Key result
Right ventricular-pulmonary arterial (RV-PA) uncoupling in ARDS rapidly leads to right ventricular dilation, decreased left ventricle filling, and systemic circulatory collapse.
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Right ventricular-pulmonary arterial (RV-PA) uncoupling is a critical mechanism driving hemodynamic instability, right heart dysfunction, and mortality in patients with ARDS.
Acute right-sided heart dysfunction is a critical complication present in up to 20% to 50% of patients with ARDS, significantly driving hemodynamic instability and mortality.1 In ARDS, right ventricular-pulmonary arterial (RV-PA) uncoupling—representing a mismatch between right ventricle (RV) contractility and pulmonary vascular load—occurs rapidly because of hypoxic pulmonary vasoconstriction, hypercapnic acidemia, and positive-pressure ventilation. Understanding this ventriculoarterial interaction is vital, because a sudden increase in effective pulmonary arterial elastance exceeds the acute adaptive limits of RV contractility, leading to RV dilation, diastolic septal shift, decreased left ventricle (LV) filling, and systemic circulatory collapse.
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Gasca-Aldama et al. (2026) conducted a review in ARDS. Right ventricular-pulmonary arterial (RV-PA) uncoupling was evaluated. Right ventricular-pulmonary arterial (RV-PA) uncoupling in ARDS rapidly leads to right ventricular dilation, decreased left ventricle filling, and systemic circulatory collapse.
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