Ultraprotective ventilation allowed by extracorporeal CO2 removal improves the right ventricular function in acute respiratory distress syndrome patients: a quasi-experimental pilot study.

ABSTRACT

BACKGROUND: Right ventricular (RV) failure is a common complication in moderate-to-severe acute respiratory distress syndrome (ARDS). RV failure is exacerbated by hypercapnic acidosis and overdistension induced by mechanical ventilation. Veno-venous extracorporeal CO2 removal (ECCO2R) might allow ultraprotective ventilation with lower tidal volume (VT) and plateau pressure (Pplat). This study investigated whether ECCO2R therapy could affect RV function. METHODS: This was a quasi-experimental prospective observational pilot study performed in a French medical ICU. Patients with moderate-to-severe ARDS with PaO2/FiO2 ratio between 80 and 150 mmHg were enrolled. An ultraprotective ventilation strategy was used with VT at 4 mL/kg of predicted body weight during the 24 h following the start of a low-flow ECCO2R device. RV function was assessed by transthoracic echocardiography (TTE) during the study protocol. RESULTS: The efficacy of ECCO2R facilitated an ultraprotective strategy in all 18 patients included. We observed a significant improvement in RV systolic function parameters. Tricuspid annular plane systolic excursion (TAPSE) increased significantly under ultraprotective ventilation compared to baseline (from 22.8 to 25.4 mm; p < 0.05). Systolic excursion velocity (S' wave) also increased after the 1-day protocol (from 13.8 m/s to 15.1 m/s; p < 0.05). A significant improvement in the aortic velocity time integral (VTIAo) under ultraprotective ventilation settings was observed (p = 0.05). There were no significant differences in the values of systolic pulmonary arterial pressure (sPAP) and RV preload. CONCLUSION: Low-flow ECCO2R facilitates an ultraprotective ventilation strategy thatwould improve RV function in moderate-to-severe ARDS patients. Improvement in RV contractility appears to be mainly due to a decrease in intrathoracic pressure allowed by ultraprotective ventilation, rather than a reduction of PaCO2.