Background: Patients with chronic heart failure show impairment of ventilatory efficiency, defined as the relation between ventilation and carbon dioxide output. It is caused by ventilation of excess physiologic dead space. We hypothesized a role of active vasoconstriction in the increase of physiologic dead space, presumed to lead to alveolar hypoperfusion.
Methods and results: In 57 patients with chronic heart failure (New York Heart Association classification II through IV, ejection fraction 25.6%+/-10.4%) and 7 control subjects, gas exchange at rest and on exercise was compared with hemodynamic measurements and, in a subgroup of 15 patients, with endothelin-1, epinephrine, and norepinephrine levels in the pulmonary and systemic circulation. Ventilatory efficiency at rest (VE/VCO2 ratio) correlated with ventilatory efficiency on exercise (VE vs VCO2 slope). Impairment of ventilatory efficiency correlated strongly negative with exercise tolerance (maximal oxygen uptake: r = -0.67) and cardiac output (r = -0.66) and positive with pulmonary hypertension (mean pulmonary artery pressure: r = 0.69, pulmonary vascular resistance: r = 0.60). None of the vasoconstrictors correlated with reduction of ventilatory efficiency in the subgroup studied.
Conclusions: Impairment of ventilatory efficiency in chronic heart failure is correlated with resting pulmonary artery pressures and associated with the impairment of exercise capacity. An imbalance of pulmonary vascular tone probably leads to both pulmonary hypertension and alveolar hypoperfusion.