in anatomical VD/VT, resulting in a small positive Y‐intercept in the ventilation vs. metabolic CO2 output relationship (Whipp's law). Remarkably, patients with congestive heart failure compensate for their abnormally large alveolar VD/VT with augmented ventilation, maintaining isocapnia at rest and during exercise without CO2 retention despite their decreased exercise tolerance. Thus, the control law governing isocapnic exercise ventilatory response is not merely determined by metabolic CO2 output per se but is responsive to an apparent (real‐feel) metabolic CO2 load that also accounts for the adverse effect of physiological VD/VT on pulmonary CO2 elimination. (Supported by HL067966 and RR028241)