Guia, Miguel FilipePaula, FernandaPinto, PaulaFroes, Filipe2020-09-162020-09-162020Rev Port Cardiol. 2020;39(9):551-5520870-2551http://hdl.handle.net/10451/44381© 2020 Published by Elsevier España, S.L.U. on behalf of Sociedade Portuguesa de Cardiologia. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).Management of respiratory failure (RF) in pulmonary hypertension (PH) is a complex subject, since positive pressure ventilation (PPV) can reduce right ventricular (RV) output. During PPV there is an increase in intrathoracic pressure, increasing right atrial pressure. This leads to lower venous return and consequently to decreased RV preload and output. Furthermore, pulmonary vascular resistance (PVR), the main determinant of RV afterload, is directly affected by changes in lung volume, since when the lung is hyperinflated, alveolar distension occurs, leading to compression of the alveolar vessels. On the other hand, low lung volumes result in terminal airway collapse and hypoxic vasoconstriction, and parenchymal vessels also become more tortuous and predisposed to collapse.All the above factorstend to reduce left ventricular output, leading to systemic hypotension.engjournal article10.1016/j.repc.2020.01.0092174-2030