Excessive exercise ventilation in moderate left heart dysfunction. Influence of postural changes in central haemodynamics and blood gases

To evaluate the relative importance of pulmonary congestion and peripheral hypoxia as causes for the excessive exercise ventilation in left heart dysfunction, seven patients with excessive ventilation and distinct left heart dysfunction during moderate exercise (LHD), and seven control patients with essentially normal exertional functions (CTR), had ventilation, central haemodynamics, arterial and mixed venous blood gases examined at rest and exercise, 32 W (25-40) in the LHD group and 44 W (33-49) in the CTR group, in lying and sitting positions. Change from lying to sitting exercise, led to fall in pulmonary artery wedge pressure (PAWP) from 31.0 +/- 5.5 to 8.8 +/- 5.0 mmHg in the LHD group, compared with from 13.7 +/- 1.0 to 2.1 +/- 2.4 mm Hg in the controls, while ventilation/O2 intake ratio (V/VO2) and physiological dead space/tidal volume ratio (VD/VT) showed a tendency to rise, from 36.3 +/- 8.8 to 39.2 +/- 7.4, and from 0.35 +/- 0.11 to 0.39 +/- 0.09, respectively, in the LHD group, and from 27.5 +/- 3.1 to 28.7 +/- 5.3, and from 0.19 +/- 0.09 to 0.21 +/- 0.12 in the controls. Mixed venous O2 tension (PvO2) showed a marked decline from 3.60 +/- 0.33 to 3.26 +/- 0.36 kPa in the LHD group, as compared with from 3.94 +/- 0.28 to 3.71 +/- 0.29 kPa in the controls, while the calculated physiologic shunt (Qs/Qt) suggested improved alveolo-arterial gas exchange. The data fit in with recent studies ascribing the excessive exercise ventilation to a combination of signals from hypoxia-induced changes, particularly in the exercising muscles, and augmented ergoreflex and central and peripheral chemoreceptor activity, partly to changes in the integrated control of ventilation and circulation, not to mechanisms related to pulmonary congestion.