Background: Patients with chronic heart failure have an excessive ventilatory response to exercise, characterised by an increase in the slope of the relation between ventilation and carbon dioxide production (VE/VCO2 slope). Patients have an altered respiratory pattern with an increased respiratory rate (f) at a given tidal volume (VT), which may result in increased anatomical dead space ventilation.
Methods: The ventilatory responses in 88 patients with chronic heart failure and 43 age matched controls during maximal incremental treadmill exercise were analysed. Peak oxygen consumption (VO2), VE/VCO2 slope, and the slope of the relation between f and VT were derived. Anatomical dead space was estimated from a standard formula and anatomical dead space ventilation calculated.
Results: Peak VO2 was greater (mean (SD)) (33.2 (8.5) v 19.4 (6.7) ml/min/kg; P < 0.001) and the VE/VCO2 slope lower in the controls (25.96 (4.16) v 35.14 (9.80); P < 0.001). During matched submaximal exercise VT was higher (1.97 (0.92) v 1.68 (0.62) 1; P < 0.05) and flower in the controls (18.23 (6.48) v 24.28 (7.58); P < 0.001). At peak exercise there was no difference in f, but VT was higher in the controls (2.66 (0.97) v 1.90 (0.61) 1; P < 0.001). The VT/f slope was the same (0.04 (0.04)) in both groups. The intercept of the relation was greater for the control group (1.31 (1.28) v 0.59 (0.83); P < 0.001). Anatomical dead space ventilation was lower in the controls at submaximal work load (4.17 (1.56) v 5.58 (1.93) l/min; P < 0.001). At peak exercise anatomical dead space ventilation was the same in both groups, but was lower expressed as a percentage of total VE in the control group (9.8 (3.3) v 13.5 (4.0); P < 0.001). There were weak relations within the heart failure group alone between VT/f slope and peak VO2 and VE/VCO2 slope.
Conclusions: The relation between anatomical dead space ventilation and VE/VCO2 slope is expected: as f increases, so do VE/VCO2 slope and anatomical dead space ventilation. The VT/f slope was the same in patients with chronic heart failure and controls, so change in respiratory pattern cannot explain the increase in VE/VCO2 slope. The stimulus causing the increased f has yet to be identified.