The Vicious Cycle of Dyspnea and Heart Failure - The 65th Annual Conference of the Israel Heart Society & The Israel Society of Cardiothoracic Surgery, 24-25 April 2018

אנה פיינגרש Biomedical Engineering, Technion - Israel Institute of Technology, Haifa, Israel Shmuel Rispler Cardiology, Rambam Health Care Campus, Haifa, Israel Eugenia Nikolsky Cardiology, Rambam Health Care Campus, Haifa, Israel Yuval Cohen Cardiology, Rambam Health Care Campus, Haifa, Israel Arthur Kerner Cardiology, Rambam Health Care Campus, Haifa, Israel Sergey Yalonetsky Cardiology, Rambam Health Care Campus, Haifa, Israel Amnon Eitan Cardiology, Rambam Health Care Campus, Haifa, Israel Ariel Roguin Cardiology, Rambam Health Care Campus, Haifa, Israel Amir Landesberg Biomedical Engineering, Technion - Israel Institute of Technology, Haifa, Israel

Introduction: Heart failure (HF) is characterized by decompensation phases. We hypothesized that (1) decompensation results into dyspnea, mainly due to increased respiratory effort; (2) dyspnea degree can be quantified by respiratory effort severity; (3) increase in respiratory effort causes further heart failure deterioration.

Methods: The study enrolled a total of 13 patients undergoing right-heart catheterization to clarify dyspnea diagnosis. Additionally to the standard parameters, measurements of respiratory flow and chest wall dynamics were obtained using facial mask and three motion sensors. Pulmonary wedge pressure was separated into two waves: the respiratory wave (P_RESP) and the capillary transmural pressure (P_CT).

Results: According to right-heart catheterization, 3/13 patients had primary pulmonary hypertension, 8/13 left-sided HF (preserved or reduced) and 2/13 had no evidence of pulmonary hypertension. Remarkably, P_RESP values were very high - up to 43 mmHg in HF patients, and there was high correlation between P_RESP (surrogate of dyspnea) and P_CT (r = 0.76). Namely, every 1.6 mmHg elevation in P_RESP corresponded to 1 mmHg increase in P_CT. This raises the question of cause/consequence relationships. An increase in the wedge-pressure increases pulmonary capillary pressure, leading to "capillary stiffness“ resulting into decreased lung`s compliance. The associated congestion increases lung`s viscosity. These two mechanisms intensify the required respiratory work. As for the vicious feedback, elevated P_RESP increases LV afterload, while elevated P_CTaffects the RV afterload. In addition, the left and right atrial V-waves (filling) were significantly and oppositely modulated by respiration. An increase in P_RESP in HF patients was associated with more pronounced RA filling and with lower LA filling, possibly contributing to further lung congestion.

Conclusions: The respiratory dynamics and P_RESP may be used as a surrogate of the respiratory effort and allow quantification of dyspnea severity. The respiratory effort plays a pivot role in the vicious cycle of cardiac decompensation.

Capillary transmural pressure vs. respiratory pressure. Circles - mean values, whiskers - the range, thick black line - mean values linear fitting (correlation coefficient = 0.76).