The 67th Annual Conference of the Israel Heart Society

The cardiopulmonary vicious cycle; An increase in the respiratory effort immediately and proportionally intensifies the hemodynamic congestion

Noa Markovitch 1 Anna Faingersh-Klebanov 1 Shmuel Rispler 2 Yair Feld 2 Amir Solomonica 2 Sergey Yalonetsky 2 Ariel Roguin 3 Arthur Kerner 2 Amir Landesberg 1
1Faculty of Biomedical Engineering, Technion-Israel Institute of Technology, Israel
2Department of Cardiology, Rambam Health Care Campus, Israel
3Department of Cardiology, Hillel Yafe Medical Center, Israel

Introduction: An increase in the pulmonary wedge pressure (PCWP) is associated with an increase in the respiratory effort and the sensation of dyspnea. However the interrelationships between the PCWP and respiratory effort are not well-defined. We hypothesize that an increase in the inspiratory effort decreases the intrapulmonary transvascular pressures and the vascular diameters, especially at the venous side, leading to an increase in the post-capillary resistance to flow and elevation of PCWP.

Methods: We investigated the cardiopulmonary interactions by simultaneously measuring hemodynamic and respiratory indices in patients undergoing right heart catheterization. The immediate effects of the respiratory effort were analyzed by asking the patients to perform short events of apnea and vigorous breathing. 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: The resting end-expiratory PCWP rose with PRESP, by 0.7±0.11 mmHg and 0.41±0.05 mmHg for every 1 mmHg of PRESP in the heart (n=30,p=0.04) or isolated lung (n=9,p=0.11) patients, respectively. The pulmonary artery pressure (PAP) rose with PRESP by 1.35±0.15 mmHg in the heart group (p<0.01).

Intentional changes in the respiratory effort had immediate effect on PCWP, within a single breathing-cycle (t =1.72±0.36[sec]) in all patients (n=39). A tight linear correlation was found between breath to breath changes in the end-expiratory lower PCWP envelope and the PRESP. Interestingly, similar changes in the PCWP with PRESP were obtained in all the patients (slope of 0.42±0.16 between the two). Apnea was associated with significant decrease in the PCWP.

Conclusions: An increase in the respiratory effort is not just a result of cardiac decompensation. The respiratory effort has immediate detrimental effects on the PCWP, PAP and the workloads of both ventricles, leading to a cardiopulmonary vicious cycle, where the respiratory effort plays a pivotal role.









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