Haemodynamics, dyspnoea, and pulmonary reserve in heart failure with preserved ejection fraction

Abstract

Aims: Increases in left ventricular filling pressure are a fundamental haemodynamic abnormality in heart failure with preserved ejection fraction (HFpEF). However, very little is known regarding how elevated filling pressures cause pulmonary abnormalities or symptoms of dyspnoea. We sought to determine the relationships between simultaneously measured central haemodynamics, symptoms, and lung ventilatory and gas exchange abnormalities during exercise in HFpEF.

Methods and results: Subjects with invasively-proven HFpEF (n = 50) and non-cardiac causes of dyspnoea (controls, n = 24) underwent cardiac catheterization at rest and during exercise with simultaneous expired gas analysis. During submaximal (20 W) exercise, subjects with HFpEF displayed higher pulmonary capillary wedge pressures (PCWP) and pulmonary artery pressures, higher Borg perceived dyspnoea scores, and increased ventilatory drive and respiratory rate. At peak exercise, ventilation reserve was reduced in HFpEF compared with controls, with greater dead space ventilation (higher VD/VT). Increasing exercise PCWP was directly correlated with higher perceived dyspnoea scores, lower peak exercise capacity, greater ventilatory drive, worse New York Heart Association (NYHA) functional class, and impaired pulmonary ventilation reserve.

Conclusion: This study provides the first evidence linking altered exercise haemodynamics to pulmonary abnormalities and symptoms of dyspnoea in patients with HFpEF. Further study is required to identify the mechanisms by which haemodynamic derangements affect lung function and symptoms and to test novel therapies targeting exercise haemodynamics in HFpEF.

Figure 1

(A and B) Pulmonary capillary wedge pressure and Borg dyspnoea score as a function of workload in heart failure with preserved ejection fraction and control subjects. (C) The increase in pulmonary capillary wedge pressure from rest to peak exercise was directly correlated with the change in the Borg dyspnoea score in subjects with heart failure with preserved ejection fraction, but not in controls (P = 0.3, data not shown). (D) Peak pulmonary capillary wedge pressure correlated inversely with peak oxygen consumption. (E and F) Elevations in pulmonary capillary wedge pressure and pulmonary artery mean pressure during peak exercise were related to Ney York Heart Association class in heart failure with preserved ejection fraction subjects, but not in control subjects. *P < 0.05 between groups. ^aDetermined by Pearson’s correlation analysis. ^bDetermined by Spearman’s correlation analysis.

Figure 2

Baseline, low-level (20 W) and peak exercise for (A) respiratory rate, (B) tidal volume (V_T), (C) minute ventilation (V_E), (D) inspiratory drive [tidal volume/inspiration time (V_T/T_I)], (E) dead space ventilation relative to tidal volume (V_D/V_T), and (F) peak oxygen consumption in heart failure with preserved ejection fraction and control subjects. *P < 0.05 between groups.

Figure 3

Correlation of peak V_D/V_T ratio with peak pulmonary vascular resistance, pulmonary arterial compliance. ^aDetermined by Pearson’s correlation analysis. ^bDetermined by Spearman’s correlation analysis.

Figure 4

(A) Compared with controls, subjects with heart failure with preserved ejection fraction displayed less increase in V_E during peak exercise. (B) This was explained by impaired increase in V_T in heart failure with preserved ejection fraction. (C and D) The change in V_T varied directly with peak oxygen consumption, and peak V_T was correlated inversely with peak pulmonary capillary wedge pressure. Error bars indicate SE. ^aDetermined by Pearson’s correlation analysis.

Take home figure

Linkages between haemodynamic derangements, symptoms, ventilatory abnormalities and gas exchange alterations in patients with heart failure with preserved ejection fraction. See text for details.