Right-sided heart failure in acute respiratory distress syndrome

Right-sided heart dysfunction (RHD) has emerged as a critical yet often underappreciated aspect of acute respiratory distress syndrome (ARDS). This review describes the role of RHD in ARDS, providing an updated overview of its pathophysiology, diagnosis and potential treatments. Several mechanisms contribute to increased right ventricular (RV) afterload in ARDS, including hypoxic vasoconstriction, hypercapnia, acidosis, in situ thrombosis and an imbalance between pulmonary vasoconstrictors and vasodilators. Mechanical ventilation, a cornerstone in ARDS management, can worsen haemodynamic instability due to impaired lung compliance. Systemic implications of RHD include renal dysfunction due to impaired organ perfusion and venous congestion. Volume overload further exacerbates RV strain, setting off a vicious cycle of deteriorating RV function, interventricular septal bowing, reduced left ventricular preload and ultimately circulatory failure. The diagnosis and management of RHD in ARDS require an integrated approach that combines invasive haemodynamic monitoring, imaging techniques and noninvasive assessments. Specific treatment options targeting RHD in ARDS remain limited. Titration of positive end-expiratory pressure plays a critical role in mitigating RHD. Prone positioning has shown inconsistent effects on RV function which require further investigation. Inhaled pulmonary vasodilators, such as nitric oxide and prostacyclins, are commonly used to modulate pulmonary vascular tone in ARDS. Small studies suggest that levosimendan and commonly used vasoactive drugs such as norepinephrine, epinephrine, vasopressin and milrinone may improve RV function in ARDS. However, no pharmacologic treatment is specifically approved for ARDS-associated RHD. Large-scale clinical trials are necessary to identify the most effective treatment strategies for specific patient populations.