Ventilation and dyspnoea during exercise in patients with heart failure

Patients with chronic heart failure have an increased ventilation/carbon dioxide production ratio (VE/VCO2) during exercise. Recently it was discussed whether the cause of this increase was a ventilatory stimulus driven other than by CO2. Dyspnoea during exercise is thought to be related to impaired respiratory function. However, clinical confirmation is scarce. Ninety-two patients (age 51 +/- 9 years) with heart failure due to idiopathic dilated cardiomyopathy exercised on a bicycle ergometer to exhaustion, and measurement of ventilatory gases and Swan-Ganz catheterization were performed. The maximal oxygen consumption corrected for body weight (VO2max. kg-1) was 16.6 +/- 5.5 ml x min-1 x kg-1. The increase in (VE/VCO2) during exercise was related to an increase in respiratory rate (r = 0.43; P < 0.00001) but not to an increase in cardiac index or capillary wedge pressure. Nineteen patients stopped exercising because of dyspnoea. Their maximal tidal volume and VO2max . kg-1 were lower than the 67 patients who stopped exercise because of fatigue (P < 0.001 and P < 0.00001 respectively). Other variables showed no significant difference. In conclusion, the increase in VE/VCO2 during exercise may reflect a non-CO2 driven ventilatory stimulus as it cannot be attributed to increased pulmonary vascular pressures or an insufficient increase in cardiac output leading to a ventilation-perfusion mismatch. Low oxygen uptake is a prominent finding in patients with chronic heart failure who experienced dyspnoea during exercise, and dyspnoea is in part related to impaired respiratory function.