Hemodynamics is a key factor in the management of acute respiratory distress syndrome (ARDS), as hemodynamic compromise is associated with mortality and its incidence is between 50 and 70% [1]. In around one half of ARDS patients with hemodynamic compromise, the main mechanism is right ventricular (RV) failure related to an abrupt increase in pulmonary vascular resistance with loss of perfused vascular tissue bed because of microthrombi, pulmonary vasoconstriction, and endothelial dysfunction, but also because of the consequences of mechanical ventilation itself with its generated excessive transpulmonary pressure. In the other half of patients, hemodynamic compromise is due to sepsis, which is frequently associated with ARDS. The Berlin Consensus defined ARDS and recommended a respiratory strategy, unfortunately only based on the PaO₂/FiO₂ ratio without any mention of hemodynamic status [2]. A more recent guideline recommended avoidance of excessively high a positive end-expiratory pressure (PEEP) when it induces hemodynamic worsening [3]. This high PEEP strategy, when combined with an aggressive recruitment maneuver, worsens hemodynamics and increases mortality [4]. Hemodynamic failure interferes with blood gases which seriously limits the evaluation of ARDS severity based on oxygenation. A low cardiac output at constant shunt can overestimate the degree of lung injury by decreasing PaO₂ through a decrease in PvO₂; conversely, it can decrease the computed shunt fraction, thus underestimating severity; finally, RV overload can re-open the patent foramen ovale leading to intracardiac shunt.