Right ventricular-protective ventilation in acute respiratory distress syndrome: phenotypes, monitoring and ventilatory management.

Despite the widespread implementation of lung-protective ventilation, mortality in acute respiratory distress syndrome (ARDS) remains substantial, underscoring the importance of extrapulmonary determinants of outcome. Right ventricular (RV) dysfunction is recognised as a frequent and clinically meaningful complication of ARDS, affecting a sizeable proportion of patients and consistently associated with adverse outcomes. ARDS-related pulmonary vascular injury, including hypoxic pulmonary vasoconstriction, hypercapnia and acidosis, microangiopathy, and an imbalance in vasoconstrictor/vasodilator signalling, reduces the functional pulmonary vascular bed and increases pulmonary vascular resistance, thereby imposing an acute afterload challenge on the thin-walled right ventricle. Mechanical ventilation may further exacerbate RV stress through alveolar overdistension, increased intrathoracic pressure and decreased venous return, promoting RV dilation, RV-pulmonary arterial uncoupling and circulatory collapse in severe cases. In this review, we summarise the pathophysiological basis of RV injury in ARDS and propose a physiology-informed clinical framework integrating RV phenotyping with multimodal monitoring. This includes echocardiography as the bedside cornerstone, selected invasive haemodynamic assessments and emerging noninvasive techniques such as electrical impedance tomography, as well as advanced cardiac imaging modalities and serological biomarkers for complementary assessment. We further discuss key components of RV-protective ventilation, including limitation of tidal volume and airway pressures, haemodynamics and recruitability-guided positive end-expiratory pressure titration, cautious use of permissive hypercapnia, avoidance of excessive mean airway pressure, prone positioning, appropriate application of spontaneous breathing and extracorporeal support to facilitate ultra-protective lung ventilation. Finally, we highlight unresolved clinical questions and emphasise the need for prospective studies incorporating standardised RV phenotypes and RV-centred end-points.