Cardiopulmonary interaction during spontaneous breathing and mechanical ventilation

Cardiopulmonary interaction is a fundamental physiological process during spontaneous breathing, but it is profoundly altered in critically ill patients receiving mechanical ventilation (MV). Positive-pressure ventilation modifies intrathoracic, pleural, and transpulmonary pressures, with major effects on pulmonary vascular hemodynamics and right ventricular performance. Among these consequences, acute pulmonary hypertension (aPH) has emerged as a clinically relevant yet frequently underrecognized complication. This review summarizes the current evidence on cardiopulmonary interaction during spontaneous breathing and MV, with particular emphasis on the mechanisms driving aPH and right ventricular dysfunction in critically ill patients. A narrative review was performed using PubMed, Embase, Scopus, Web of Science, and the Cochrane Library. Free-text terms and controlled vocabulary related to positive-pressure ventilation, right ventricular dysfunction, pulmonary hypertension (PH), pulmonary vascular resistance (PVR), right heart catheterization, intensive care, and respiratory compliance were combined using Boolean operators. Priority was given to studies involving adult patients, including systematic reviews, observational studies, clinical trials, and relevant reference lists. During spontaneous breathing, cardiopulmonary interaction is governed by negative intrathoracic pressure, venous return (VR), transpulmonary pressure, and physiological ventilation-perfusion relationships. In contrast, MV reverses this physiological pressure profile and may reduce VR, increase right ventricular afterload, impair ventricular interdependence, and increase PVR. High tidal volumes, excessive positive end-expiratory pressure, increased plateau pressure, hypercapnia, hypoxemia, alveolar overdistension, and diffuse lung injury all contribute to aPH, potentially disrupting right ventricle-pulmonary artery coupling and promoting right ventricular dysfunction. MV profoundly reshapes cardiopulmonary physiology and may precipitate aPH and right ventricular dysfunction. Early recognition of these mechanisms and the application of protective ventilatory strategies are essential to reduce pulmonary and hemodynamic complications.