The Cardiopulmonary Vicious Cycle; A Novel Paradigm for Understanding Cardiac Decompensation

Background: Dyspnea is the cardinal symptom of heart failure (HF) and the main limit during exercise. The underlying mechanisms are not well-known. We hypothesize that an increase in the inspiratory effort decreases the transvascular pressure, especially at the venous side of the pulmonary system, leading to an increase in the post-capillary resistance to flow. Consequently, an increase in the respiratory effort is associated with an increase in the pulmonary capillary wedge pressure (PCWP) and a decrease in lung compliance. Thus, there is a cardiopulmonary vicious cycle, whereby an increase in the respiratory effort increases the loads of both ventricles and decreases lung functions, leading to progressive cardiopulmonary deterioration.

Methods: We investigated the cardiopulmonary interactions by simultaneously measuring hemodynamic and respiratory indices in patients undergoing right heart catheterization (n=40) for the diagnosis of dyspnea. The PCWP was decomposed into cardiac and respiratory waves. The respiratory effort (P_RESP) was defined as the respiratory wave amplitude that modulates the PCWP.

Results: In all patients (HF, lung, Mix, normal), both PCWP and pulmonary artery pressure (PAP) rose with P_RESP, by 0.84±0.04 mmHg and 1.23±0.11 mmHg for every 1 mmHg of P_RESP, respectively. Changes in respiratory pattern and P_RESP had immediate (t =1.72±0.36[sec]) effects on PCWP and a tight linear correlation was found between P_RESP and the minimum end-expiratory PCWP in all the patients (slope of 0.42±0.16).

Conclusions: An increase in the respiratory effort is not just a hallmark of cardiac decompensation. The respiratory effort plays a pivotal role in the vicious cardiopulmonary cycle.