ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) is associated with high mortality (up to 46%) despite best standards of supportive care. 1 One of the major determinants of mortality in severe ARDS is hemodynamic instability, in particular pulmonary vascular dysfunction and right ventricular (RV) dysfunction/failure 2,3 ; however, cardiopulmonary interactions in the context of ARDS are not understood fully. In most ARDS studies, RV failure is defined as "acute cor pulmonale" (ACP), which refers to an abrupt increase in RV afterload. On echocardiography, this is characterized by septal dyskinesia and RV dilatation with a ratio of RV end-diastolic area (RVEDA) to left ventricular end-diastolic area (LVEDA) 4 0.6 and 41 for severe ACP. 4,5 A recent risk score developed for the prediction of ACP in ARDS demonstrated several important clinical and physiologic parameters: (a) pneumonia as a cause of ARDS, (b) ratio of arterial oxygen partial pressure to fractional inspired oxygen (PaO 2 / F i O 2) o150 mmHg, (c) arterial carbon dioxide partial pressure (PaCO 2) Z 48 mmHg, and (d) driving pressure Z18 cm H 2 O. 5 The aforementioned variables have a statistically significant correlation with development of ACP with a reported incidence of 19%, 34%, and 74% in ARDS patients with risk scores of 2, 3, and 4, respectively. 5