Background: Heart Failure (HF) is associated with severe dyspnea and elevated pulmonary capillary wedge pressure (PCWP). The research investigates the interactions between the cardiac and pulmonary systems and the role of the respiratory effort in the development of decompensation.
Methods: We have simultaneously measured the hemodynamic indices and the respiratory mechanics in patients undergoing right heart catheterization (n=56) for the diagnosis of dyspnea. The PCWP was decomposed into cardiac and respiratory waves. The respiratory effort (PRESP) was defined as the respiratory wave amplitude.
Results & Discussion: The HF patients (n=35) exhibited huge PRESP of 9.6±3.7mmHg [2.6-16.7], 5-8 fold the normal PRESP, of about 2mmHg. Their lung compliance decreased with increasing PCWP (2.0±0.4%/mmHg of PCWP). Interestingly, both PCWP and PAP rose with PRESP, by 0.92±0.36mmHg and 1.68±0.47mmHg, for 1mmHg of PRESP, respectively. Moreover, PCWP always exceeded PRESP, leading to the stipulation of a novel fundamental constraint/law: the continuous pulmonary flow throughout the entire respiratory cycle requires that PCWP > PRESP. This constraint imposes a positive feedback of PRESP on pulmonary circulatory pressures. The bigger rise in PAP than in PWCP is attributed to the increase in the pulmonary vascular resistance with PRESP (0.3±0.06wood for 1mmHg PRESP). The latter constructs additional novel positive feedback of PRESP on the workload of both heart ventricles.
Conclusions: The study highlights the bidirectional interactions between the pulmonary vasculature and lung mechanics, where dyspnea/PRESP is not just a result of HF but plays a pivot role in the vicious cardiopulmonary cycle that can accelerate decompensation.