The Cardiopulmonary Vicious Cycle in Patients with Heart Failure, a Mechanism for Accelerated Decompensation

Anna Faingersh-Klebanov 1 Shmuel Rispler 2 Eugenia Nikolsky 2 Yuval Cohen 2 Sergey Yalonetsky 2 Arthur Kerner 2 Ariel Roguin 3 Amir Landesberg 1
1Biomedical Engineering, Technion - Israel Institute of Technology
2Cardiology, Rambam - Health Care Campus
3Cardiology, Hillel Yaffe Medical Center

Background: Heart Failure (HF) is associated with elevated pulmonary capillary wedge pressure (PCWP) and hemodynamic congestion that leads to clinical congestion. 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 hemodynamics 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 that modulates the PCWP.

Results & Discussion: The HF patients (n=35) exhibited huge PRESP of 9.6±3.7mmHg [2.6-16.7], 5 fold the normal PRESP (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. Interestingly, PCWP always exceeded PRESP, in both HF (n=35) and lung (n=14) patients, leading to the stipulation of a novel fundamental constraint/law: the continuous pulmonary flow requires that PCWP > PRESP, otherwise the capillary pressure will decrease below the alveolar pressure during the inspiration phase and the pulmonary circulation will collapse during inspiration. 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. The respiratory effort is not just a result of HF but plays a pivot role in the vicious cardiopulmonary cycle. An increase in the respiratory effort increases the PWCP, pulmonary vascular resistance and the afterloads of both ventricles, thereby accelerating cardiac decompensation.

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