Severe acute respiratory distress syndrome (ARDS) confers significant in-hospital mortality despite implementation of evidence-based ventilatory strategies.^1–3 Acute right ventricular (RV) injury characterized by abnormal RV and pulmonary vascular biomechanics is one of the major determinants of short-term mortality in patients with severe ARDS.^4,5 The reported prevalence of RV injury in ARDS (defined as RV dysfunction, acute cor-pulmonale (ACP), RV dysfunction with hemodynamic compromise, or RV failure) is 21%.⁴ A universal RV injury definition is however lacking and a spectrum of different phenotypes and subphenotypes (from RV diastolic dysfunction to advanced RV injury/failure) have been linked to mortality in patient populations with ARDS.^6–9 The main mechanisms of pulmonary vascular dysfunction and RV injury in ARDS include: obstruction due to thrombosis and remodeling; compression due to elevated extravascular lung water and injurious invasive ventilation; and constriction due to hypercapnia, hypoxemia, and acidemia. The resultant acute pulmonary hypertension and negative diastolic interaction between the right and left ventricle (LV) may lead to RV dilatation with or without systemic venous congestion, uncoupling between the RV and the pulmonary circulation, reduced LV filling and shock.^7,10