Interplay of pulmonary circulation, cardiac filling pressures, and sympathovagal balance in exercise-induced hyperventilation among cardiopulmonary disorders.

Abstract

Although chemosensitivity plays a role in exercise-induced hyperventilation in cardiopulmonary disorders, the integration of the underlying reflexes with cardiac hemodynamics is not fully understood. We aimed to explore the interplay between right- and left-heart pressure overload, right ventricular-pulmonary arterial (RV-PA) coupling, cardiovascular autonomic modulation, and ventilatory response in patients with cardiopulmonary disorders. Forty patients underwent echocardiography, cardiopulmonary exercise testing, and right heart catheterization. Spectral analysis of heart rate variability (HRV) was used to assess cardiovascular autonomic modulation of low- (LF) and high-frequency (HF) components, with LF/HF ratio as an index of sympathovagal interaction. Heart rate recovery (HRR) quantified vagal reactivation. RV-PA coupling was calculated through the tricuspid annular plane systolic excursion (TAPSE)/systolic pulmonary artery pressure (PAPs) ratio, and V̇e/V̇co₂ slope defined ventilatory inefficiency. Patients were classified as NoPH (no pulmonary hypertension, n = 13), PCPH (precapillary pulmonary hypertension, n = 15), and LVDD (left ventricular diastolic dysfunction, n = 12). V̇e/V̇co₂ slope was higher in PCPH than LVDD and NoPH (53.9 vs. 43.7 vs. 42.2, P < 0.01). The LF/HF ratio was similar in PCPH and LVDD but higher in NoPH (P < 0.01), whereas HRR was significantly blunted in PCPH compared with LVDD and NoPH (P < 0.01). TAPSE/PAPs was significantly reduced in PCPH and LVDD vs. NoPH and was significantly correlated with all HRV parameters. Our findings support a tight interconnection between left- and right-heart hemodynamics, pulmonary circulation, sympathovagal control, and ventilatory response during exercise. Although additional mechanisms are involved, cardiopulmonary efficiency, captured by RV-PA coupling, emerges as a key determinant linking cardiopulmonary hemodynamics to autonomic modulation and ventilatory inefficiency.NEW & NOTEWORTHY The results underscore a multifaceted interaction among cardiopulmonary hemodynamics, right heart pressures, ventilatory response, and autonomic regulation. In particular, altered RV-PA coupling correlated with heightened sympathetic drive, indicating that cardiopulmonary efficiency and hemodynamics may influence central autonomic outputs. This suggests that mechanical stress or overload in the right heart could modulate sympathovagal balance, thereby contributing to altered autonomic responses during exercise in patients with cardiopulmonary disorders.