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Background Hemodynamic congestion appears days prior to the development of clinical congestion. Lung congestion is associated with increased respiratory effort and dyspnoea. The effects of increased respiratory effort on pulmonary circulation were not well-defined. Purpose The study investigates the cardiopulmonary interactions and the role of the respiratory effort in the development of decompensation. It is well-accepted that lung congestion affects the lung mechanics and increases the respiratory effort. On the other hand, changes in the intrathoracic and alveolar pressures, due to the increase in the respiratory effort, may have detrimental effects on the pulmonary circulation and the workloads of the heart. Methods We have simultaneously measured the hemodynamic indices and the respiratory mechanics in patients undergoing right heart catheterization (n=56) for the diagnosis of dyspnoea. The patients were classified either as heart failure (HF) or lung disease, according to their clinical history, symptoms and signs. The pulmonary capillary wedge pressure (PCWP) was decomposed into cardiac and respiratory waves. The respiratory effort (Presp) was defined as the respiratory wave amplitude that modulates the PCWP. Lung compliance was calculated as the ratio of the tidal volume to Presp. Results and discussion The HF patients (n=35) exhibited huge Presp of 9.6±3.7 mmHg [2.6–16.7], ∼4 fold the normal Presp, of about 2–3 mmHg (figure below). Their lung compliance decreased with increasing PCWP (2.0±0.4%/mmHg of PCWP). Both PCWP and pulmonary artery pressure (PAP) rose with Presp, by 0.92±0.36 mmHg and 1.68±0.47 mmHg, for 1 mmHg of Presp, respectively (Figure below). Interestingly, PCWP always exceeded Presp, leading to the stipulation of a novel fundamental constraint/law: the continuous pulmonary flow throughout the respiratory cycle requires that PCWP > Presp (above the identity line in figure A), otherwise the capillary pressure will decrease below the surrounding alveolar pressure and the pulmonary circulation will collapse, especially during inspiration. This constraint imposes a positive feedback of Presp on the pulmonary circulatory pressures. It is also supported by the increase in PWCP with Presp in the patients with lung diseases (Figure A). The bigger rise in PAP than in PWCP is attributed to the increase in the pulmonary vascular resistance (PVR) with Presp (0.3±0.06 wood units for 1mmHg Presp). The latter constructs additional positive feedback of Presp on the cardiac workload. A decrease in the intrathoracic pressure that surrounds the heart increases the LV apparent afterload. The increase in PAP and PVR elevates the right ventricle afterload. PCWP (A) and PAP (B) vs. Presp Conclusions The respiratory effort is not just a hallmark of HF but plays a pivotal role in the cardiopulmonary vicious cycle. An increase in the respiratory effort increases the PWCP, PAP, PVR, and the afterloads of both ventricles, and thereby may accelerate cardiac decompensation.