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Right ventricular dysfunction in acute respiratory distress syndrome: from cardiopulmonary mechanisms to precision management—a narrative review
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DOI：10.1016/j.bja.2026.07.002.png)
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Abstract
En 中文
Acute respiratory distress syndrome (ARDS) is defined by severe hypoxaemia and bilateral pulmonary infiltrates, yet clinical outcomes are not determined by gas exchange alone. Increasing evidence suggests that right ventricular (RV) dysfunction is a frequent and clinically relevant complication, reflecting the combined effects of pulmonary vascular injury and mechanical ventilation. In this narrative review, we examine the mechanisms through which inflammatory lung injury, pulmonary vascular dysfunction, and mechanical ventilation contribute to RV–pulmonary arterial uncoupling. We discuss how hypoxic vasoconstriction, microvascular thrombosis, endothelial dysfunction, hypercapnia, driving pressure, intra-abdominal pressure, transpulmonary and transdiaphragmatic pressures, and inappropriate PEEP together increase pulmonary vascular load beyond the adaptive capacity of the RV. Extracardiac factors, including fluid accumulation, venous congestion, and abdominal–thoracic interactions, further influence RV loading conditions but are often under-recognised in ARDS. We also review the clinical features of acute cor pulmonale and its association with increased mortality. We emphasise the importance of systematic bedside assessment integrating echocardiography, invasive haemodynamics, ventilatory variables, while acknowledging the limitations of current biomarkers and diagnostic tools. Finally, we discuss the therapeutic implications of RV dysfunction, outlining how ventilatory management, fluid strategy, vasoactive support, prone positioning, and extracorporeal life support can be informed by RV physiology. Recognition of RV dysfunction can improve physiological assessment and individualised cardiopulmonary management in ARDS.
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